February 17, 1998
AM Session
STATE OF MINNESOTA
DISTRICT COURT COUNTY OF RAMSEY
SECOND JUDICIAL DISTRICT
File No. C1-94-8565
The State of Minnesota, by Hubert H. Humphrey, III, its attorney general, and Blue Cross and Blue Shield of Minnesota,
Plaintiffs,
vs.
Philip Morris Incorporated, R.J. Reynolds Tobacco Company, Brown & Williamson Tobacco Corporation, B.A.T. Industries P.L.C., Lorillard Tobacco Company, The American Tobacco Company, Liggett Group, Inc., The Council for Tobacco Research-U.S.A., Inc., and The Tobacco Institute, Inc.,
Defendants.
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THE CLERK: All rise. Ramsey County District Court is now in session, the Honorable Kenneth J. Fitzpatrick now presiding.
(Jury enters the courtroom.)
THE CLERK: Please be seated.
THE COURT: Good morning.
(Collective "Good morning.")
MR. CIRESI: Proceed?
Thank you, Your Honor.
(Videotape played.)
MR. CIRESI: Your Honor, the exhibit that will now be identified in the deposition is trial Exhibit No. 3681.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 1504 is Trial Exhibit No. 3683, and we will offer that.
MR. GARNICK: No objection.
THE COURT: Could you stop the deposition, please.
(Videotape stopped.)
THE COURT: Trial Exhibit 3683 will be received.
Could you wait until it's been -- if there's been an offer, wait for any objection and the determination by the court, please.
Thank you.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, we will offer Trial Exhibit 3684, which is identified in the deposition as Exhibit 1505.
MR. GARNICK: No objection.
THE COURT: Court will receive 3684.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Exhibit 1506 in the deposition is Trial Exhibit No. 3685, and we offer it.
MR. GARNICK: No objection.
THE COURT: Court will receive Trial Exhibit 3685.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 103 will be offered as Trial Exhibit No. 2513.
MR. GARNICK: No objection.
THE COURT: Court will receive 2513.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 1514 will be Trial Exhibit No. 3693, and we'd offer it.
MR. GARNICK: No objection.
THE COURT: Court will receive 3693.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 126 will be offered as Trial Exhibit No. 2536.
MR. GARNICK: No objection.
THE COURT: Court will receive 2536.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 1516 will be offered as Trial Exhibit No. 3695.
MR. GARNICK: No objection.
THE COURT: Court will receive 3695.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, the next exhibit will be Deposition Exhibit 1517, which will be offered as Trial Exhibit 3696.
MR. GARNICK: No objection.
THE COURT: Court will receive 3696.
(Videotape continued to be played.)
MR. CIRESI: The next exhibit is Deposition Exhibit 1518, which will be offered as Trial Exhibit 3697.
MR. GARNICK: No objection.
THE COURT: Court will receive 3697.
(Videotape continued to be played.)
MR. GARNICK: Objection to the next question and answer, Your Honor, as being inconsistent with the court's order. Counsel is testifying, and the question relates to periods of time that go beyond Dr. Osdene's tenure.
THE COURT: The objection is sustained.
MR. CIRESI: The next exhibit, Your Honor, will be --
THE COURT: Counsel, excuse me, counsel. As I understand it, that's page 93, lines nine through 12; is that correct?
MR. CIRESI: That is correct.
MR. GARNICK: Yes.
MR. CIRESI: Through 13, Your Honor.
MR. GARNICK: Through 13.
THE COURT: Through 13. I just want the record to show that.
MR. CIRESI: The next deposition exhibit will be 1519, which will be offered as Trial Exhibit 3698.
MR. GARNICK: No objection.
THE COURT: Court will receive 3698.
(Videotape continued to be played.)
MR. CIRESI: The next deposition exhibit is 1520, which will be offered as Trial Exhibit 3699.
MR. GARNICK: No objection.
THE COURT: Court will receive 3699.
(Videotape continued to be played.)
MR. GARNICK: Objection. Same basic grounds as before that is in Your Honor's order, it goes beyond the document, and also it's not limited in time to Dr. Osdene's tenure.
MR. CIRESI: Just asking whether he recalled, Your Honor, which is limited by its question to the time that's related to the exhibit.
THE COURT: The objection is sustained.
MR. GARNICK: And that would be page 132, line 20, to page 133, line two.
MR. CIRESI: The next deposition exhibit, then, would be 145, which will be offered as Trial Exhibit 2554.
MR. GARNICK: No objection.
THE COURT: Court will receive 2554.
(Tape continued to be played.)
MR. CIRESI: Your Honor, the next deposition exhibit, 279, is offered as Trial Exhibit 2688.
MR. GARNICK: If they're offering it, we have no objection.
THE COURT: Court will receive 2688.
(Videotape continued to be played.)
MR. GARNICK: Objection, page 140, line 15 through 21, goes beyond the document, it's not limited in time to Dr. Osdene's tenure, and it is testimony of counsel.
MR. CIRESI: It is directly related to the preceding question, which was the final full paragraph on the second page, and he's being asked a question directly related to that paragraph.
THE COURT: You may respond.
(Videotape continued to be played.)
MR. CIRESI: Exhibit 91 is being offered as Trial Exhibit 2501, Your Honor.
MR. GARNICK: No objection.
THE COURT: Court will receive 2501.
(Videotape continued to be played.)
MR. GARNICK: Objection, again goes beyond the document, beyond that it mischaracterizes Dr. Charles' testimony. And this objection relates to page 142, lines 15 through 21.
MR. CIRESI: This is preparatory to Dr. Charles' testimony which will be offered, Your Honor, and it's also preparatory to asking him a question with regard to his recollection, and it relates specifically to the document in question.
THE COURT: Okay. I'll allow the testimony as subject to a motion to strike after the testimony is received of Dr. Charles.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Exhibit 1529 from the deposition has the Trial Exhibit No. 3708, and we'll offer Exhibit 3708.
MR. GARNICK: No objection.
THE COURT: Court will receive 3708.
(Videotape continued to be played.)
MR. CIRESI: Your Honor, Deposition Exhibit 148 will be offered as Trial Exhibit No. 2557.
MR. GARNICK: No objection.
THE COURT: Court will receive 2557.
(Videotape continued to be played.)
THE COURT: We'll be taking a short recess at this time.
THE CLERK: Court stands in recess.
(Videotape paused at deposition page 229,
line 20.)
(Recess taken.)
THE CLERK: Ramsey County District Court is again in session.
(Jury enters the courtroom.)
THE CLERK: Please be seated.
MR. CIRESI: Thank you, Your Honor. We would offer two previous exhibits that we had not, Your Honor, but were the subject of Dr. Osdene's testimony: Exhibit 3680, which was Deposition Exhibit 1501, and it was at page 37 of the deposition, and Trial Exhibit 3681, which was Deposition Exhibit 1502, and it was at page 41 of the deposition.
MR. GARNICK: No objection.
THE COURT: Court will receive 3680 and 3681.
MR. CIRESI: And the questions now are by Philip Morris's attorney, Mr.
Webb.
(Videotape started at page 230, line 24.)
MR. CIRESI: We have to roll the tape for the next part, Your Honor; that's why it's taking a while.
(Videotape continued to be played.)
MR. CIRESI: That completes the deposition of Dr. Osdene, Your Honor.
We would call Dr. Scott F. Davies to the stand, Your Honor. Dr. Davies.
(Witness sworn.)
THE CLERK: Please state your name and spell your last name for the record.
THE WITNESS: Scott F. Davies, D-a-v-i-e-s.
MR. CIRESI: Doctor, you may want to attach that to your belt. The other -- the other part, not -- there you go.
SCOTT F. DAVIES called as a witness, being first duly sworn, was examined and testified as follows:
BY MR. CIRESI:
Q. Good morning, doctor.
A. Good morning.
Q. Doctor, you reside at 2100 East 43rd Street in Minneapolis, Minnesota?
A. Yes, I do.
Q. And you're presently the director, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine at the Hennepin County Medical Center in Minneapolis?
A. Yes, I am.
Q. And you're also the medical director, chief of medical staff at Vencor Hospital in Golden Valley, Minnesota?
A. Yes, I am.
Q. Doctor, you're here to testify about chronic obstructive pulmonary disease, one of the major smoking-caused diseases?
A. Yes, I am.
Q. Doctor, before we get to your testimony itself, I'd like you to review just briefly your background and education for the jury and the court.
You obtained your B.A. degree from the College of Holy Cross in Massachusetts?
A. Yes, I did.
Q. And then you obtained your M.D. in 1974 from the University of Minnesota?
A. Yes.
Q. And from 1974 to 1975, you were an intern in internal medicine at the University of Minnesota?
A. That's correct.
Q. And from 1975 to 1977, you were a resident in internal medicine at the University of Minnesota; correct?
A. Correct.
Q. With regard to your licensing and certifications, you're a diplomat of the American Board of Internal Medicine?
A. Yes, I am.
Q. You're also a member of the Pulmonary Medicine Subspecialty Boards?
A. Yes.
Q. And you have critical care certification; correct?
A. Correct.
Q. And from 1979 to 1994 you were an assistant professor of medicine at the University of Minnesota Medical School?
A. Yes.
Q. And 1985 to 1994 you were an associate professor of medicine at the University of Minnesota Medical School?
A. Yes.
Q. And from 1994 to the present time you are a professor of medicine at the university's medical school; correct?
A. Yes.
Q. And at the present time you are a course director at the University of Minnesota Medical School in a course entitled "Pathophysiology, Respiratory Medicine?"
A. Yes, I am.
Q. And 1979 to the present time you've also been on the faculty for clinical rotations in pulmonary medicine and critical care medicine at the Hennepin County Medical Center for medical students, medical residents and pulmonary fellows and critical care fellows; is that correct?
A. That is correct.
Q. Can you describe that program a little bit, please, doctor.
A. Well Hennepin County Medical Center is a teaching hospital, one of the four major teaching hospitals of the University of Minnesota. It's a urban, city hospital, and as medical students in their last two years of their training get clinical experience, they rotate and take different rotations or elective rotations at our hospital. And for example, they might do six weeks on an internal medicine ward, and they might do six weeks in an intensive care unit, and they might do six weeks studying pulmonary diseases and that -- by seeing patients and working with the faculty.
The patients in the hospital are generally taken care of by a team, and that team has often a medical student, and then a resident, who's someone who has finished medical school but training to become boarded in internal medicine, and then a faculty member, working together to take care of that patient. And so the students -- about 35 percent of all clinical rotations of Minnesota -- University of Minnesota students are spent at our hospital. It's one of the major teaching sites. And I work with those students and those residents, but in the process of taking care of the patients who come for various different problems.
Q. And doctor, from 1980 up to the present time, how many students at the University of Minnesota Medical School have you taught respiratory medicine to?
A. The second-year course that Mr. Ciresi is referring to is a lecture-type course that goes six weeks in the second -- in the fall of the second year of the medical school, and all the students take that course; it's their introduction to lung diseases. And there's about 200 students, and I've taught the course for 18 years, so basically every student who's come through, over 3,000 students would have taken that course since 1980.
Q. And do you also serve on the faculty at many local and regional post- graduate courses sponsored by various institutions?
A. Yes, I have.
Q. And those institutions would include the Mayo Clinic?
A. Yes.
Q. The University of Michigan?
A. Yes.
Q. And the University of North Dakota?
A. Yes.
Q. And doctor, are you also a member in various professional societies?
A. I am.
Q. Does that include the American Thoracic Society?
A. Yes, it does.
Q. And the American College of Chest Physicians?
A. Yes.
Q. And have you also held various offices and committee assignments in the professional societies that you belong to?
A. Yes, I have.
Q. Have you been the chairman of the Cardiopulmonary Infection Steering Committee of the American College of Chest Physicians?
A. Yes, I have.
Q. Have you also been the president of the Minnesota Thoracic Society?
A. Yes, I have.
Q. Have you also been on the Tuberculosis and Pulmonary Infection Program Committee of the American Thoracic Society, Scientific Assembly on Microbiology?
A. Yes, I have.
Q. And in 1987 to 1982 did you serve as the Governor for the State of Minnesota, the American College of Chest Physicians?
A. Yes, I did.
Q. And doctor, with respect to your primary areas of research at the present time, does that include deep fungal infections?
A. Yes, it does.
Q. And can you describe what that is, please.
A. There are a variety of chronic pneumonias. Most pneumonias are -- we think of, you take an antibiotic and the pneumonia goes away in a week or two, and there's some chronic infections in the lung that last a lot longer and require different antibiotics over a longer period of time, and the one that's most common would be tuberculosis that most people would know about that doesn't go away in a week like a pneumonia, it requires many drugs for many months, and it's sort of more subacute or chronic. There are other chronic pneumonias caused by fungal organisms that you inhale from the soil. Some of them are common in southern Minnesota and northern Minnesota. And they also present like -- not like a bacterial pneumonia where it goes away in a week with an antibiotic, but requiring many months of treatment and presenting a little bit differently. And I've studied the epidemiology of those diseases and the treatment and various clinical -- clinically-related aspects of those diseases.
Q. And have you also done major research in obstructive sleep apnea?
A. I'm part of the faculty at the Minnesota Regional Sleep Disorder Center, which has been in existence since 1978, and it's done a lot of research learning different things about sleep disorders.
Q. And you can tell us what sleep apnea, doctor?
A. Sleep apnea is sort of -- everyone has seen someone snore. It's the far end of snoring where the snoring gets so loud that it's not just rattling the room, but the patient actually sort of chokes and obstructs and then has to wake themselves up again to get breathing again. And those snorers get very tired during day because their sleep is so fragmented and choppy and disruptive. That's what sleep apnea is.
Q. And doctor, during the course of your career have you published in excess of a hundred articles in peer-reviewed journals and books that are used by other physicians?
A. Yes, I have.
Q. And with respect to your practice itself, doctor, is about 20 percent of it spent in treating chronic obstructive pulmonary disease?
A. Ten to 20 percent of my inpatient practice and a slightly higher percentage of my outpatient practice would be seeing patients with chronic obstructive lung disease. I see them every single day when I'm in the hospital and every single day when I'm in the clinic, patients with this problem.
Q. Doctor, can you describe what is chronic obstructive pulmonary disease?
A. The -- the pulmonary part, "pulmonary" just means lung, so it's a lung disease, and the "disease" itself is explanatory. What "obstructive" means is that there's a problem with emptying the lungs. The lungs can't empty normally, so there's obstruction to air flow during exhaling, exhaling is impeded and slowed. And the "chronic" means that the condition is permanent, that it cannot go away. It can partly get better sometimes, but it cannot go away. So "chronic" means a permanent condition in which there's obstruction or slowing of expiration, the patients can't exhale normally. And the "pulmonary" is just that it's the -- it involves the lung and that it is a major disease.
Q. Doctor, how does that compare with like asthma?
A. Asthma also has airflow obstruction and patients with asthma can't empty their lungs. And it's a pulmonary disease. But asthma, the obstruction is due to spasm of the smooth muscles around the little air tubes, and secretions, so that it is not a chronic disease, it can -- in the sense that an attack of asthma can reverse. And someone with asthma can come in at another time when they've been well treated and are not having symptoms and have normal lung function with no obstruction. So it's a reversible obstructive airway disease would be asthma, whereas COPD is a chronic, irreversible sort of like an asthma attack that can never end, that will last forever.
Q. Doctor, we've had Drs. Hurt and Dr. Samet and Dr. Robertson describe for the jury and the court the anatomy of the lung. But I'd like to have you touch briefly on it with respect to how it will impact your testimony here.
Could you go to the exhibit book in front of you and please direct your attention to Exhibit 30054.
MR. CIRESI: Which we would offer for illustrative purposes, Your Honor.
MR. MONICA: Your Honor, I object to counsel summarizing or attempting to summarize testimony from prior witnesses and ask that counsel be instructed to just ask direct questions.
THE COURT: Well I think the question is pretty preliminary.
MR. CIRESI: It was, Your Honor.
THE COURT: I'll let it stand.
MR. CIRESI: Is there an objection to 30054 for illustrative purposes?
MR. MONICA: There is no objection.
THE COURT: The court will receive 30054.
BY MR. CIRESI:
Q. Doctor, if we can start with maybe the depiction in the upper third and work our way down, and if you could describe what is being represented by this exhibit.
A. It's my understanding that you've been shown some normal anatomy of the lungs and how the windpipe is the biggest tube, and then it divides into ever- smaller tubes, so there's a series of branching tubes that carry the air out into the lung tissue. And where we're starting, up on the right part -- this won't show on the screen, but if we start on the very upper right is one of the very small tubes that's already branched 15 times, so it's getting through the -- what's called the conducting airways or the tubes that bring the airway to the lung and it's getting close to the business end of the lung where the oxygen actually goes into the blood and the carbon dioxide comes out into the gas so you can exhale it. This last -- the bronchus at the upper right entering the screen is labeled "Terminal Bronchiole," and that's because it's one of the small terminal broncioles that leads to the business end of the lung where the gas exchange comes to. And then you can see that the next branch of tubes has a few little sacs off the edges, it starts to get little tiny sacs around the edges, not all the way along, but sort of scattered along that tube, and that's called the respirator bronchiole, of which there are several branchings of that. So it means they have some parts in gas exchange because there's little sacs, air sacs actually coming off the tubes, and then it goes all the way to the end, you can see that the little air spaces have sacs all the way around them, and that's all they do. It's done conducting air down, and that's just where the air sits and gas exchange occurs. So this is sort of the terminal, business-end of the lung.
Q. And doctor, at the end you were talking about the alveolar sacs?
A. The alveolar sacs are these little tiny sort of blisters around the edge of those round alveolar ducts at the end.
Q. Can you then describe what is being depicted in the middle third, doctor, of this Exhibit 30054.
A. What --
Can we come down just one second to the top again?
Q. Yes.
A. Because what -- what's important is that when we talk about obstruction, or patients not being able to exhale the air from their lungs, it's chronic obstructive lung disease, and where that happens is in these very small airways, the very small airways are -- that sort of limiting factor for air getting out of this lung and back up into the windpipe and the other bigger pipes that carry it out of -- out of the lung. And the -- the -- so that right where you see the respiratory broncioles is where the obstruction and the problem with can't exhale develops. Patients can't exhale because of problems right in that particular area.
And the two kinds of problems that occur are both related to smoking, and the first is that there are inflammatory cells that gather in that area, inflammatory cells just like would gather in a boil, if you had a boil on your skin they gather there, and they can cause scarring and secretions and narrowing, and that can sort of block the exit of air from the lungs. And the second thing that happens is the lung starts to dissolve right at that point, and the --
In fact, expansion of these air spaces beyond the terminal bronchiole is what the definition of emphysema is, and you've all heard the word "emphysema." It's just large air spaces beyond the terminal broncioles.
So that if we can go up to the second picture, this shows what's called centrilobular emphysema, which is just called that because it's right where these -- these small air tubes come off the respiratory bronchiole, before you get out to the little alveolar sacs at the end. And as the lung tissue gets dissolved, these spaces get larger and larger and larger. So that -- normally they're microscopic, and they become so large that they're even visible to the naked eye as the lung expands.
The next -- the bottom one just shows what's called panlobular emphysema, where the whole air space is totally dissolved, not only the proximal tubes, but all the way out, involving the little tiny air sacs. And it's changes in this -- in this lung, it's -- it's anatomic and pathological changes in this lung that make it not empty, as I'll show you in a minute. But this is where the action occurs, and this is why patients have obstructions. Can't --
Chronic obstructive lung disease, the obstruction is cannot empty the lung of air, and the chronic means it's an irreversible condition.
Q. Doctor, can you direct your attention now to Exhibit 30056.
MR. CIRESI: Which again, Your Honor, we'd offer for illustrative purposes.
MR. MONICA: No objection.
THE COURT: Court will receive 30056 for illustrative purposes.
A. Now there is a little schematic that's just taking one of those respiratory bronchioles that were coming off -- the first branch that were coming off there, starting to get little air sacs, entering the -- the business unit of the lung, and cutting it in side -- sideways, so it's a cross-section of one of these little terminal broncioles. It's a schematic, I drew it, and it's not an actual picture of tissue, but it illustrates what's happening at that point in the lung.
So it says at the top COPD is an obstructive lung disease, that means the lungs cannot empty and that the obstruction, the site of major obstruction occurs in these small peripheral airways. And it has several features why this lung won't empty. Normally when you just relax your lungs -- lungs empty all by themselves. One of the reasons is that there's all these inflammatory cells that gather in and around this airway, and they're marked by little while circles, and they cause swelling and they cause edema and they cause scarring.
Q. What's edema, doctor?
A. Edema is just swelling in the tissue like you might get if you get a burn, and right over a welt -- you know, fluid would come into the tissue and you can see it and it would be raised over your skin.
And the infection-fighting cells are exactly what would happen if you have a boil, and the boil, you know, if you puncture it, there's yellow pus in there, and the cells come in and sit around the airway like that, and even through the wall of the airway. And then in the center I'm trying to show that there are secretions and pus that are in the airway. And you can hear people cough this up when they have -- when they have to get that deep phlegm out of these airways.
So that the two things that this inflammation at this site does is it causes fibrosis and scarring on this airway, which narrows it, and that keeps the lung from emptying. But it also -- these cells are loaded with elastases, and elastases are like meat tenderizer and they break down various tissue structures. And what they will do is start dissolving some of these alveolar walls that normally connect to these small airways. Because the airways have to go through the lung, and so there's lung tissue around them, and normally that lung tissue helps hold them open when you breathe out. And as these alveolar walls are destroyed by the elastases, that's how you get these bigger spaces in the same area, these air spaces that are emphysema.
So when that happens, when these airways are no longer tethered open by tissue, then they tend to be floppy and collapse as you breathe out. So that's the second way in which obstruction occurs, is that these small airways are not supported, they're not tethered open, so they tend to narrow and collapse as the patient breathes out. That's why it's an obstructive disease.
Q. Doctor, we've all had the experience of blowing up a balloon and it's elastic.
A. Right.
Q. And then it loses its -- its resilience, if you will.
A. Right.
Q. Is there any analogous situation?
A. I think on the next slide I was going to show exactly that.
Q. Let me direct your attention, then, to Exhibit 30053.
MR. CIRESI: And we'd offer that for illustrative purposes, Your Honor.
MR. MONICA: No objection.
THE COURT: Court will receive 30053 for illustrative purposes.
A. So in the --
On the top is just the normal situation, again very schematic. Here there's only two alveoli or two air spaces being shown, when in reality there's a hundred million of them. So it's a two-compartment little schematic. And it shows that that's what the normal lung looks like, and the pipes leading to this air space are fairly rigid and they're not narrowed, and they're also stretched open by the tethering tissue around them. Also, the alveoli themselves, as they're stretched, have an elastic property like a balloon, so that they tend to want to empty as soon as you've inflated your lungs. You do the work taking the breath in, and you just relax and the breath empties very naturally without you feeling it or doing any work or using any muscles, and part of that is you stretch the lung and it's like a balloon, and then the pipes are open, and the pipes are well supported and the pipes aren't narrow, and the air just comes out very naturally without any sense of work.
Now the bottom two slides show what happens in COPD. And on the left is illustrated simply the fact that if all this inflammation of these tiny airways causes scarring and secretions and narrowing, that those balloons are not going to be able to empty through those narrowed pipes. So it's a disease where you cannot exhale. And on the right shows you an area of the lung where the supporting tissue has been dissolved, the alveolar walls have been dissolved, and these air spaces are -- are bigger and larger.
And that has two different effects. One is that the airways aren't tethered open by tissues so they tend to just collapse and are floppy, but the other effect is that the balloon has lost all of its elastic properties, so it can't empty partly because it's just distended, and so all of the walls and all the elastic tissue has been dissolved, and just like -- thinking of a rubber balloon that's made of thick rubber and is very hard to blow up, it's going to empty very easily, whereas if you made a balloon of something that was like -- more like Saran Wrap and didn't have any elastic, it's just going to sit there and it's not going to empty very well.
So there's three main factors related to the can't empty part, and all of them are permanent, that's why we call it chronic obstructive lung disease, and the obstruction is related to three factors, scarring and secretions and narrowing of these small airways due to the inflammatory cells, lots of tethering due to the dissolving of the little connections that hold the airways open, due again to the inflammatory cells that gather there, and finally destruction of the lung so it becomes a balloon that hasn't got thick rubber any more and it can't sort of empty forcefully when you relax.
And for all those reasons, what we're used to is taking a breath again, and with an active use of our diaphragm and our muscles, and then relaxing and the lung will just empty, nice and normal. And in these patients, they can not empty, the lungs can't empty normally, and that's what the word "obstruction" is talking about.
Q. Now doctor, do we have some human lungs here that were freeze dried to show a normal lung and one with emphysema?
A. Yes, we did.
Q. Could you step down, please.
MR. CIRESI: Your Honor, could the doctor step down?
Q. Maybe you could -- I could move this up for you, doctor.
A. Well these are --
It's interesting, I saw some of the videos you showed and they looked like just this. But these are real --
MR. MONICA: Your Honor, excuse me, may I lodge an objection, pleases? Your Honor, these lungs, a foundation has not been established as to where they came from and whose lungs they are, and I don't know that this witness has that knowledge, and I would ask that before they be shown to the jury and discussed, that that be established.
MR. CIRESI: Your Honor, these are only being used for illustrative experience. The doctor has had experience in dealing with lungs his entire career, and they're being used for illustrative purposes only to explain to the jury the concept that he's just shown on the illustrative depictions that we've put in, Exhibits 30054, 30056 and 30053.
THE COURT: I think it's appropriate so long as it's just for illustrative purposes.
MR. MONICA: Your Honor, --
MR. CIRESI: Your Honor.
MR. MONICA: -- excuse me, may I go over?
THE COURT: Please.
MR. CIRESI: The normal lung then is Exhibit 30269, 30269, and it's being offered for illustrative purposes only. And he also has a sliced part of the lung, which is Exhibit 30270.
Go ahead, doctor.
A. Okay. First piece is the lung, and it looks like sponge, and you can actually feel it. It's not -- it's sterile and it's not going to cause any harm.
Because these little air sacs are very microscopic, they're tiny, tiny air sacs, just like in a sponge has microscopic, and a sponge has a lot of sponge to it, a lot of tissue to it, and the same is with these lungs, so they have a fairly good structure. And basically as you breathe in through the little air tubes, all the little air sacs inflate, and then you relax and everything empties out to its resting position just naturally with no trouble.
Q. Doctor, could you just maybe move around this side --
A. Sure.
Q. -- so the court and all the jury can see it.
A. Now this is a piece of a similar lung, a normal lung, that's just been sliced with a saw, and what you can do in looking at this is that you can't even see the air sacs. They're so tiny that they're really microscopic, the things I've been showing you on the screen, they're invisible, just like a sponge, you can't look at it and see the individual holes in the sponge, even though you know when you squeeze it and open it, it's going to hold water in those little holes. You can see some of the --
You will see there are holes here in the center, and these are the blood vessels that carry blood to the lung or they're the bigger air tubes that branch through the lung, getting out to the small -- small part. And the units that I'm showing you schematically are very tiny little terminal units of which there are about 60,000 units supplied by one of those, what I showed, terminal broncioles up in the right upper corner of that. And you can all look at this and -- and see that there really is --
Maybe I could pass it around in the tray.
Q. If you put it in the box. If we could, Your Honor.
A. And you can look at this and see that there really is not any visible holes, that the holes are sort of beyong --
Q. Doctor, the clerk will --
You have to let the clerk do that.
(Clerk displays the exhibit to the jury.)
A. I noticed that none of you wanted to really touch it, but if you push on this with your thumb, and it's sort of firm, it's like a firm sponge, and it has tissue to it.
Q. And doctor, do you also have a freeze dried lung of emphysema?
A. We have another lung prepared in the same manner of a patient who died with severe emphysema from -- who was a long smoker.
MR. CIRESI: Your Honor, for illustrative purposes, the doctor will be referring to the Exhibits 30272 and 30273.
A. Now this --
MR. MONICA: Your -- Your Honor, excuse me, we object to these two exhibits. The witness has stated one of them, at least, is from a smoker. That has not been established. I think a foundation needs to be established. I'm not even sure whether this witness has ever seen these before today. And we object to them on that basis.
THE COURT: I think you should establish some foundation.
BY MR. CIRESI:
Q. Doctor, how do you know that that's a smoker's lung?
A. These are from the collection of the pathology laboratory at the University of Minnesota, and the person who has custody of this collection told me that he had in his record that this patient was a smoker.
MR. MONICA: Your Honor, I --
MR. CIRESI: We offer it for illustrative purposes, Your Honor.
MR. MONICA: Your Honor, I object. It's based upon hearsay, and the witness has no first-hand knowledge of these particular lungs.
THE COURT: Okay. I'll allow it for illustrative purposes only.
MR. CIRESI: Doctor, make sure you turn around so everybody can see.
A. Yes, I'm sorry. So this is a lung fixed in the exact identical manner, and this is the whole lung, which doesn't illustrate too much, except that a lot of the tissue has been dissolved, and you can see that it's crinkly and does not have very much substance to it, and that's because these small alveolar sacs have been dissolved and that the spaces with air in it are much, much bigger, and they aren't these microscopic. And that's what emphysema does, is it dissolves the lung tissue. Now we couldn't --
We prepared some sections here, and they're in plastic bags, and you'll notice that the others aren't in plastic bags, and that's because they're so much more fragile that they would fall apart if they weren't in a plastic bag. And when you see at these sections you can actually see the visible holes in the terminal air spaces in the lung that you couldn't see before. When I pass them around, you can just glance at the outer rim and see that there are holes that are so big that they're totally visible to the naked eye. And if you hold it up to the light, you can actually see through it; it's a moth-eaten, dissolved lung where all the tissue that's supposed to form these alveolar walls and hold the gas exchange units in the lung has been dissolved. And this is what emphysema is, it is a dissolving of all these spaces so that the lung becomes moth-eaten and the spaces -- the air spaces beyond the terminal bronchiole are enlarged many times beyond what these normal spaces would be enlarged. And that's what contributes in the three ways that I told you about the inability of this lung to empty. The lung cannot empty. It's an obstructive disease where the patients cannot exhale any more and cannot release the lung -- the air from their lungs because the small air tubes have been narrowed and because there's bigger air spaces so that the -- what air tubes there are are not tethered open by the structure and the tissue of the lung, and because there's no elastic recoil. The other lung snaps back to shape when you stretch it by taking a breath because it's like a thick balloon, and this is just a moth-eaten tissue that has totally lost its structure and can't snap back, so it won't have any elasticity and it can't empty.
MR. CIRESI: Your Honor, could we have the clerk pass those.
(Clerk displays the exhibits to the
jurors.)
Q. Doctor, in the course of your work, do you need to measure lung capacity?
A. Yes. I mentioned, you know, the chronic obstructive lung disease, the obstruction is the fact that the patient can't exhale, and how we determine if someone has it and how we determine how bad it is is by making direct measurements of how well the patient exhales air from their lungs. I told you that the basic problem was that if the person couldn't exhale, that they couldn't empty their lungs normally. And you have to sit and try to think how am I going to -- how am I going to measure that? Eventually, you know, you come up with the idea that you have the patient take a deep breath and blow out as fast as they could, and just measure in some way how fast the air would come out, and that would tell you if there's obstruction to air flow. And that's exactly what we do in the pulmonary lab, is the standard diagnostic test for finding out if you have airway obstruction and finding out how bad it is.
Q. And have you prepared an exhibit which would illustrate what is done, --
A. Yes, I have.
Q. -- and that's 30268?
A. Now --
MR. CIRESI: Your Honor, we would offer 30268 for illustrative purposes.
MR. MONICA: No objection.
THE COURT: Court will receive 30268.
A. Okay. Now this is a graph, and first of all we start at the vertical axis of the graph, and you'll see it says volume, and we're measuring the volume of air that a person can breathe out and we're measuring it in liters, so that there's one, two, three, four and five liters of air. Someone can hold about five liters of air in their lungs. And that volume of air is measured as someone blows it out. And on the right you see it says time, and here in this graph the time is in seconds, one, two, three, four, five, six seconds.
And what we do is we take -- tell the patient, "I want you to take a deep breath, fill your lungs as full as you can with air, and then I want you to breathe it out as hard and as fast as you can until your lungs empty, till they're empty." And we measure exactly what happens to their volume.
And I want you to look only at the top curve for a second, and that's a normal what's called -- this is called the spiro -- spirogram -- spiro is just breathing, gram is a graph of breathing -- and the top line is what's called the normal spirogram. And when the patient -- what you can see is that when the patient breathes out, that little dot where it says FEV1 --
Q. What is FEV, doctor?
A. FEV1 means the --
The F just means that we ask the patient to breathe hard, that they forced their expiration. And E is just the exhaled volume. So it's the forced exhaled volume. The patient takes a big breath and they force it out as fast as they can with a forced exhalation. And the little one just means that that is how much air came out in one second. And that's why if you look where that dot is, it's right above the one second mark on the graph.
And what that shows you is that when a normal person breathes out hard, 80 percent of the air comes out in one second. His lungs -- they're stretched when you take a deep breath, they're really elastic like a stiff balloon, and the pipes that conduct the air out them are held open and they're big enough to empty the lung. And so when you breathe out hard, 80 percent of the air comes out in one second. The rest of the 20 percent comes out in another second or two. So within -- within two or three seconds all of your lung is empty and no more air is coming out, you're just going flat along that curve. So that's what normal lungs are supposed to do. You take a deep breath to the size of your lungs, and if you blow out hard -- you can all try this, you blow out hard and your lungs will be empty in just a second or two and there won't be any more air coming out.
And that's how we measure whether someone has COPD, is by doing a test like this.
Q. Now what is depicted with the second line, which is titled "Moderate Obstruction?"
A. Well the second line is someone who has COPD that's moderately severe, and by -- we mean moderately severe is it's gotten bad enough where in a normal-sized person only about one and a half to two liters of air will come out in one second. And that that reduction is due to the mechanisms that we talked about, the narrowing of the pipes, the dissolving of the tethering of the pipes, and then the loss of elasticity of the lung tissue itself.
And you can see several things about that curve that are different. First of all, if you go up on one second, only about one and a half liters came out, and that's only about a quarter of the air came out in the first second. Instead of 80 percent comes out in the first second, only a quarter of the air came out in the first second. And as long as the patient keeps breathing out and out and out, the lung keeps emptying and emptying and emptying. So it doesn't really get emptied, it just continues emptying until the patient has to stop and take another breath. So this is a lung clearly that can't empty very well. The patient cannot empty the lung.
Then the third graph is just -- it shows what someone with severe, terrible obstruction, and I want you to pay close attention so this because we're going to talk about a patient who has this -- has obstruction this severe and show you an illustration of this. But this is where the FEV1, the amount of air that comes out in one second here, is under one liter of air, so it's about maybe 600 -- .6 tenths of a liter, so it's maybe 20 -- you know, 10 or 20 percent of the lung volume can come out in one second. And you can see that it's slow to come out all the way along the way. It's just the lung cannot empty, and just a little air comes out piece by piece by piece by piece rather than the lung just snapping empty and going right down to empty within two seconds. And that would be someone with very severe obstruction.
And people with moderate obstruction and terrible obstruction, it's not just something you measure in the lab, it's something that translates into real symptoms that cause people real difficulties in -- in living their lives.
Q. How does this manifest itself in terms of a person breathing?
A. Well everybody is -- is different, but patients who have mild obstruction can normally do things pretty well in their day-to-day life. They couldn't run a marathon very well, they couldn't do highly athletic things, but they could walk from place to place and carry on a relatively sedentary job and do okay and not be very bad. When it gets down to moderate obstruction, patients begin to get shortness of breath that interferes with the heavier things they have to do in their day-to-day lives, like walking upstairs, they go to church and there's ten steps up, or if there's a little something unusual or if they have to -- they may be fine walking in from the car, but if they have to carry a 20-pound bag and they get breathless and short of breath and feel hungry for air.
And then when you get to the bottom, the terrible, when the FEV1 gets under a liter, that's where any little activity -- you know, even if the patient is okay at rest, any little activity, walking a few feet, saying eight words, have to take another breath. Doing -- you know, just conversing, walking a little bit, carrying a very light things, anything like that would make the person short of breath. And eventually they end up being in a wheelchair because people have to move them, or a little motorized cart, and they end up with oxygen. Most of the patients have oxygen who have FEV1s under one liter, they have severe obstruction, and they end up with really being very, very disabled. Disabled from work, but disabled also from normal human activities that they're required to have a high quality of life by the severity of the shortness of breath that they have.
Q. Doctor, when someone is breathing with moderate or -- or heavy obstruction or terrible obstruction, is their breathing pattern different than the normal person would have?
A. Well they breathe faster. There's a number of things that -- that they do. They breathe faster because they're short of breath and they're hungry for air, but they also tend to --
One of the problems is because the lung can't empty, when they're ready to take another breath there's already air in the lung. In fact the tubes have collapsed, so the only way you could get a breath is to take a breath on top of a partly-filled lung already. So that they tend to -- the lung volume tends to walk up and up to a higher lung volume so they can keep some little amount of air going in.
When the lung gets up to a very high volume, which it has to be so you can get some emptying -- so the lung can't empty, so the next breath has to be on top of that, can't empty so the next breath has to be on top of that, you end up with a patient who is breathing way up high with big, inflated lungs, and the work of breathing at that mechanical place is very, very hard, and one of the reasons is that the diaphragm is the main breathing muscle, this is the big piston-like muscle that's right under the rib cage. When you breathe in you can see your belly contents will come out as the diaphragm comes down, and what happens is if your lungs get too big, then the diaphragm is totally flat at the beginning of the breath and can't help you, so your main breathing muscle, because of the mechanical problems of not -- of lungs that can't empty, becomes absolutely unable to help you take the next breath. So all you have left are your muscles of your neck and your muscles of your upper chest. And you can sort of watch people who have very big barrel-chest, severe emphysema, and you'll watch them breathe and they use all these neck muscles to breathe, we call them accessory muscles, and all their chest muscles to breathe, and it's very, very hard work, very, very hard work to breathe when the lung is -- when the chest wall's expanded and the diaphragm is flat and won't work and they're having to use all these extra muscles to get a little air on top of these great big lungs that can't empty normally because of this problem.
So you'll see people breathing visibly, you can watch their neck muscles tighten as they sort of fight to take a -- to take a breath in, especially when they work, but sometimes even at rest.
Q. And doctor, have you prepared another graph which shows the effect of smoking in COPD over a period of time?
A. Yes, I have. And I think what it --
I made another graph to show you sort of the natural history of COPD and to talk a little bit about how this happens to a person over a lifetime when they get obstruction of their air tubes, when they get this chronic permanent obstruction of their air tubes.
Q. Can you direct your attention to Exhibit 30059. Is that the illustrative exhibit that you have prepared, doctor?
A. Yes, that --
Yes, it is.
MR. CIRESI: Your Honor, we would offer Exhibit 30059 for illustrative purposes.
MR. MONICA: No objection.
THE COURT: Court will receive 30059.
A. Just like before, I want to go over this graph and just set up the vertical and the horizontal axes. And you can see that the vertical axis is the same, it's volume, and it's volume in liters. And this is the volume of air that comes out in the first second on one of these tests, so this is the F -- the forced exhalation volume in one second, and one liter, two liters, three liters, four liters and five liters. And on the horizontal axis, just like before, we have time, but here instead of time in seconds I have time in years, and time over the whole lifetime of an individual. What happens to your breathing tests from the time you're 20 until the time that you're 70? So it's timing that's marked off in decades of life on the bottom axis.
And if you just start at the -- like I told you before, look at the dotted lines crossing the graph, when obstruction to air flow gets bad enough where your FEV1, the amount you can get out is about one to -- and a half to two liters is where people begin to get shortness of breathe where they do anything unusual, so you can call that shortness of breath with moderate activity. And when you get down below a liter is when you have shortness of breath with any minimal activity where you're really breathless, where you're really disabled, where you face a risk of dying, where you get on chronic oxygen, where you struggle to breathe and fight to breathe even to do normal human activities of your life. So that's where the two liters is moderate obstruction and the one liter is severe obstruction.
Now if you look at the very top line on here, you can see that a 20-year-
old person has a FEV1 -- and I'm using as -- as an example a 20-year-old male who is 70 inches tall, because that's the average height, and that person has an average FEV1 of four and a half liters. The F --
The total size of your lungs is determined by your body size, by your age and by your sex to a certain extent. So we're going to use an example of an average-sized male who is 20 years old. They can blow four and a half liters of air out of their lungs in one second, just like that -- exactly like the top line on the last graph that I showed you.
What happens if you take that person who doesn't smoke and has a normal life experience and follow their breathing tests throughout their whole life? And what you find is that there's a slow, gradual decline in the FEV1 of about 30 cc's per year. That's about like a shot glass smaller. So each year your breath -- the breath that you can force out of your lungs gets about one shot glass smaller over your entire lifetime.
Why is that? Part of it is due to your chest cage getting a little stiffer. It's due to mechanical things as your ribs and your articulation of your ribs with your spine changes a little bit. Even changes in your spine. Part of it is due to the elastic tissue in your lungs gets less tensile, less elastic as you get older. There's physical/chemical changes in elastic tissue. So for whatever reason there's a small dropoff in your first-second volume that happens over your whole lifetime.
But you notice when you're at 70, you're still at three and a half or four liters, you still got double the breathing power that you would need to -- before you even get down into that beginning symptomatic range, and people live out their lives without ever being limited by their breathing power. Their lungs always empty well.
Now the second line shows you that a certain percentage of smokers, probably in the range of 15 to 20 percent of smokers, are -- basically develope an accelerated loss of lung function over their entire lifetime, and those smokers -- what happens to them is that they begin to lose their lung volume faster. Their FEV1 drops about a hundred cc's a year, so roughly about three times faster. And that seems to occur from an early age, from 20 or even earlier. They -- when these subjects start to smoke, their breathing power starts to drop off faster and faster.
And you can see that they're not going to run out of breathing power in their twenties, this is because these two curves are only separating at 50 cc's a year, so it takes a long time and years and years of exposures, but they are losing lung function in an accelerated fashion right from the beginning. And what happens is if they continue to smoke and are susceptible to the effects of smoke, that they gradually in their early forties begin to get into the area of mild obstructive lung disease that we can measure and pick up with these tests.
By the time you follow this other line, when you -- by the time they hit the one liter mark, in other words, a large group of patients who have developed severe COPD, these are the patients that you see riding a cart, oxygen in their nose, unable to walk around the store, disabled people working hard to breathe, those type of patients have an average FEV1 of about a liter, and they reach that at an average age of about 58.
So that the average person with severe COPD is a 58-year-old person who has smoked their whole lifetime and has had this gradual accelerated drop in lung function over their whole span of their -- of their smoking life. And by the time they're 58, they cross that line into severe respiratory disease, severe COPD.
Now what does that mean, to have an FEV1 of a liter when you're 58? Well different doctors have followed large groups of patients where they -- with chronic -- that's irreversible, they tried to treat all the reversible parts and what's left is chronic obstructive lung disease with an FEV1 of one liter about, and they followed them for years in studies and so to see what happens to these people. And when you pick up people right where that line crosses the second -- the bottom dotted line, 50 percent of them die of their lung disease within five years. So these patients are dying of their COPD in their early sixties, late fifties, early sixties to a large -- to large part.
This is a very severe disease which not only causes a lot of shortness of breath, suffering, distress in even doing day-to-day activities, but also leads you to lose your life early and to die of -- of -- a breathless death in your early sixties. And to lose out on that part of your life, your sixties and your seventies where you're retired and where your grandchildren are being born and -- and being raised, and it's -- it's a very tragic and unfortunate time point. Now --
Q. Doctor --
MR. MONICA: Excuse me.
Q. Doctor, when you --
MR. MONICA: Excuse me, Mr. Ciresi. Your Honor, I move that the -- at least the last portion of that answer be stricken as a gratuitous statement, comment by the doctor on philosophy of life or whatever it was. And also I would ask that counsel ask a question and answer instead of a running narrative, Your Honor. I object.
THE COURT: All right. Well the last portion was not responsive to the question.
Try and ask questions, counsel.
MR. CIRESI: All right.
BY MR. CIRESI:
Q. Doctor, when you get to the severe stage, will cessation of smoking help?
A. When you get down to the very severe stage where the FEV1 is a liter, cessation of smoking can help you have less secretions, can improve the quality of your life a little bit, but it does not change the gradual decrease in lung function and it does not change the mortality. So at that point there's some subjective benefits in terms of how much coughing and how much secretions and how many infections, but it does not alter the natural history in terms of the progressive nature of the disease from that point or the dying of the patient from that point.
Q. And the line that's sort of the broken line which says ex-smoker, can you describe what is being depicted there?
A. Well that's one of the most important things, I think, of this whole area, is that if patients have obstructive -- chronic obstructive disease that's still moderate, then if at that point they quit smoking, it can make a drastic difference in the eventual outcome and the natural history of their disease. And that's what lung doctors like myself do, is to try to find people who are developing obstructive lung disease when it's still in its moderate stage when they're in their early forties and work with them to get them to quit smoking.
And what you can see is on that line, there's a line where the hatch line goes off, and the patient is in their mid-forties and say the FEV1 is 22 -- 2.2 liters or 2200 milliliters. What I use in talking to my patients and teaching my patients is I use how much left -- they have left to spend before they have severe COPD.
So if you came in and you were 46 years old and you'd smoked since you were 15 and your FEV1 was 2.2 liters, I would tell you you have 1200 cc's left to spend and -- before you develop this point of severe lung disease. If you continue to smoke during the next 10 or 15 years and you spend it at 100 cc's per year, you're going to reach that point in your mid- to late fifties and you're going to be in this group of people with severe symptoms and major disability.
On the other hand, if you can quit, then you go back to losing it at 30 cc's a year. You don't get your lung function back, you don't jump up to that top line, but you go back to losing it at 30 cc's a year. And if you have 1200 to spend and you spend it at 30 cc's a year, that's going to last you decades, and the middle part of your life is going to have a different course than it will if you run out of breathing power when you hit that dotted line at -- at -- in -- in your late fifties.
Q. So that if they can quit, they will reduce the degenerative condition of the lung; is that right?
A. They will slow the rate of decline of their lung function from the point where they quit, and it can make a drastic difference clinically.
Q. Doctor, can you direct your attention to Exhibit 30057. Is this an illustration of the type of breathing that you described a little bit earlier?
A. Yes, it is.
MR. CIRESI: Your Honor, for illustrative purposes we would offer Exhibit 30057.
MR. MONICA: No objection.
THE COURT: Court will receive 30057 for illustrative purposes.
BY MR. CIRESI:
Q. Can you describe, doctor -- and we'll try to bring it up as you talk about different parts of the exhibit --
A. All right.
Q. -- can you describe what is being depicted here?
A. Now this -- this is an illustration by a famous medical illustrator named Frank Netter, and he's drawing his perception of what someone with bad emphysema looks like as they're trying to breathe. On the top left you can see the schematic of the lung, shows the things that we've talked about. See those two arrows that are vertical in the middle are where the airways are narrowed so they can't empty, and then it shows the big air space with the positive dots in it, which is the emphysema, the sort of holes in the lung because the lung has been dissolved, and the loss of that tissue has -- gets rid of the little tethering structures that hold the airways open and loss of that tissue loses the elastic ability to empty the lung. So this lung can't empty for all those reasons. There's no recoil because the lung has been dissolved and is moth-
eaten. The tethering part of the lung can't open the little airways and the little airways are scarred and narrowed. And this is showing the exact physiology that we talked about.
The reason that I wanted to put this in is that it shows a couple things. If you show me the picture of the patient -- the drawing rather. It shows, for one thing, that -- that this patient's lungs, because of these -- this obstruction, don't empty. He has chronic obstructive lung disease, irreversible, problem exhaling, and so he's trying to compensate and get as comfortable as he can to breathe, and one of the things is the very bottom where the diaphragm is, that big piston that moves air in, you can see that that's flat. Contracting that is not going to do anything for him. He can't get any more air in because that diaphragm is already totally flat. So what he does is lean forward and roll his shoulders forward a little bit and use these big muscles of his neck and his upper chest to get that little bit of air in on top of his lungs that can't empty, to get a little bit of air in on top. And you've seen people breathe like that.
The other thing he's doing is if you look at that top arrow pointing at his lips, one of the ways in which a patient like this can get a little more air out is actually make -- put some backpressure in into the airway. It tends to splint it open just a little bit so there can be more airflow. And on the bottom right, if you can go up again, the bottom right just shows that schematically, is that here on the left that airway is totally collapsed and can't empty at all, and on the right there's a couple of positive plus signs in the airway that the patient has made a little backpressure that just keeps that last little airway from collapsing so he can get a little airway out.
And patients do this automatically. When they take a breath, they sort of give backpressure by (demonstrating by pursing lips) -- just to hold their lung open a little bit and splint these airways so it can empty. And you don't have to teach them to do that, although they do at certain breathing classes, but the patients will do that automatically.
So if we go back up to the picture of the patient, you can see that patient is leaning forward, they don't have a diaphragm any more because their lungs are so inflated and because they can't empty, they're sucking -- they're basically using the anterior chest and their neck muscles to get that little piece of air in, and then to try to empty a little bit they're pursed-lip breathing, closing their lips and (demonstrating by pursing lips) to -- to give back pressure.
We're going to show you a patient who is breathing, and I want you to pay attention during the video part to her lips and just watch how she automatically adjusts to this to try to get that little last little bit of air in. I don't want --
I want you to realize how much difficulty this is to breathe like this. One of the things is that the average size of these lungs is very near to what's called total lung capacity at the end of a breath. Okay? So that their lung capacity is nearly at total lung capacity at the end of a breath, and that means all their breathing has to be done on top of that. So it -- what -- if you do is you just take a very big breath until your lungs are totally full and then pretend you have to start your breath there, and if I do that, the only way I have to get a little more air in is to pull with my neck muscles and my upper chest, and that's it. You know, that's the only way to stay alive is to take that next breath way at the top using the accessory muscles, leaning forward, pressing the stomach in. And it's very much work, the patients get exhausted from breathing hard and doing this intense work of breathing.
And eventually these muscles fail and the patient ends up in the hospital on life support machines, being rested and being taken care of in trying to treat whatever little reversible piece, whatever little infection, whatever little bronchospasm there is.
Q. Now doctor you said -- you mentioned we have a video, and this is illustrative of this breathing that you've been describing?
A. Yes, it is. It shows -- just shows a patient with severe COPD and, you know, the kind of work it entails to just to regular day-to-day activities.
Q. Can you describe the individual that we'll be seeing?
A. The individual is a patient of mine that I've taken care of for 12 years, and she's 52 years old at this time. She's a nurse. She started smoking cigarettes at age 13, was smoking a pack a day by age 14, was -- and has never been able to quit despite really heroic attempts. She's used every resource in the community and every resource that a doctor could give her to help her to quit, including smoking sessions, smoking cessation classes, groups, nicotine gum, nicotine spray, nicotine patches --
MR. MONICA: Excuse me, Your Honor. May I make an objection. I object to the witness carrying on this narrative and describing what his patient has done. This is rank hearsay, Your Honor, and it's a narrative form of hearsay by the witness, and I object to it.
THE COURT: I don't see where this is hearsay. These are the doctor's observations.
MR. CIRESI: That's correct, Your Honor.
THE COURT: And I think they're appropriate. There should be a question directed to the doctor, however.
MR. CIRESI: I will do that, Your Honor.
BY MR. CIRESI:
Q. Did the --
Does this patient have any history of asthma or allergies?
A. No.
Q. How many times has she been hospitalized?
A. Seven times, first time at about age 40 or 41, and in recent years about one time per year, usually for about a week and usually for a bad infection that just sort of tips her over the edge and tips her to the point where she needs help to stay alive.
Q. And doctor, you said she was a nurse. Where did she work?
A. At the University of Minnesota Hospital.
Q. And what was her position there?
A. She was a very senior --
She was a very senior nurse supervisor, managing very a large sophisticated unit for a number of years. Had to take disability retirement in '96 at age 50.
MR. CIRESI: Your Honor, we would offer, then, for illustrative purposes the video. It is Exhibit 30049.
MR. MONICA: Your Honor, we object to the video. It is not a proper representation of what it purports to be, and in addition it's duplicative of Exhibit 30057.
THE COURT: Court will receive 30049 for illustrative purposes only.
(Videotape played.)
Q. Can you describe what we see.
A. There is a patient taking a treatment with a bronchodilator, with a little inhaler that makes a mist containing the medicine to open up the airways a little bit.
Now the the patient is just sitting, and you see there's oxygen in her nose and she has an oxygen tank.
And as she works harder doing some little activities, you'll see that she starts to breathe even more with her lips.
You note she has to stop on the way back up and then stop again in the garage to sort of catch up, coming up this little slope here, this driveway.
THE COURT: We'll recess for lunch, reconvene at 1:45.
THE CLERK: Court will recess, reconvene at 1:45.
(Recess taken.)
THE CLERK: Please rise. The court is again in session.
(Jury enters the courtroom.)
THE CLERK: Please be seated.
MR. CIRESI: Thank you, Your Honor.
Good afternoon, ladies and gentlemen.
(Collective "Good afternoon.")
BY MR. CIRESI:
Q. Good afternoon, doctor.
A. Good afternoon.
Q. The patient that we saw in the video, was that her ordinary condition on a day-to-day basis?
A. I think one of the hard things about that tape is that that portrays her at a time when she was very good. You'd seen her taking a breathing treatment before to get every little bit of oxygen from the breathing treatment. She was wearing her oxygen. The secretions were white. She wasn't sick so that she needed to come to the hospital or anything else. That was during a time when she was really near her optimal good part of her range.
Q. Doctor, can you turn on your microphone. I think it may be off.
A. Excuse me.
(Discussion off the record.)
BY MR. CIRESI:
Q. Now doctor, looking at the effect of chronic obstructive pulmonary disease from a medical standpoint, how many yearly United States hospitalizations are attributable to chronic obstructive pulmonary disease?
A. I think it's important to realize how very common a problem that this is, and it -- right now probably 10 to 15 percent of all hospitalizations, all hospitalizations in the United States are for treatment of this problem. It's a very, very common problem.
Q. And with regard to leading causes of death in the United States, where does it rank?
A. Right now COPD ranks as the fourth leading cause of death in the United States, behind heart disease, cancer, and I think cerebrovascular disease. But it's the fourth leading cause of death in the United States.
Q. And approximately how many people in the United States per year die from chronic obstructive pulmonary disease?
A. About -- approximately 100,000 deaths per year from this condition.
Q. And what is the overwhelming cause of chronic obstructive pulmonary disease?
A. The overwhelming cause for -- for this condition is smoking cigarettes. It overwhelms all other causes.
Q. Are there any other causes, doctor?
A. There are other causes of COPD that do -- that do exist, and some of them are -- there's a very rare genetic disease where the patient has no -- has -- misses an enzyme that protects you against the substances that dissolve the lung, and this is an anti-elastase. And that -- if you were born without that enzyme, then you get COPD at an early age. But even there smoking plays a dramatic effect on how fast you get it. If you don't smoke, about half of the people get short of breath by age 40 and about half of them have tied by age 55 of COPD, and this is non-smokers. If you smoke, half of them are short of breath by age 30 and half have died by age 40. So that even in that condition, smoking accelerates it.
And I think you have to put that in perspective because the incidence of that rare condition is about one in a hundred thousand patients, so if you look at the whole -- like the metropolitan area, there's 20 or 30 patients with that condition. That's a rare condition. Whereas if you look at the number of patients with COPD, it's in the tens of thousands to upwards toward a hundred thousand. So that you're talking about a rare genetic defect with 20 or 30 patients in this metropolitan area versus something that is incredibly common as a clinical condition.
Q. Are there any other causes other than this rare genetic disease and smoking?
A. We've mentioned that the "chronic" part of chronic obstructive means the irreversible part, the damage to the lung that can't get better, and we talked briefly that asthma is an acute obstructive disease, that if you get the proper treatment, you'll go back to breathing normally and feeling normal. For example --
And that's what so, so terrible about this disease is it is like a asthma attack that isn't going to go away. No matter what you do, it's going to be with you like the patient that we watched. You just want to say "Well let me help you do that. Let me" -- you know, when you're watching her, you want to stop her and help.
And asthma ordinarily is very treatable, but there are some patients with asthma whose asthma condition, as they age and as they have more and more attacks, develops an irreversible part to the asthma so that the asthma itself becomes a chronic obstructive lung disease. But numerically those cases are very tiny; at most five -- five percent of the entire group of COPD.
Q. Now doctor, directing your attention to the medical treatment and medical management of COPD, have you put together a chart which categorizes medical management? And if you could direct your attention to 30060.
A. Yes, I have it.
MR. CIRESI: Your Honor, for illustrative purposes we'd offer Exhibit 30060.
MR. MONICA: No objection.
THE COURT: That's 30060, counsel?
MR. CIRESI: 30060.
THE COURT: That will be received for illustrative purposes.
A. This is just a list highlighting some general topics, more to keep me from forgetting certain things as I go through it.
What we're talking about here is the medical management of COPD, what can a -- can a doctor do for patients with this problem. We've talked --
Q. Doctor, let me ask you one thing first. Is the management of the problem on an overall basis costly?
A. It's extremely costly.
Q. All right. Can we --
A. All parts of the treat -- all parts of the management are very expensive.
Q. Can you then start going through each part of the medical management regimen and describe each one as we go along.
A. Yes. Yes, I will.
We've talked a little bit about the natural history and the effect of smoking cessation on the natural history. COPD is something that occurs in this group of smokers who start smoking early and over decades. They have an accelerated loss of lung function until in their late fifties they reach the severe point where they need a lot of treatment and a lot of support and have severe disability and shortness of breath.
We've talked about smoking cessation as being important, especially early on, at changing the slope of decline of breathing function, so that they can still have an adequate, functional life for years or even decades. And patients do a lot of things to try to quit smoking, a lot of which are very expensive. They, you know, join self-help groups, they take nicotine replacement in various forms, gum, patches, and even a nicotine nose spray. You can see these in any kind of a drug store right on the counter next to the cigarettes. They're for sale without a prescription, over-the-counter, and they're very costly. They cost well over a hundred dollars a month, a hundred dollars a month to replace the nicotine.
There's also for smoking cessation a trial of using anti-depressant drugs which blunt the craving -- are believed to blunt the craving or help a bigger percentage of people quit, and those drugs are expensive.
And then some patients even go so far as to get -- do inpatient. Hazelton and the Mayo Clinic both offer inpatient treatment, quitting regimens, which no insurance pays for, so the patients have to pay for themselves. The program at Hazelton is several weeks long and it's about as much as if you went on a cruise. You know, that's what I tell my patients, spend the money there, see if you can get off rather than doing something enjoyable.
So a lot of money goes into smoking cessation, and a lot of doctors' visits and doctors' work goes to try to help people stop smoking.
MR. MONICA: Your Honor, I object to the running narrative of the witness's answer. The answer was given in the first few sentences, and I ask that the witness be instructed to answer the question directly and to not ramble on. I realize he has to explain his answer, I have no problem with that, but these long, rambling answers, Your Honor, I object to them.
THE COURT: Okay. Ask another question, counsel.
MR. CIRESI: Yes.
BY MR. CIRESI:
Q. Now directing your attention to bronchodilators, can you tell us what that is, sir?
A. Bronchodilators are medicines that relax the smooth muscle part of the bronchiole wall, and they're very common treatment for asthma, and they treat the small asthmatic piece of COPD. A lot of patients with COPD have a little bit of spasm as part of the obstructive disease, those same small airways can have some spasm, but instead of like, for example, someone with bad asthma, their FEV1 might be one liter, and after full treatment it might go to four liters, so it would be completely reversible and the patient will go back to being normal. With COPD it might be one liter when they're sick and have an infection, and with all the extra bronchodilator therapy it might go to 1.3 liters. So they get like a 15, 20 percent improvement. Now that's not much, but sometimes it's crucial for them to be able to live their life and do their job and function.
So the bronchodilators are used and they're either inhaled -- little puffers like asthmatics use. You've seen people with little, you know, meter dose inhalers and they puff on that and it relieves asthma. In some cases they put a liquid right in a little mister, like you watch the patient use in the beginning of that video, and they breathe in over 10 or 15 minutes to get a higher dose. And those bronchodilators cost in the order of probably a hundred dollars a month for this kind, and two hundred dollars a month for the inhaled kinds. And there's a number of different kinds that are -- with slightly different mechanisms, but they're basically asthma-type treatments.
Q. Okay. And doctor, the corticosteroids, can you describe that management.
A. Well drugs like cortisone are very powerful anti-inflammatory drugs and they're used for arthritis and they're used for lots and lots of conditions, and when people are really sick and almost dying with COPD, sometimes just reducing the inflammation in the lung can sort of get them over a very bad spot. Does not fix the lungs, but it can get them over a severe problem. So that oral steroids, like by pill, prednisone pills, are used to get them over very tough spots. And the inhaled cortisone on a chronic basis are sometimes used to try to alter the course. The trouble with inhaled -- inhaled steroids is trying to reduce the inflammation and calm the lung down, and they're never as powerful as directly deeply inhaling something that causes inflammation 20 times a day.
So they do not counteract the effect of smoking, they are nowhere near that powerful, but they are used in this condition. And again, the cost of the inhaled steroids is like a hundred dollars a month. The oral steroids are cheaper, but -- by pill, but they have more side effects.
Q. And doctor, antibiotics, how are they used in the medical management of COPD?
A. Well one of the things that gets people in trouble so they have to go into the hospital, like if they get the flu last month or this month, it's not just the fever and aching -- you know, aching and being sick for a few days, they also can't breathe, and then they can get a secondary infection with bacteria where they cough up green pus and they're infected. And they don't have enough reserve to have a bronchitis, so it sort of tips them over the edge when they have to go into the hospital. And when they get a bacterial infection in the bronchial tree or a bronchitis, they need antibiotics, and the antibiotics are expensive and have to be taken for episodes of bronchial infection.
Q. Are individuals who have COPD more susceptible to other illnesses or diseases?
A. Yes, they're -- they're certainly susceptible to either having the disease more often, like episodes of bronchitis, or not having the reserve so they get sicker and are in danger with the same kind of illness that someone with more reserve could do fine with.
Q. And doctor, how is oxygen used in the medical management of COPD?
A. Now oxygen is very important. And you saw her carrying her oxygen tank. And oxygen is one of the few treatments that actually has been shown to prolong life in severe COPD. And it only works for a small group, maybe a quarter of the patients, because not all patients with COPD have very low oxygen. But the ones that have very low oxygen, either at rest or with exercise, who use oxygen, it -- it basically has been shown to prolong their life by up to two or three years. So that all patients who have resting low oxygen or whose oxygen drops either at night or with exercise, we put on chronic oxygen, and they use that not only to be able to exercise better, to avoid turning blue when they try to exercise, but they also use it as an actual life-prolonging measure. And it -- it prolongs life on the average of -- of two to three years.
It costs two to four hundred dollars a month, depending on whether you have a concentrator, whether you have extra tanks that you carry around.
The patient in the video, when she -- her oxygen level was about 90, which is sort of the low end of normal, and when she would walk 50 feet it would drop below 80, which means blue basically, she would turn blue with walking 50 feet without oxygen. With the oxygen she could walk twice as far without dropping the oxygen level. So it did improve her capacity to exercise. And again what you saw was her exercise with the help of oxygen, with the help of the bronchodilator.
Q. And doctor, pulmonary rehabilitation, how is that utilized in the medical management of COPD?
A. Pulmonary rehabilitation is sort of a controversial subject, because it's not really proven that it prolongs anybody's life by going through different rehab programs, but it definitely makes people able to walk further and gives them a little -- it teaches them to be more relaxed with their breathing, what to do with they run out of breath, it teaches them how to do the pursed-lip breathing, make sure that they're using all their inhalers correctly. It's sort of a setup where they go through all the details of this chronic disease and try to optimally handle all of the details. Can either be done as an outpatient, and there's programs at most of the hospitals that run for like twice a week for six weeks or something like that. I use the program at Abbott Hospital quite a bit because it's right in the neighborhood of our hospital, and my patients, you know, do feel more confidence with their disease, learn about their disease, have a better functional life after going through that program. They don't live any longer.
And the other way you can do it is an inpatient program, and there are several hospitals in town including Vencor, which is the chronic subacute hospital that I work at that has an inpatient program, so people can actually go into the hospital for two weeks and get help with their secretions, with their bronchodilator use, with learning how to take care of their oxygen equipment, with pursed-lip breathing, with all the details of doing as well as they can with a chronic, incurable problem.
Q. Doctor, you talked about a chronic subacute hospital such as Vencor. What is a chronic subacute hospital?
A. Well it's a licensed --
Hospitals are usually licensed as acute hospitals, like the University of Minnesota, Mayo Clinic, St. Mary's down there, Hennepin County, Abbott, but there are a couple hospitals that -- that are licensed under a subacute hospital where the average length of stay, instead of being three or four or five days for acute problems, is more like 30 or 40 days for things that sort of get better week by week and require a rehab component to it rather than the things that are getting better day-by-day. And in -- in the metro area there's two of those hospitals, ones in the west metro, in Golden Valley, and one's Bethesda, which is not too far from here, near downtown St. Paul.
Q. Doctor, hospitalization, is that required in the medical management of COPD?
A. Again it's 10 or 15 percent of all hospitalizations to acute hospitals in the United States, much higher percentage of hospitalizations in chronic long-term acute hospitals. So that many patients, especially when they get a bronchitis or an infection or some intercurrent problem, they have to go into the hospital, be stabilized and get their breathing back up to where it's good.
Q. What's the cost of hospital stays for COPD management?
A. Well they vary according to what needs to be done. But in general if the patient is in a ward bed getting an antibiotics and intensive treatment and things like that, the cost would be in the range of a thousand dollars a day. If they're in an ICU on a breathing machine, on life support, the cost would run from two to three thousand dollars a day. So that the -- you know, hospitalizations have become incredibly expensive, and even a week in the hospital to treat a bad infection associated with COPD would be ten thousand dollars, easily.
Q. All right. Now doctor, it's also mentioned here single lung transplant or lung reduction surgery.
Let's talk about the single lung transplant. Can you describe that aspect of medical management of COPD.
A. Uh-huh. The two things on the right I put in parentheses because they're sort of surgical management rather than medical management, but there are a couple things that are done occasionally to try to help people who are near the end of their life and are desperately short of breath from COPD. And sometimes, like you say, if these lungs are so rotten and so worn out and so terrible, why don't we just give them a new lung, you know, new lungs? And that is done. There are certain number of people, especially people who are young, who don't have other diseases, you know, who have not had other chronic diseases, who get a lung transplant. And they go from not being able to breathe at all to being able to walk and live -- live their life and get a tremendous relief. So that for some of these patients, that can be almost a miraculous type of improvement.
Q. Are there many available lungs in the United States to do lung transplants?
A. The problem is partly in organ -- is in cost, in the complications, and the organ availability. There is at least probably eight to ten thousand people right now in the United States who would benefit from a lung if it were available, and there's only three or four to five hundred a year that are available. So most patients simply can't have one because there aren't available lungs that can be used for transplantation.
Q. Is it an expensive procedure?
A. The cost of a lung transplantation in the first year would run over a hundred thousand dollars, in the range of a hundred thousand dollars.
And the patient -- it's really done for lifestyle reasons. The patient is so short of breath that each breath, they feel like they're suffocating, and they would do anything to get rid of that sense of dyspnea. Because a third of these patients die in the first three months of either rejections or of infections, so the patient that wants to go for lung transplant -- one, they have to get incredibly lucky, a lung has to become available when they need it, and they have to have a chance, a 30 percent chance of dying within months in order for -- you know, to take that chance for what's at the other end, is some patients who get relief of their symptoms.
Q. Are there other sequelae or consequences of a lung transplant other than death?
A. Well a lot of people get rejection of the organ which causes obstruction itself and leads to a recurrence of the shortness of breath. And the patients on transplant -- on -- with lung transplants have to take high doses of immunosuppressive drugs, and they get infections from those drugs. And they have to take high doses of cortisone, which leads to softening their bones, fractures of their spines, necrosis of their hips, they need hip surgery in many cases, cataracts with cataract surgery, so that there's a whole complication of the regimen of drugs that you have to take to keep from rejecting that lung, and it's simply not an available treatment for the tens of thousands of patients who have COPD as they reach the end of their life. It's something that is done in a few -- a few patients.
Q. Doctor, with regard to lung reduction surgery, can you describe that, please.
A. Well that's sort of an interesting story, too. One of the problems that I mentioned to you is these lungs are just too big, and one of the consequences of being too big is the diaphragms, that big muscle that works as a piston for breathing, is flat and can't work, and so people have come up with the idea of removing part of the lung to make the lung smaller so the diaphragm can work again and so that gas exchange with improve, and they actually are helped in this by the fact that emphysema tends to be worse in the top of the lung than in the bottom. There's some regional differences in the disease. So they remove the top third of each lung. They do a surgery where they split the sternum, just like heart surgery, and take out the top third of each lung and then -- then close the patient. And some patients get substantial relief of their shortness of breath, they double their ability to walk, and that lasts for up to a few years.
And that is surgery that's being evaluated to try to figure out which subgroup of these COPD patients have the most benefit and the least risk, so we can pick out people that actually help them with that treatment.
Q. And doctor, is that an expensive treatment?
A. I would guess that the minimal cost for that would be in the range of $20,000. And if you get persistent air leaks or other surgical complications, it can run into ten of -- many tens of thousands of dollars.
Q. Doctor, do some of the COPD patients require permanent life support?
A. Now some patients when -- when they have a bad problem and they have an acute worsening of their disease, they would have to go on life support with a breathing machine. And they either have a tube down their nose into their lung or in their mouth into their lung, or sometimes even a tracheostomy so that they can be put on assisted ventilation with a breathing machine. And hopefully they will get better from their infection, whatever caused them to worsen suddenly will be treated and they will be able to come off that breathing machine.
Sometimes it happens when they get influenza. They have bad COPD and they get influenza, and they can't live without at least temporarily being supported with life support.
Q. Is that treatment expensive?
A. That treatment is -- you know, during the time that you need it, is thousands of dollars a day. And the problem is that some people never get well enough to come off of that breathing machine, and then they sort of have to make the decision whether to come off and be helped to be comfortable with drugs like morphine, or whether to try to make their life as a disabled person as well as they can with chronic life support. If they get to that point, then the costs are tens of thousands of dollars a month for that type of support.
Q. Doctor, if smoking were eliminated as a cause of COPD, would we see a reduction of this illness in the United States?
A. If -- if smoking would gradually disappear and there were no smoking in our culture, in one generation COPD would be a rare condition. It would be something that most doctors didn't see, it would be something that most families didn't have patients or relatives -- it would be an unusual, rare condition rather than the fourth leading cause of death in the United States and the cause of 10 to 15 percent of all hospitalizations in the United States. It would be that dramatic an impact on the incidence of COPD.
MR. CIRESI: Thank you, doctor. I have no further questions.
MR. MONICA: Your Honor, may we have a few minutes to move the Elmo over here?
THE COURT: Let's take a short recess.
(Recess taken.)
THE CLERK: All rise. Court is again in session.
(Jury enters the courtroom.)
THE CLERK: Please be seated.
THE COURT: Counsel.
MR. MONICA: May it please the court.
Good afternoon.
(Collective "Good afternoon.")
BY MR. MONICA:
Q. Good afternoon, doctor.
A. Hello.
Q. Doctor, my name is John Monica and I represent Lorillard Tobacco Company, and I'm going to be asking you some questions this afternoon, not only on behalf of my company, but the other companies, as we have a -- the court has asked us to just have one attorney ask questions of every witness, and we're trying to do that. And so I'll be the attorney who will ask you questions this afternoon.
If you don't understand my questions, please tell me. I'll be glad to repeat them.
A. Okay.
Q. Doctor, chronic obstructive pulmonary disease, is it correct that that disease consists of mainly two subparts, emphysema and chronic bronchitis?
A. The -- the -- it's kind of a -- of a clumsy term because it incorporates two main things, emphysema, which is a pathological description, and chronic bronchitis, which is a clinical description regarding cough and sputum production. So that --
But the reason that it's used so often is that it represents the changes in the lung mainly due to -- to cigarette smoking and almost nobody has pure emphysema or pure chronic bronchitis. So that most patients have features of both of these. The airways are -- have some changes and the lung tissue has been dissolved and they have a mixture of two, so rather than trying to divide a group right in half into emphysema and bronchitis, which really doesn't divide because most patients have features of both, this is sort of a lumping term that's used to describe patients with -- who have to have obstruction, they have to be trouble exhaling, and it has to be irreversible.
Q. But there are gradations in between, but basically at the one end and at the other you have emphysema and chronic bronchitis; right?
MR. CIRESI: Objection, asked and answered.
THE COURT: No, you may answer that. You may answer.
A. As I said, most patients have some of the clinical features which would be described as chronic bronchitis, some of the anatomic features which would be emphysema, and they have features of both of these. So that at the very far end would there be someone with pure emphysema and someone with pure bronchitis? There could be someone whose clinical picture fit more closely pure emphysema and whose clinical picture fit more purely with the bronchitic, but they would be uncommon.
Q. And to -- and to determine where they are -- where the patient is at on the spectrum, you of course would have to review that patient's chart and medical records and talk with the patient; isn't that correct?
A. You can't really totally determine where someone is on that record because emphysema is a pathological diagnosis, and most of the time our diagnosis is made by that spirogram where we do breathing tests, and what we're measuring is actually the degree of obstruction, and we don't get accurate --
So we would never think in terms of putting someone along this -- the area. We would say they have COPD and this is how bad their obstruction is based on the -- the breathing test.
Q. Okay. And by "COPD," we're talking about the disease that we've been -- you've been testifying about today; correct?
A. Yes.
Q. That's the shorthand term for it, "COPD;" correct?
A. That --
Yeah, that's the term we spent a lot of time trying to explain.
Q. Yes.
Now let's try to put things in perspective. Isn't it true, doctor, that if you take lifetime smokers, people who have smoked for their entire lives, that only 10 to 15 percent of lifetime smokers develop symptomatic COPD? Isn't that true, doctor?
A. About 15 percent of people with -- who are lifetime smokers develop symptomatic COPD.
Q. And by the same token, conversely, that means that 85 to 90 percent of smokers do not ever develop symptomatic COPD; isn't that correct?
A. That's correct to a point, although the -- that doesn't mean they have normal breathing tests and that they haven't developed some degree of airway obstruction. That has never been shown, what percentage have absolutely normal lung function. But there are a substantial majority who never get to the point of being disabled by the airflow obstruction.
Q. In fact, it's more than a substantial majority, it's the vast majority. It's 85 to 90 percent.
A. It's about 85 percent.
Q. Yes, sir. And as far as the disease COPD, I believe you said about 10 percent of your inpatients you treat for COPD, about 10 percent of your patients have COPD that requires treatment in a hospital; is that correct?
A. I didn't say that, no.
Q. Well is --
Let me ask you the question, then, directly.
A. Uh-huh.
Q. Isn't it true, doctor, that of your practice, only about 10 percent of your COPD patients require hospitalization?
A. I didn't -- that's --
I didn't mean to say that or imply that at all. I -- I stated that about 10 to 15 percent of all hospital admissions in the United States are due to COPD, but I don't have any number for the percentage of my own patients with COPD who are ever in a hospital. It would be -- I don't have -- have that accurate number.
Q. All right. So you don't know what percentage of your patients require hospitalization --
A. No.
A. -- because of COPD; do you?
A. No.
Q. And you talked about some of the cost figures and in that regard, the last exhibit we had, which is Exhibit 30060 -- and I'm going to put this up just to remind you of which one I'm talking about, and I've -- I've written on mine here, but this is the exhibit I'm talking about, doctor. You went through some cost estimates, do you recall, just a few moments ago on that?
A. Yes, I did.
Q. I'm going to be talking to you about some of those cost estimates. But have you been advised, doctor, that the plaintiffs in this lawsuit are seeking reimbursement for costs that they spent to treat some of the patients who have COPD?
MR. CIRESI: Objection, Your Honor, that's outside the scope of this witness's testimony.
MR. MONICA: Your Honor, this clearly is --
He's talking about costs with regard to this lawsuit, costs for treatment of patients that are relevant to this lawsuit.
THE COURT: Counsel, I don't recall any testimony with regard to costs for this lawsuit. I think you can inquire about his statement on costs generally.
MR. MONICA: Okay.
Q. Doctor, with regard to the costs that you have estimated here, isn't it true that you did not make any kind of a particular study of the costs? These are just your general experience, your general impression?
A. I did make a few phone calls to our pharmacy and ask them how they price out these items, how much one inhaler costs. I called an oxygen -- one of the biggest oxygen vendors. And I have very personal experience of hospital charges and costs from some of the administrative things I did. So I never meant to present it to you as a study of any kind, but I think it's an accurate estimate of some of the costs that are involved in these -- in these items.
Q. And in fact, doctor, as you said, it was not a detailed study or any kind of a study on your part; was it?
A. It was -- it was not a study, no.
Q. It was kind of based upon your experience and a few conversations you had.
A. I stated what it was based upon.
Q. And doctor, let's see if we can establish the extent of what you did do.
Now bear with me, I'm not an artist, but I thought it might be helpful just to put this up. I'm going to try to draw the state of Minnesota here first, doctor.
MR. CIRESI: Is it all right if I look at this one, Your Honor?
THE COURT: If you want to.
MR. CIRESI: We'll see if he's as good as Mr. Bernick.
MR. MONICA: I make no representations.
THE COURT: I think we're going to bring Mr. Bernick back.
THE WITNESS: There's a little bump on the top.
MR. MONICA: That almost looks like Texas. But I --
MR. CIRESI: We can tell you're from Kansas City.
MR. MONICA: I think the -- we can go through the points I wanted to make, even though that is a very crude drawing, I admit.
Q. But anyway, this is the Twin Cities area right -- right here, doctor.
A. Yes, it is.
Q. Now you --
When you were making your inquiries, you -- for example, you didn't check with anyone up here in the Moorhead Fargo area; did you?
A. No.
Maybe put Willmar on there, which is halfway to the South Dakota border straight left. I do outreach there one day a month for several years, and I -- I did talk to some of -- their pharmacy when I was out there. So I have looked at a little at outstate. I'm also from a small town, and I have a family who use some of these products, so --
Q. You didn't check with anyone up in International Falls; did you?
A. No, not up in that bump.
Q. And how about over here by the lake, Duluth. You didn't --
A. No, I did not check Duluth.
Q. Okay. So my point is, as far as the studies -- or the inquiries that you made, they were fairly well localized on the Twin Cities area with a couple of outlying. Is that a fair statement, doctor?
A. That's a fair statement, sure.
Q. And so your --
And admittedly this is a crude drawing, but your -- your inquiries and the cost estimates, then, are really only really relevant and pertinent to the Twin Cities area; aren't they, doctor? They're not a state-wide, they don't purport to be a state-wide figure.
A. No, this is true, but in all fairness, like drug stores are becoming more of a national chain, and if I buy an Albuterol inhaler in a Snyder's store in Minneapolis and in Duluth and in Rochester and in Albert Lea, they may be off by a few pennies, but they're not off by an order of magnitude. These are products that there's a profit margin on. Just like cigarettes wouldn't be double the cost in the Twin Cities as in Willmar, they would be roughly in the same general frame because they're a product with a profit margin.
Q. But doctor, you -- as you said, you didn't actually check in these areas that I've mentioned to see how close the prices were; did you?
A. That is correct.
MR. CIRESI: Objection, asked and answered, Your Honor.
THE COURT: It's been asked and answered now.
BY MR. MONICA:
Q. Now in -- in determining whether a cost, a particular cost is -- is reasonable, doctor, don't you have to look at what was done for that particular charge?
A. I'm not --
I don't exactly know what -- what you mean. Where --
Q. I'll try to rephrase.
A. Maybe you can use an example.
Q. Well to -- let's take an example. Let's, for example, look at a bronchodilator.
A. All right.
Q. To know if that charge is -- is appropriate, wouldn't you have to know if the procedure was really necessary and appropriate?
A. You would have to assume that the patient had some benefit from the treatment. Is that what you're asking?
Q. And not all patients use bronchodilators; do they?
A. Not all patients do use them.
Q. So you'd have to consider whether the individual patient really needed a bronchodilator before you would know if that cost --
A. Right.
Q. -- for that dilator was reasonable, wouldn't you, sir?
A. Right. And that would be determined by the individual doctor working with that patient, testing them, and the patient -- to see if they had an appropriate clinical response to that drug so that the benefit to them was worthwhile.
Q. And doctor, is the same true for all of these entries on this chart that we have on the -- on the screen here?
A. There's --
Q. You got --
A. -- some exceptions. For example, oxygen, it's federally paid for -- I mean the federal payors, like Medicare, you're required to document very precisely what the oxygen level is in the blood. So in order to give oxygen, it's not -- I can't give you oxygen because I think you might feel better. I'm required to show what your PO2 level is or what it does with exercise. There's very stringent criteria for that oxygen and you can't have it unless you meet very uniform standard criteria where it's been shown to do you some good.
The oxygen vendor that we use actually started in Duluth, it's pretty much become a -- it's Arrowhealth, and they -- you know, a lot of the companies have amalgamated, and so I think the oxygen costs throughout the state would be pretty close. And certainly you just can't have a doctor decide to give oxygen. It doesn't work that way. You have to say what are the criteria? Well it's a PO2 less than 60, and you have to show that. The lab that does the blood test has to be certified and you have to present that documentation at the time that you give the oxygen. So I would assume that at least for oxygen, everybody getting it would -- would be -- represent people who would benefit from it.
Q. Yes. But on the other ones that we've talked about, the bronchodilators, the antibiotics, the pulmonary rehabilitation, you'd have to -- to take a look at the individual patient and his chart or her chart to determine whether the cost was necessary and appropriate; wouldn't you, doctor?
A. A doctor would have to be ordering the treatment for an appropriate -- for an appropriate patient. That's -- that would be true.
Q. And in fact, in order to determine if these treatments are necessary, you would want to know, for example, whether a patient had a history of exposure to environmental -- certain undesirable environmental exposures; wouldn't you, doctor? Like say they worked in the coal mine or something like that, you'd want to know that; wouldn't you?
MR. CIRESI: Your Honor, I'm going to object to that as being outside the scope. It's also in improper form.
THE COURT: Sustained.
BY MR. MONICA:
Q. Well doctor, when you are evaluating a patient to determine if that patient has COPD, what are some of the things that you ask the patient? When they -- when they come in to sit down with you for the first time, what are some of the things you ask the patient about?
MR. CIRESI: Objection, Your Honor, outside the scope.
THE COURT: No, you can answer that.
A. Uh-huh. Well a patient often comes with a particular problem. They have a presenting complaint, there's something -- some reason that they're going to the doctor. And if you talk -- so the patient might make an appointment because they have a complaint, something that they're troubled with. Usually that would be shortness of breath on exertion. They've noticed that when they try to do heavy work or carry something or do more work, that they would be short of breath.
The other main symptom would be cough, that they have developed a chronic cough, that they cough up phlegm from their chest and they have a deep, barky cough that persists and just won't go away like a cold would, and they're concerned about that. So those would be the two main symptoms.
Sometimes the patient is just there for a routine exam, and you might question whether they had COPD based on their physical exam, their pattern of breathing, observing them doing the things you do in giving a regular physical examination.
Q. And doctor, you would ask the patient for the family background; wouldn't you?
A. If the patient came in with a complaint, like on a complaint-centered visit, I might not. But if this was my patient, I would have as part of their medical record a complete family history, social history, and a complete review of systems. If I was seeing a new patient that was coming to me for the first time, then I would get that information and it would be part of -- of their record.
Q. And you would need that information to diagnose the patient; correct? That's why you ask the patient for the information.
A. I would need that -- that information to fully understand that person and their health history and their various problems.
Q. For example, you'd want to know if the patient had HIV; wouldn't you?
A. I would -- if it --
I would certainly want to know if the patient had a history of -- of being exposed, having risk factors, having been documented to have HIV. But to my knowledge, that has nothing to do with the question of COPD.
Q. Don't people who have HIV get pneumonia and other respiratory illnesses much more frequently?
A. Patients with HIV do not get COPD.
Q. Don't --
Would you answer my question? Do they get pneumonia more frequently, Your Honor -- ah --
A. Patients are susceptible to a variety of bad infections. One of the problems is that their immune system is wiped out, so they get a whole variety of respiratory and other infections which have to be managed as part of a chronic illness, but --
Q. Which if --
A. -- it has nothing to do with COPD.
Q. Which if they are not managed properly can move into COPD.
A. No.
Q. Wouldn't you want to know if -- if your patient had worked in a factory and had worked grinding fiber glass every day? Would you want to know that?
A. I would want to know what work my patients have done, yes.
Q. And wouldn't you want to know if your patient had worked in a paint factory where the paint was in the air all day and they had breathed the air all day every day while they worked at that paint factory, wouldn't you want to know that?
A. I would want to know what occupations my patients have -- have done, what they've done for work.
Q. And doctor, did -- did you know that we've taken some depositions in this case of Medicaid recipients, and that one woman that I deposed myself has had all these experiences I just mentioned to you?
MR. CIRESI: Excuse me, Your Honor, I'm going to object. And I'm sorry to interrupt, counsel, but he knows that's an inappropriate question. It's already been ruled on.
THE COURT: Counsel, that is an inappropriate question, that has been ruled on in the past. Move on.
MR. MONICA: All right.
BY MR. MONICA:
Q. Doctor, have you examined the individual medical records of any of the Medicaid recipients for whom plaintiffs claim damages in this lawsuit?
A. I don't know who those claimants are. All I can say is that they -- I've taken care of patients every day of my work life for 19 years, and I've certainly represented -- I've certainly taken care of many patients who are receiving Medicaid within the state of Minnesota. So again, I don't know the parameters of -- of the details.
Q. And -- and so then, obviously, doctor, you're not in a position to say if any of those people have COPD because they smoked; are you, doctor?
A. I don't know --
I do not have a list of any of the patients you're talking about. I have no personal knowledge of any such a list.
Q. And by the same token, doctor, you're not in a position to say that any of the medical costs incurred by those patients is reasonable and necessary; are you, doctor?
MR. CIRESI: Objection, Your Honor, there's no foundation for that.
THE COURT: Sustained.
Q. Doctor, when you look at a patient for the first time, you said you're looking for -- you're looking for two things, shortness of breath and -- what was the other one, doctor?
A. I said when a patient comes to me with a complaint, and they come in because they have a patient-centered complaint, that the two most common ones would be shortness of breath and a cough, chronic cough.
Q. And --
A. That's what the patient -- what the patient would bring to me as a complaint.
Q. And if they had those two symptoms, then, you would want to investigate whether or not they were being caused by COPD; correct?
A. Yes.
Q. And by the same token, those same two symptoms can be manifested as a result of other diseases, non- COPD diseases; right?
A. Yes.
Q. And what are some of the other diseases that manifest those two symptoms, non-COPD diseases?
A. Well asthma could present with either shortness of breath on exertion or with cough, and various types of diseases of the lung tissue could present with shortness of breath and/or cough, like pulmonary fibrosis or sarcoidosis. In fact any lung disease -- the lung doesn't have too many ways that it can tell you that it's going bad, and almost any lung disease can present with shortness of breath or with -- or with cough.
Q. So you'd have to investigate those various possibilities in order to determine whether it was COPD you're looking at or one of those other diseases; right?
A. That's -- that is my job.
Q. And again you'd have to look at the patient's chart and the medical history and things like that.
A. Uh-huh.
Q. Correct, doctor?
A. That would be part of the information I would gather.
Q. All right. And as you said, you haven't done that for any patient in this litigation, any Medicaid patient.
MR. CIRESI: Objection, asked --
A. I don't know if that's true or not.
MR. CIRESI: Excuse me, doctor. Objection, it's been asked and answered.
THE COURT: It's been asked and answered.
Q. Doctor, have you talked with any of the damages experts in this case and given your input to any of them?
A. No.
Q. So you're not testifying on any element of damages in this case, to your knowledge?
A. I'm testifying about COPD as one of the severe medical conditions caused by chronic smoking and about the medical management of -- of that condition.
Q. But as far as you know, doctor, your work is not being used in any regard to compute damages.
A. To my knowledge, it is not.
MR. MONICA: I have no further questions.
MR. CIRESI: I have no further questions, Your Honor. Thank you, doctor.
THE COURT: You may step down.
MR. CIRESI: Your Honor, we need to --
THE COURT: Side bar.
MS. NELSON: Your Honor, plaintiffs call Dr. Kenneth Graham to the stand.
(Witness sworn.)
THE CLERK: Please state your name and spell your last name for the record.
THE WITNESS: Dr. Kevin J. Graham, G-r-a-h-a-m.
THE CLERK: Please be seated.
THE WITNESS: Thank you.
MS. NELSON: Good afternoon, ladies and gentlemen.
KEVIN J. GRAHAM called as a witness, being first duly sworn, was examined and testified as follows:
BY MS. NELSON:
Q. Good afternoon, Dr. Graham.
A. Good afternoon.
Q. Dr. Graham, is your mike on?
A. Is it on?
Q. Yes. Okay.
Dr. Graham, would you please briefly explain the expertise you bring to the court and the jury today.
A. What my purpose in appearing today to the court is to talk about cardiovascular disease and the clinical presentation of cardiovascular disease, specifically coronary artery disease or the development and presentation, clinical presentation of blockages in the coronary arteries of the heart, stroke and the loss of blood in some way to the brain, and peripheral vascular disease or decrease in blood flow to the extremities.
Q. And when you say "clinical presentation," what do you mean by the word "clinical?"
A. Much like Dr. Davies, I am a clinician, and every day when I get up it's my job to go and see patients, and that's -- so we deal with patients who present with clinical problems, or hopefully to prevent those clinical problems.
Q. Dr. Graham, before we get into the substance of your testimony, I'd like just to take a moment to review with you your education and your training.
It appears that you graduated from the University of Minnesota Medical School in 1981; is that correct?
A. Yes, ma'am.
Q. And in 1985 you completed an internal medicine residency at Hennepin County Medical Center; is that correct?
A. Yes, ma'am.
Q. Could you just briefly describe to the jury what a residency is in internal medicine?
A. After the completion -- successful completion of medical school, there is a competitive arrangement to go to top internal medicine residency programs. Through the internal medicine program you learn essentially all the inpatient and outpatient modalities of the treatment of the adult patient.
Q. And then you were awarded a cardiology fellowship at the University of Minnesota; is that correct?
A. Yes, ma'am.
Q. And you completed that fellowship in 1988.
A. Yes, ma'am.
Q. So that was a three-year post-residency fellowship.
A. Yes, ma'am.
Q. Could you explain to the jury what the medical field of cardiology involves.
A. After a three-year residency, learning the spectrum of adult medicine and the various specialties within that, touching each of those, a cardiology subspecialty fellowship concentrates on diseases of the vasculature, most specifically the heart, but also dealing with wherever blood flows in the body.
Q. And then, doctor, you received board certification in internal medicine in August of 1985; is that correct?
A. Yes, ma'am.
Q. And then you received a subspecialty board certification in cardiovascular medicine in November of 1989; is that correct?
A. Yes, ma'am.
Q. Now where do you currently practice cardiology?
A. I am a consultant in cardiology at Minneapolis Cardiology Associates, at the Minneapolis Heart Institute, practicing primarily quaternary practice and tertiary practice out of Abbott Northwestern Hospital.
Q. Could you take a moment to describe the work of the Minneapolis Heart Institute.
A. The Minneapolis Heart Institute is a confederate of over now 50 cardiovascular specialists, surgeons, three surgical groups, one cardiology group, which is our group, which is approximately 29 cardiologists, cardiovascular anesthesiologists, interventional radiologists who deal mostly with peripheral vascular disease, and the pediatric cardiologists.
Q. Is the Minneapolis Heart Institute the largest provider of cardiac care in the entire Twin City area?
A. Yes, ma'am, it is.
Q. And have you over time received national recognition for your work with the heart?
A. The Minneapolis Heart Institute has approximately a 20-year history of being a premier single-specialty cardiovascular group. Dr. Robert Van Tassel, who founded the group, brought forth the concept of working with primary care physicians in a single-specialty group, giving high clinical medicine, but then returning the patient almost to the primary care physician for continued ongoing primary care.
Q. Could you briefly describe for us the number of cardiovascular procedures that the Minneapolis Heart Institute does, say, in one year's time.
A. We have roughly somewhere over 25,000 patient visits per year. We physically go to 28 outreach sites in Minnesota and western Wisconsin where one of our cardiologists will drive to Grand Rapids or Willmar or New Ulm to provide outreach consultative services to communities.
We perform about 4,500 diagnostic coronary angiograms a year, roughly 1400 angioplasties, catheter-based interventions which we'll talk a little bit about a little bit later, about the same number of open-heart procedures a year, roughly 1400, putting in approximately 450 pacemakers last year, approximately 150 cardiac defribillators. We have the active transplant program doing approximately 25 heart transplants a year. So we try to offer the entire spectrum of clinical cardiovascular care.
Q. Now limiting your response now to your own practice, could you describe for the court and the jury what the nature of your practice is.
A. I am director of preventive cardiology at the Minneapolis Heart Institute. I spend approximately 95 percent of my time in acute patient care. Of approximately -- of the 95 percent of my time, 75 percent of the time is spent with the full spectrum of cardiovascular care, approximately 15 to 20 percent is -- dealt with what's called primary prevention, which is trying to keep a patient from having the first heart attack, and I have a special interest in what we call secondary prevention, which is once a patient's had a heart attack, keep that patient from coming back again and again by addressing the causative agents that caused them to come for the first time.
Q. Doctor, are you also the chief operating officer and board chair of a company called ProMedicus Systems, Inc.?
A. I am.
Q. And could you briefly describe for us what the work of that company is?
A. It's an offshoot of our medical environment in the metropolitan area, which for most of you in this room I don't have to expound on. We saw the biggest issue over the past half a dozen years or so of being appropriate care, getting the right care to the right patient in the right setting, whether that's in a primary care setting or whether the patient needs to get to a specialist to try and maximize the efficiencies of serving that patient, so that wherever they come, they are served appropriately.
What we have done first through the Heart Institute and now through this company is to try, with a web-based computerized service, to give specialized help to primary care physicians so that they will have specialty help wherever a patient presents. The spectrum of medical knowledge is tremendous and the pressures on primary physicians are tremendous in this atmosphere with that environment that we live in, so we try and give as much help in -- in -- in line with what the mission of the Heart Institute has been since day one, to work with primary care physicians to give best patient care wherever the patient presents.
Q. Doctor, in the early '80s were you medical director and chief of staff at the McNamara Hospital and Nursing Home in Fairplay, Colorado?
A. I was.
Q. Please tell us your experience in working with that nursing home.
A. Between my first and second year of residency, I took a one-year sabbatical, and with that ran a small hospital, 16-bed nursing home, emergency room and clinic that was 88 miles southwest of Denver. It was probably one of the best learning experiences I've ever had to understand what a primary care physician feels, especially in a rural area, when they don't have some specialist right around the corner.
Q. And then between your residency and cardiology fellowship, did you work as director of utilization review for Midway Hospital here in St. Paul?
A. I did.
Q. And what was the nature of that work, doctor?
A. Again focusing on quality of care, I was employed to review charts in order to try and make sure and work with physicians to make sure that patients were appropriately treated in a hospitalized setting.
Q. Now doctor, are you a member of a number of medical associations and societies?
A. I am.
Q. Are you a member of the American College of Physicians?
A. Yes, ma'am.
Q. And the American Medical Association?
A. Yes, ma'am.
Q. And the American Heart Association and its Council on Clinical Cardiology?
A. Yes, ma'am.
Q. And have you served on the board of directors of the American Heart Association, Minnesota affiliate?
A. Yes, ma'am.
Q. And have you worked as the chair of the Physician Cholesterol Task Force of the American Heart Association, Minnesota affiliate?
A. Yes, ma'am.
Q. Is it fair to say, Dr. Graham, that some of your primary interests in cardiology are the secondary prevention of cardiac events, and the delivery of appropriate care throughout health care?
A. Yes, ma'am.
Q. Now that we've learned about your training in clinical cardiology, let me ask you these questions:
Are you an expert in epidemiology?
A. I am not.
Q. Are you an expert in biostatistics or health economics?
A. No, ma'am.
Q. Doctor, I'd like to begin our discussion today with the anatomy of the heart. We have heard from previous experts in this case about the gas exchange that takes place in the lung. I'd appreciate it, with the permission of the court, if you would step down and describe for us how the oxygenated blood gets from the lungs to the heart.
A. I first have to apologize for my drawing before I take the first stroke, but what we would like to show -- this is a heart, and the heart is a pump. And if you think of it very simply as a pump that you would pump out your basement with or anything else, it becomes an easier concept. The blood, after it is used up -- the blood basically delivers nutrients and oxygen. When the blood delivers its oxygen to the tissues it becomes blue, and we look at that as a darker color and we call that blue blood. And as the blue blood comes back to the heart from the top, the superior vena cava and the inferior vena cava, it comes back to a place called the right atrium. We'll just say RA there. And that right atrium then is filled with blue blood that goes into the right ventricle. Ventricles are the bottom chambers of the heart, atria are the top chambers. And the job of the right ventricle is to push the blood in a fairly low-pressure system to the lungs.
Now once it goes to the lungs, as Dr. Davies has very exquisitely talked about, it picks up oxygen and comes back to what is now the left atrium, the top chamber on the left side of the heart -- this is if I was facing you like this -- and then into the left ventricle, which is the biggest, most powerful chamber of the heart, and is responsible for pumping blood to the body. And the blood pressure that we take and that you may be familiar with, 120, 140, whatever like that, is generated in this pumping chamber, and then the red blood is directed to the body, all right, through the aortic valve out to the body. Okay? And once that happens, if this pump does not work appropriately, there is decreased flow, just as if the sump pump in your basement didn't work, you would have water in your basement. With that there is decreased flow, and there can be back- pressure of blood back to the lungs, which causes the person to be short of breath.
One of the things that Dr. Davies talked about is shortness of breath. There's also a question: Is it the heart or is it the lungs? Many of the people that I see it's the heart, where the heart is no longer pumping well, and the blood pushes back towards the lungs and makes somebody feel short of breath.
MS. NELSON: Dr. Graham, let's just mark your picture as Trial Exhibit 25023. And Your Honor, at this time we would offer 25023 for demonstrative purposes only.
MR. MARTIN: No objection.
THE COURT: Court will receive 25023.
BY MS. NELSON:
Q. Now doctor, if you would take a look at Exhibit 30111, is that, although enlarged, an anatomically correct model of the heart?
A. I believe it is.
MS. NELSON: Your Honor, we would at this time offer Exhibit 30111 for illustrative purposes only.
MR. MARTIN: No objection.
THE COURT: Court will receive 30111.
BY MS. NELSON:
Q. Doctor, can --
Using the heart, can you explain to the jury how the body gets its blood supply?
A. I can. This again --
Your heart is about a little bigger than your fist, so if everybody makes a fist in this courtroom, if you have a big -- big fist, you probably have a big heart, and if you have a little fist, your heart is probably a little bit smaller, so this is many times bigger than any of our hearts. The arteries that flow on the surface of the heart are about as big as a lead pencil. Okay? And so they're -- they're just a few millimeters in diameter.
And I want to just first open up this heart, and of course we can't do that in real life, but this is the right ventricle that pushes the blood out to the lungs, the blue blood, then it comes back to the heart, to the left atrium, this very thick muscle, the pumping chamber of the heart called the left ventricle. And if this doesn't work, if the pump doesn't work, then nothing works and you die.
And with that, when it's pumped out here to the aortic valve, it comes through what's called the aortic arch. These are the vessels that feed the head. The head is the most sensitive organ in the body, the brain -- six seconds it can only be deprived of oxygen and then it stops working. And then this aortic traverses down and feeds the various organs of the body there. And this is the pump, and I'm a little prejudiced being a cardiologist, but I think this is -- you know, if the heart doesn't work well, nothing else works well.
Q. Doctor, then how does the heart muscle itself get its blood supply?
A. The heart is like the hands, the legs, anything, it needs -- it needs blood and it needs oxygen, and there are various ways that the heart can get oxygen, but the -- the primary way and the way that you and I at this moment are getting our oxygen, I will sketch out again for you, and I again --
The aorta, as I -- as you saw it there, comes out and gives its branches to the head and to the arms and then continues on down like this. The arteries that feed the heart are run on the surface of the heart. And I will try my best to sketch those arteries out for you. And what they look like when we look at pictures of them is essentially tree roots that keep branching. And when they branch, they give the various nutrients, oxygen and sugar -- that's all that's delivered to the heart -- but it's crucial. The heart muscle like any other muscle needs the nutrients.
This again, if I was facing you, this would be the right coronary artery here -- and we will talk more about this as we go on -- this is called the left main coronary artery, because it's the main artery going in the left side of the heart, this is the left anterior descending coronary artery or LAD. In most people that's the most important artery because -- and I'll show -- because it feeds this thick front wall of the heart. This is the LAD coming down here on the surface of the heart. Convenient for bypass surgeons and all that it happens to be located on the surface. But with that, that's LAD comes down here, the circumflex coronary artery circles around the back of the heart. Okay? And that's usually a little smaller in most people, but you can see it circling around back here. All of us have these, that's how our heart get its blood supply. The blood supply then goes through the heart from the outside to the inside after these arteries continue to branch.
MS. NELSON: Your Honor, we will mark Dr. Graham's drawing of the coronary arteries as Trial Exhibit 25024, and offer it for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 25024.
BY MS. NELSON:
Q. Now Dr. Graham, I'm going to ask you to get your notebook of slides, please.
If you would turn to Trial Exhibit 30018, please. Dr. Graham, is that an anatomically correct illustration of the arterial system?
A. Should I show them?
Q. No, not yet. Just "yes" or "no."
A. Yes.
MS. NELSON: Your Honor, we offer Exhibit 30018 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30018.
BY MS. NELSON:
Q. If you would, Dr. Graham, please describe what is depicted on 30018.
A. Of course, again, a little biased cardiologist, but the heart is the center pumping organ. When the aortic arch comes around as I drew here, in much nicer fashion is shown the innominate system here that gives a branch to the arm, the right carotid artery that feeds the right side of the brain, the left carotid system and the left subclavian, and then the aorta that comes down here and feeds the various intestinal organs, kidneys coming off here, and then this upside down Y is the iliac arteries that goes to the femorals and down and feeds the legs. Again it's much the same as the diagram that I show here, it's a branching tree almost like tree roots that then feed each of the respective organs downstream.
Q. Now doctor, I'd like to turn your attention to Trial Exhibit 30021 in your notebook, doctor.
A. Excuse me. Which number?
Q. 30021.
Is that an anatomically correct illustration of the coronary arteries that would aid you in illustrating your testimony?
A. Yes, ma'am.
MS. NELSON: Your Honor, we would offer 30021 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30021.
BY MS. NELSON:
Q. Dr. Graham, would you please describe what we see on Exhibit 30021.
A. Again this is a much prettier drawing of the -- of my drawing right here. And the aorta is coming out here. The valve that I show, the aortic valve, which is the trap door between the heart and the aorta, is under the pulmonary artery here, but you can see the right coronary artery coming out here again, branch -- giving branches off, the aorta coming out here. The very important big left anterior descending coming down the front of the heart where the big pumping portion is, and then the circumflex then circling around the back of the heart.
Q. Doctor, what is the size of a coronary artery?
A. As I had mentioned before, a coronary artery in most people is roughly the size of a pencil. And so when you -- when we talk about working inside that and doing angioplasties and stuff, we're basically working inside a pencil.
Q. Now doctor, I want to turn your attention to the subject of arteries developing blockages.
Could you briefly describe for us -- and you might as well stay right there because we're going to use exhibits here -- how arteries develop blockages.
A. Again, I -- I think a simple drawing can -- can tell a lot in something like this.
An artery is a pipe. It has to deliver the goods downstream like any of the pipes we have in our own home. I'm just going to draw for you what would be a pipe here. And with that we'll look end-on at the same pipe here. And over time an artery can develop -- and I might -- must admit by the time -- we're going to look at some angiograms later and all -- by the time we see something on an angiogram, it's a quite large blockage. And if you looked in all of our arteries by virtue of living in Western society, we would have abnormal arteries. And I'll explain a little bit more about that later. But by virtue of having higher lipids than is necessary, with other insults to the artery, over a period of time a small plaque can form in that artery. And it's just like any other blockage in a pipe or anything, and over time that can increase in size with that.
If we look then end-on, a beginning of flow limitation happens when that plaque blocks off that artery. We think most of the time a flow limitation has to be 70 percent or more to really impede blood flow down the artery.
Q. Now doctor, would you take a moment in your notebook and look at the following exhibits for me: 30022, 30040, 30015 --
A. Wait, wait, wait.
Q. Actually, 30015 is a model. 30033 and 30043.
Doctor, are each of these exhibits either actual microscopic photographs of coronary arteries or accurate portrayals of coronary arteries?
A. Yes, they are.
MS. NELSON: We would offer, Your Honor, 30022, 30040, 30015, 30033 and 30043 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: The court will receive those into evidence.
BY MS. NELSON:
Q. Turning your attention, Dr. Graham, first, to 30022, could you please describe what this exhibit portrays.
A. What this exhibit portrays are two examples of a relatively normal artery here, again a pipe in cross-section here that looks relatively normal, and this would be a far advanced atherosclerotic plaque, "atherosclerosis" meaning a blockage that develops over time that has end-on narrowed the artery severely, on lengthwise, caused a -- probably we would call that an 80 percent or more blockage, impeding flow, blood flow in the artery.
Again with a microscope, though, when you look at a coronary artery disease or atherosclerosis in general, it tends to be a diffuse disease, but with a focal clinical presentation. And we'll talk a little bit about that.
Q. Doctor, atherosclerosis, is that a disease of the artery that's characterized by the blockages that you've been describing?
A. Yes. Atherosclerosis, again, is a diffuse disease. And I think we will have to draw the distinction between atherosclerosis -- and again, almost everybody in this room, by virtue of living in Western society, has some degree of atherosclerosis. It's the question of who is going to present with clinical events, when is that atherosclerosis going to accelerate into a clinical event that becomes the most important thing.
Q. Now what risk occurs when the coronary artery creates blockages?
A. Again we talk of the coronary artery, if we look at the model or model there or something, if the blood doesn't flow down the pipe, within four to six hours all the muscles downstream die. And that's what heart attack is. A heart attack is when the area here closes off and a clot forms there, if the -- if -- the heart muscle downstream here then would die from that. And that's what a heart attack is.
Now when people come to the emergency room in most places in the country, they will be given a clot-dissolving medicine to try and reopen the artery. About 70 percent of the time it works, 30 percent of the time, unfortunately, it doesn't. And only about 40 percent of patients who are eligible for that get to the emergency room in time to get the clot-dissolving medicine.
Q. Now focusing for a moment what is portrayed on that exhibit as -- it looks like little white lines, what does that depict?
A. What -- what the -- what the white lines here would depict, there is a lipid core here that -- that is -- and then there's a fibrous cap over that, the body caps that, and then that cap, for reasons that we really don't understand, can break down. When that happens, the goo of the lipid core, which is a little -- a little bit like a little Jell-O in all of our coronary arteries, can then pour out and it causes a clot to form there.
Q. Now you used the term "plaque." What did you mean by that term?
A. "Plaque" just means blockage, I think. And I think in keeping it as simple as we can, which we try to do for patients to understand, is if a plaque remains stable, it can -- it can be there for a long time. But a plaque we say is basically a blockage.
Q. Now what is portrayed by the central gray area in that coronary artery?
A. This is a depiction, an artist's depiction of a clot that is formed after this area in the artery has cracked open and some of this goo has come out here and causing a blood clot to form right there.
Q. Now I would phoning us your attention on Trial Exhibit 30040 and ask you to describe what we see in that exhibit.
A. This is an actual photomicrograph of a coronary artery plaque. Again the coronary artery itself used to be this big, and over time a fat-filled lipid plaque has built up here. This is the fibrous cap, which is like a band that covers that, that is the border between where the plaque or the blockage is and where the blood flows down now. This area here has been filled with a white contrast material that opens the artery up, and this is a post-mortem examination.
This now we may consider to be a 60 percent, 70 percent blockage. It is my job as a cardiologist, it's very important to find out whether that's in the left main coronary artery or whether it's way downstream here in the distal mainstream artery, because the treatment is much, much different. Any one can cause pain.
This is the type of patient who presents with what we call stable angina, and as the patient walks down the street, gets a little chest pain, stops and the chest pain goes away, because as the heart demands more blood flow, there is this blockage that has impeded the blood flow from getting there. And with that, we then have to work it up and say where is this blockage and what do we need to do about it?
People who have coronary blockage, as far as treating them, there's only three initial treatments; one is medicine, the second is angioplasty or stenting, the third is coronary bypass surgery for people who have severe or life-threatening disease.
Q. Now doctor, would you look at the model that we have that's been marked 30015 --
No, it's right here.
A. Oh, sorry.
Q. Is that an accurate or inaccurate depiction of the clogging of a coronary artery?
A. This is an inaccurate depiction --
Q. Could you --
A. -- for most coronary arteries.
Q. Could you explain why.
A. Intuitively we used to think that you would have no blockage, then a 25 percent blockage, then a 50 percent blockage, then it goes 60, 70, 80, 90, and finally to a hundred percent blockage. We've learned that that is not true. If you had to pick one blockage here that is most likely to cause a heart attack, this one; it's the 30 to 50 percent blockage that suddenly, like a popcorn seed, pops, and when it pops, it can pop like one of Orville Redenbacher's finest and go out into the lumen of the artery and block it off, or it can pop very small and you never know it happened.
We know that the primary cause of acute heart attacks and unstable coronary syndromes, which means unstable angina, are -- is this disruption of the plaque and a clot forming there. So we know that there are certain conditions that people's blood is stickier. When they do rupture this plaque, that they form -- are more likely to form a clot. The primary one and the most easily reversible one is cigarette smoking. Because when the blood goes through the lungs, as Dr. Davies eloquently defined to you, it goes single file. Those red cells and the platelets, which are responsible for blood clotting, when exposed to cigarette smoke, the platelets become angry or turned on, and so just as when you skin your knee, you may form a very good scab or clot there, when your artery has a skinned knee, you have a hyper response to that and form of clot that can close the artery and cause an acute heart attack.
Q. Dr. Graham, let's go back a minute. You used the word "angina." Could you explain what the word "angina" means?
A. Angina is chest pain, and it's usually caused by low blood flow to the heart. So any time somebody has -- we call it stable angina, and that would be a plaque like this where they have exertional angina and then they rest and it goes away, and we juxtapose that to unstabilized angina where they have resting pain or they've had a change in the pattern of their angina.
Q. Okay. Let's take a look at Trial Exhibit 30033. Does this exhibit portray the rupture of the plaque that you just described in the unstable angina?
A. I think this is a beautiful depiction of what happens in patients who have either unstable angina or a heart attack. This maybe just a few hours ago was a 50 percent blockage here with a fibrous cap here covering this. At that time, then, that popcorn seed popped, if you would, and the artery here -- the goo came out here, you get intense vasospasm here, this -- this relatively normal artery contracts down, formed a clot that was a fatal event in this person.
And we know now from numerous studies and from treating hundreds and thousands of patients like this, the patient who was alive that came in with a heart attack, by knowing this, we give them a clot-dissolving medicine, called TPA, in the emergency room, and again in about 70 percent of patients it opens up the artery within an hour and a half.
Q. Turning your attention then to Trial Exhibit 30043, does this exhibit, doctor, portray a clot in an artery that has atherosclerosis?
A. This again is a depiction now in a length-wise form, this has to be a pipe, again, that has to deliver blood to the muscle downstream of a -- what was a stable plaque that has now fissured or ruptured in a length-wise fashion now. You can see different colors of clots there. We know that this is coming and going, and then the fatal event in this patient was a big red cell cast here that closed off the artery entirely.
We know that 30 percent of patients who have heart attacks never make it to the front door of the hospital, and what happens is when they occlude the artery, they either drop their blood pressure or have a lethal arrythmia.
Q. Doctor, I'd ask you to look in your book at Trial Exhibit 30020.
A. 30020.
Q. Is that an anatomically correct depiction of the aftermath of a heart attack?
A. Yes, it is.
MS. NELSON: Your Honor, we would offer 30020 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30020.
BY MS. NELSON:
Q. Could you explain 30020 for the jury, doctor, keeping in mind the previous slide which demonstrated the fatal clot.
A. If you think again of a blockage, and a heart attack is a total closure of the artery, if the artery is not opened within four to six hours, the muscle downstream again, fed by this end of the root, if you would, dies, and that is now scar tissue there. And the pumping function that the heart needed -- needs to do, and this would correlate on this model to the tissue here and the tissue on the end of the heart, is now gone, and that area becomes not thick, but thin, and no longer pumps. So the patient is now compromised to the point where they have heart muscle that doesn't work. And if it's a sufficient amount of heart muscle, they can go into what we call congestive heart failure. Again, the muscle -- there is a certain amount of muscle needed to pump, and if you lose that amount of muscle needed, the blood backs up into the lungs, you get short of breath, and you don't pump enough blood forward, and the vital organs of the body are not profused or they're not getting enough blood.
The other point about this also, this area which was now dead conducts electricity differently, and people are at risk from dying from what we call arrythmias, or the heart beating chaotically after they have a full-thickness scar in their heart after a heart attack.
Q. Doctor, I want to turn your attention now to the impact smoking has on this disease of the blockage of the coronary arteries that we've been talking about.
Doctor, based on your training and experience, do you have an opinion to a reasonable degree of medical certainty as to the mechanisms by which smoking are a cause of these blockages in the arteries?
A. I think, again, for everybody in this room's benefit, I think that it's important to realize that, you know, there's a lot of vascular disease in this country and that we have to do everything we can to keep, you know, all of us out of having vascular disease.
There are four prime mechanisms which smoking causes not only the development of atherosclerosis, but the development of what we call acute events.
MR. MARTIN: Your Honor, I'm going to object to this. He has not responding to the question that was asked. I request that he do.
THE COURT: I think you should re-ask the question, counsel.
MS. NELSON: That's fine.
BY MS. NELSON:
Q. Doctor, just tell me now, do you have an opinion, "yes" or "no," to a reasonable degree of medical certainty, as to the mechanisms by which smoking is a cause of this disease of the blockage of the arteries?
A. Yes, I do, ma'am.
Q. And what is your opinion, doctor?
A. Again, I believe that there are four main ways which, looking at the model, that we have established that smoking is known to be deleterious to coronary arteries. The first is that it competes for oxygen. As I said, the blood flowing to the heart has to deliver sugar and oxygen. That's what it does. The heart doesn't use fat. And in people with lung disease, as Dr. Davies has again eloquently said, you don't get as much oxygen into the blood, and so if a normal amount of saturation of oxygen is a hundred, some -- some people may have saturations at 80, 85, you've decreased the amount of oxygen in the blood.
The second way it competes for oxygen is there is carbon monoxide, CO poisoning in cigarette smoke, and most smokers have about ten percent of their hemoglobin, which is responsible for carrying oxygen, that's what hemoglobin does, carrying oxygen in the blood to the various body tissues, ten percent of the hemoglobin is tied up as carboxylated hemoglobin, or is tied up in this almost unreversible form.
Q. Doctor, is hemoglobin commonly known as the red blood cells?
A. The red blood cells are -- contain hemoglobin. And hemoglobin's job, again it's only job is to carry oxygen to the tissues and deposit it in the tissues. So we have a double-fold, there's a competition for oxygen because of lung damage that we can't get the oxygen into the blood, secondly, the hemoglobin is then tied up, about 10 percent of it, for -- with the carbon monoxide.
Q. Doctor, if you'd look in your book at Trial Exhibit 30045, please. Does that picture accurately portray the concept of carbon monoxide competition for oxygen?
A. Yes.
MS. NELSON: We would offer Trial Exhibit 30045, Your Honor, for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30045.
BY MS. NELSON:
Q. Now could you describe for the jury and the court what you see in that exhibit, doctor.
A. This is the alveoli of the -- where air exchange happens in the -- in the lung. And it's analogy to a honeycomb with a lot of --
And this layer here is only one cell thick, so as the red cells come through and the platelets, they are exposed to, as the ingredients, oxygen, but also carbon monoxide diffuses through there and ties up the red cells so it cannot accept the oxygen molecule. We also know that from previous -- I'm sure Dr. Davies talked about that there -- as this is broken down, what I talked about, competition for oxygen, if this -- you lose some of the architecture here, the ins and outs, it's harder to get anything across here into the bloodstream.
Q. Now doctor, you mentioned that there were four mechanisms by which smoking caused these blockages in the artery. What is the second mechanism?
A. The second mechanism, and I will explain what this means, is what we call vaso -- "vaso" meaning vessel -- constriction. Vasoconstriction means a clamping down of a vessel. Okay. And what I will --
An artery, under the effects -- even a normal artery -- of cigarette smoke that is this big, then becomes this big under the direct toxic effects. There's smooth muscle around the artery that causes it to contract, and all of our -- all of our heart arteries have muscle around them, and it causes the artery to become smaller.
It becomes very important if an artery has, say, a 50 percent blockage, and then you have vasoconstriction, the blockage will remain the same size here to here, what suffers is the lumen, and suddenly what was a 50 percent blockage can become a 70 to 80 percent blockage and cause restriction of blood flow.
Q. Doctor, would you look at Trial Exhibit 30039. Does that accurately depict the impact of smoking by vasoconstriction on the arteries?
A. Yes, ma'am.
MS. NELSON: We would offer, Your Honor, Trial Exhibit 30039 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30039.
BY MS. NELSON:
Q. Could you please demonstrate to the jury the concept of vasoconstriction caused by smoking, doctor?
A. Yes, ma'am.
Again in a much prettier way than I've shown you hear, an artery that is this big under the effects of cigarette smoke becomes constricted down, and therefore the flow of blood down there is limited along the entire length of it.
Q. Doctor, what is the third mechanism by which smoking causes blockages in the coronary arteries?
A. We would best characterize this by a direct toxic effect.
Q. Now what do you mean by that?
A. In the arterial wall there is a buildup of cholesterol and there is an imperfect healing, if you would, of that plaque, that little bit of Jell-O in the arterial wall. Almost like sandpaper, the ingredients of cigarette smoke irritate that plaque when people are smoking, and it causes the lining of that to be a continual skinned knee, if you would, because there's a -- almost of a sandpaper going over that blockage up and down the artery from the direct effect of cigarette smoke.
Q. What is the fourth mechanism by which smoking causes blockage of the coronary artery?
A. The fourth mechanism, and -- and the one that --
When we talked about the first three, we were talking about the development of atherosclerosis, or the development of blockage. Again, many people in this room have atherosclerosis in various stages who have not been in the hospital or have not had bypass surgery or angioplasty for that.
The fourth event is probably the most important as far as clinical event, and that is what I would call angry or turned-on platelets.
Q. And what are platelets, doctor?
A. Platelets are parts of the blood that are responsible for blood clotting. And when you skin your knee and you begin to -- the blood stops there, and there's an initial mesh that forms over there to stop the bleeding, that is platelets that go to the area of injury. When you injure an artery or your knee, there needs to be response to that. Again, through the lung, when the platelets go through in single file with the red cells through the lung and are exposed to cigarette smoke, they get what we call turned-on or activated platelets. They are ready to clot. So when somebody has the ruptured plaque within the coronary artery, and people oftentimes will rupture plaque and they may heal down, they may not, but when somebody is a smoker they have a -- what we call hypercoagulable state or a high coagulation state, and with that they tend to form clots more easily, they tend to present with unfatal symptoms or infarctions more often when they rupture the plaque.
We know that aspirin as an anti-platelet agent -- and many people in this room may take one aspirin a day -- greases platelets so they don't stick together. We know from studies that it decreases the incidence of heart attacks in middle-aged males by about 20 to 25 percent, one aspirin per day. But the effects of smoking can even overwhelm the effects of aspirin, and that's been well-documented in the literature.
Q. Now doctor, in addition to smoking, are there other independent causative agents which substantially contribute to coronary artery disease?
A. Yes.
Q. And what are those?
A. When we look at causative agents of coronary artery disease, there are what we call the big four, which are smoking, cholesterol problems, either -- diabetes mylodus or high blood sugar, and high blood pressure. These are the big -- what we call the big four causative agents of -- of coronary artery disease.
Somebody who has one of them only may not present with coronary disease. Yet the more you have of these, there's a synergy between them that makes you more at risk for presenting with coronary disease. So we look for people with multiple risk factors, we look for people with family histories of problems with that, but at the same time, these are the major things that almost every clinician is trained to look and ask people to say are you at risk for having a heart attack.
Q. Dr. Graham, is smoking, however, an independent causative agent which substantially contributes to the onset of coronary artery disease?
MR. MARTIN: I'm going to object to the form of the question.
THE COURT: No, you may answer that.
THE WITNESS: Excuse me?
THE COURT: You may answer that.
THE WITNESS: Okay.
A. In -- in my clinical training and clinical experience, I believe that smoking is the most powerful modifiable risk factor for coronary artery disease and causative agent.
Q. Now Dr. Graham, can you think of an analogy which would explain to the jury and the court the effect of smoking synergistically with the rest of these causative risk factors?
A. Excuse me one moment, please.
Q. Sure.
A. As physicians, and especially in dealing with people with coronary artery --
MR. MARTIN: Excuse me, Your Honor. It seems appropriate, perhaps, that the doctor return to the witness chair.
THE WITNESS: Do you want me to do that?
MS. NELSON: That's fine.
THE COURT: Are you finished using the board?
MS. NELSON: Well there's a number of devices down here, but we can answer this question there, but -- but he will be returning down to explain some things.
THE WITNESS: I'll get my book.
THE COURT: I wonder if we should take a short recess at this time.
MS. NELSON: Sure. That's fine, Your Honor.
THE CLERK: Court stands in recess.
(Recess taken.)
THE CLERK: All rise. Court is again in session.
(Jury enters the courtroom.)
THE CLERK: Please be seated.
*29 BY MS. NELSON:
Q. Dr. Graham, before the break, I believe I had asked you if you can think of an analogy which explains to the jury the effect of smoking and these other causative agents on the blockages in the artery, in the coronary arteries that we've discussed in the past.
A. I think it would be helpful to -- to think of a wheat field, and if there is wheat to be grown in that field, you need to think of cholesterol and sugar as -- as fertilizer for that wheat. And let's speak to cholesterol, since it has probably been talked about a lot, and a lot of us think about that.
If there is no cholesterol, if there is no fertilizer at all, there's essentially no crop and there's no wheat to grow. And about three percent of the people in our population have very, very low cholesterols and -- and therefore probably don't have any risk of coronary artery disease. These are cholesterols less than 130. You know, we don't see them very often. We don't see those patients in our catheritization laboratory.
The truth of the matter, then, is for the other 97 percent of the population, about five percent of those people have just the right amount of cholesterol. And by virtue of living in Western society, most of us have too much cholesterol, and the wheat grows fast and furious and oftentimes, like a yard that doesn't get cut, overgrown with each other. And the same could be said for diabetes.
I liken hypertension to wind that can blow the crop, and even in severe cases lay it down, but when the wind goes away, the crop recovers.
I liken smoking to a vigorous, sudden summertime hail storm that comes in, and if there's a crop there, the -- the hail is -- damages the crop and will forever more -- while it's there, it continues to damage the crop, but even after the hail is gone or when somebody quits smoking, the crop is irreparably damaged forever and will never be the same as it would have been.
Q. Doctor, you spoke of a patient presenting with -- I think you used the term "stable angina" or "stable coronary symptoms." When that patient presents to you and complains of chest pains, are there non-invasive diagnostic tools available for you to evaluate the damage to their artery?
A. Certainly.
Q. And what are those?
A. When a patient comes, we -- we take a history, first of all, and -- and see what the patient's causative agents or risk factors are, and we'll ask if they smoke, if they have high cholesterol, if they have diabetes, hypertension, if they have a family history of coronary events, the usual questions to see how many risk factors there are, because we know the more risk factors the more likely is that patient's pre-test risk of having blockages in their coronary arteries. Then we ask the type of pain they have, whether it's the typical stable type pain where they walk down the street, they get chest pains, they stop, it goes away, and they start again, it comes. That's typical angina as opposed to somebody who may say I have a sharp pain in my left -- the right side that kind of comes and goes, that would be atypical for low blood flow to the heart.
And then we try and quantify the amount of angina. Do they get angina when they're running vigorously two blocks, or do they get angina when they walk across the room? And there's something called a Canadian angina classification between one and four, one being angina for chest pain with vigorous exercise, four being all the way down in a stepwise fashion to resting chest pain. And so we qualify a patient that way, and then if it is safe, we usually do a treadmill test if the patient is stable, if they don't have resting chest pain, in order to make sure that they can re-create their symptoms on the treadmill, and then with the electrocardiogram, which is the heart monitors that we put on them to look at their cardiographic tracings that show evidence of low blood flow to the heart.
In some patients where there's question about that, we will add a third modality called an imaging agent, which is either an echocardiogram, which gives us sound-wave pictures of the heart, or a nuclear substance to see if the heart muscle is working well, but it takes it up while the patient lays under a camera to see before and after exercise how the heart is functioning. And those are called imaging stress tests. It's a physician working -- cardiologist working with the primary care physician whose job it is to risk stratify a patient, to give them the most appropriate test along their course of presentation.
Q. Based on your experience, doctor, what is the range of cost for that type of stress testing?
A. A regular treadmill stress test with just a electrocardiogram and the belts, the walking-type treadmill that is a standardized fashion, costs about $250.00. Adding different types of imaging agents to that, there are various expenses associated with it, increases the cost anywhere from 600 dollars upwards to 3,000 dollars.
Q. If you'd look for a moment at Trial Exhibit 30029, doctor, does that accurately depict the type of stress test that you're describing to the jury?
A. Yes, ma'am.
MS. NELSON: I would offer, then, Your Honor, 30029 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30029.
BY MS. NELSON:
Q. Again very briefly, Dr. Graham, can you tell us what we see in this exhibit?
A. In this stylized drawing, there is a patient on a treadmill, much as like the treadmills that you would see at an exercise store, but the treadmill is a very standardized one that is linked to a computer, and the elevation and speed of the treadmill is -- is standardized, so that whether I do a stress test in Boston, in Minnesota or San Francisco, there is a standardization of the -- of the testing.
The patient is then monitored with the electrocardiogram, his or her blood pressure is taken about every minute during the test, and the electrocardiogram leads, which are the three electrocardiograms going across there, are monitored for evidence of low blood flow to the heart.
Q. Now doctor, before you spoke of a patient in an emergency condition who appears or presents with unstable angina or unstable coronary symptoms, such as a ruptured plaque or heart attack, what steps do you take when that patient arrives at your hospital?
A. Patients who have ruptured a plaque and who present with unstable symptoms range from very high concern to an acute medical emergency. When somebody presents and we think the artery is closed, we have four to six hours to open that artery in some fashion in order to re-establish blood flow down so the heart does not become starved. So we view the ruptured plaque and a history consistent with that as a medical emergency. The patient is hospitalized, he -- he or she is often given blood thinners intravenously. If we think they have an acute heart attack, in some hospitals they would be given a clot-dissolving medicine. At the Minneapolis Heart Institute, at Abbott Northwestern, we will take that patient directly to the cardiac catheterization laboratory and try and open the artery directly with a balloon or wire, because we have a 95 percent chance of opening it directly with some of the tools that I will show you in a few minutes, as opposed to about a 70 percent if we give the -- give the clot-dissolving medicine.
Q. Okay. Doctor, let's talk for a moment, then, about cardiac catheritization.
Can you explain to the jury what an angiogram is.
A. As opposed to the treadmill testing -- I suppose I should have said this, but as you see the picture up there, a routine treadmill in somebody who has coronary disease has about an 80 percent what we call sensitivity of identifying patients with disease, and specificity, which means that if it is abnormal, we're pretty sure the patient has disease. That means eight out of 10 patients are identified. More importantly that means two out of ten are not.
At the same time, if we add one of those imaging modalities to it, either stress echo or nuclear stress test, the sensitivity and specificity of the test goes up to about 90 percent, which means we find about nine out of 10 patients with chest pain.
The gold standard is for people that we think have a very abnormal stress test or who are unstable and we're worried about them going on to a heart attack, becomes a coronary angiogram where we actually numb up the groin area and put a catheter in the femoral artery, thread that up in reverse flow from where I showed you before coming down, with special catheters and engage both the left and right coronary arteries and inject dye down the coronary arteries to say where are their blockages, how severe are they, and how should they be treated. If the patient has blockages, initially there's only three treatments: There is medication, either oral or intravenously; and there is an angioplasty and all the things we do like angioplasty, stents, Roto-Rooters, things like that, and for the patients who have severe or life-threatening diseases, there's coronary bypass surgery.
Q. Let's start then with angiogram, and if you would look at Trial Exhibit 30044, 30028, and 30038, do these --
A. Can you read --
Can you give the second one, please?
Q. Sure. 30028 and 30038.
Do these photographs and pictures accurately -- accurately anatomically depict the process of a coronary angiogram?
A. Yes, ma'am.
MS. NELSON: We would offer, Your Honor, 30044, 30028, and 30038 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30044, 30028, 30038.
BY MS. NELSON:
Q. Focusing your attention, doctor, then, on 30044, can you describe for the jury, first of all, who's the physician in the picture?
A. That's me.
Q. Okay. And what are you doing there, doctor?
A. In the catheterization laboratory where this is depicted, with a hat and gown, with an assistant, another assistant in the background, the Cat Lab costs about two million dollars. And this is the patient's right groin here, it has been anesthetized, and I'm holding in my hand a pericutaneous needle which I will enter the artery with.
Q. And doctor, is this an entire procedure done while the patient is awake?
A. The patient is awake, but sedated.
Q. Okay. Turning your attention, then, to 30028, can you describe for us what you see here? And I'd ask you to step down at this point because we will be using some medical devices, with the permission of the court.
THE WITNESS: Is that okay?
Thank you.
A. What this depiction shows, and I think we should start over here first, we usually enter the right femoral artery. Again if you think of the diagram that was shown of the blood flowing this way to the leg, we enter the largest artery we can -- the right femoral artery is about as big as your little finger -- and that decreases our chance of complications because we actually have to perc and enter -- percutaneously enter the artery. And we then put a sheath in and then backflow into the heart up here what's called the coronary catheter that injects dye down those coronary arteries, watching under a fluoroscope as we do in making a movie x-ray of the -- of the blockages in the artery.
Q. Dr. Graham, are what has been marked as Exhibit 30007 -- over here, doctor -- 30008 and 30010, are those medical devices that you would routinely utilize in performing an angiogram?
A. They are.
MS. NELSON: Your Honor, we would offer 30007, 30008 and 30010 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30007, 30008, 30010.
BY MS. NELSON:
Q. Now doctor, if you could actually demonstrate how you perform the angiogram for the jury.
A. Again, the patient is brought to the catheterization laboratory in a lightly sedated state, and with that they are -- a few minutes is taken to sterily prepare the patient with iodine solution, and they are covered with a sterile drape from their chin all the way covering their feet. We then take some novocaine and anesthetize locally the area that we are about to enter. Once we have done -- placed a needle in the artery -- and again it takes a fair amount of training, we just perc one side of the artery -- we put a wire through the needle and pull the needle out so all that is in the artery is a wire. At that time we then, over the wire, place what's called a sheath, and the sheath stays in for the duration of the -- of the procedure. And there's a dilator and it stretches the artery, you'll see it's kind of a smooth bullet tip, as it goes into the artery. We then pull out the dilator, and there's a ball valve here that keeps the blood from coming back. We then pull the blood back and flush sterile heparinized saline in there, a blood thinner saline so the blood does not clot, and then we do our procedure through this tube that now resides in the groin or in the right femoral artery.
To reach the coronary artery, once we have done that, there is -- we have coronary catheters, which are directed over a guidewire up the aorta, and once this is in place and sitting in the coronary artery -- excuse me, in the femoral artery, we then put in --
This is a right coronary catheter, and the catheters are preshaped. This is made by -- made by SciMed, which is a Minnesota company. And we direct the --
You'll notice there's a J on the end of it. This is called a J wire. And I told you before that even though you couldn't see blockages in arteries, that they -- they were there, and -- and often times people's aorta are a cobblestone of what we call atherosclerosis. So if we put up a bare catheter, we would drag it against that cobblestone and risk knocking off pieces that would go down to the legs and cause problems. So we always use a J wire, which presents a blunt tip as it goes up the aorta against the blood flow and into the first part of the aorta.
Again this is now shown diagramatically here. When the catheter comes up here, this is a left coronary catheter that engages the artery.
So as we advance the catheter, the case -- the entire case is done through this little tube that has been placed previously.
Q. And after you've injected dye into the coronary arteries, what is it that you're able to see?
A. We're looking for blockages, and you -- we --
The camera swings around the patient, and -- and -- and once we direct this up to the coronary artery, I turn it here to direct it into the artery, and then we inject dye down the artery and take pictures as the camera swings around.
MS. NELSON: Your Honor, could we have the bailiff or the clerk pass this around, or is it permissible to do it in this fashion?
THE COURT: You don't plan to use that again, doctor?
THE WITNESS: Not unless you're volunteering.
THE COURT: Then you can pass it around.
A. So that's the diagnostic portion of -- of the case. And again, if we find blockages in there, there are -- there are only three treatments: medicines, angioplasty or bypass surgery. Angioplasty works best on people who have one or two vessels blocked. And if there are multiple or severe blockages, bypass surgery tends to work better.
Q. Now doctor --
A. So --
Q. Doctor, excuse me, but looking back up at the screen for a moment, up to the left-hand portion, it appears to be a portrayal of coronary arteries on a screen; is that correct?
A. Yes, ma'am.
Q. And is that what you see when you look at an angiogram?
A. Yes. You look under the scope and then you'll see -- and we get an initial picture on a videotape in the room, and then we develop regular 35- millimeter film or digital film and look at them after in a more refined fashion. But we almost always in the loom know what's going on while we're doing the case.
Q. And Dr. Graham, what is the typical cost for one angiogram?
A. The typical cost for one coronary angiogram is 6,000 dollars.
Q. Okay. Doctor, now you've done the angiogram and discovered that your patient indeed has some blockages. I would like to turn our attention now to the interventions that you've mentioned to the jury several times available to attempt to fix the ruptured plaque or the clot. And let's start with coronary angioplasty.
A. Okay.
Q. Could you take that back from the jury. Thank you.
A. Oh, sure. Excuse me.
(Physical exhibit handed to the witness.)
Q. Could you describe for the jury what coronary angioplasty is, without the device at this point.
A. All right. Coronary angioplasty is through the same type of catheter that I showed you, if that was a right coronary lesion, we would thread a very small catheter and a wire with a balloon on the end of the -- of the catheter, and then again watching under the fluoroscope, we would first direct a wire across the blockage, and there's a skill to threading that very thin 14-one- hundredths-of-a-millimeter-thick wire across that -- that artery or the blockage, and then we direct the balloon across and inflate the balloon to stretch the artery at that point.
At that point there is no blood flow down the artery and you need to put down the balloon and pull it out. And there's a skill that goes with that.
Q. Doctor, I show you what's been marked as Trial Exhibit 30014. Is this an accurate portrayal of an angioplasty?
A. Yes.
MS. NELSON: Your Honor, we would offer 30014 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30014.
BY MS. NELSON:
Q. Could you describe to the jury what appears on that exhibit.
A. This in cross-section -- we only have half of our pipe here, appears to be a very significant blockage in highly stylized form. And again this -- remember we're working inside a pencil, this has been blown up to a huge degree to show us. You put the balloon across, expand the balloon to push out the artery at that area. When you put down the balloon, you hope for a very good cosmetic effect to open up the artery, and a functional effect.
Q. Now doctor, turning your attention to several of these medical devices that have been marked as 30003, 30014 and 30009, are these medical devices that you would typically use to perform a coronary angioplasty?
A. Which ones?
Q. '3, '14 and '9.
A. Yes, they are.
MS. NELSON: Your Honor, we would offer 30003, 30014 and 30009 for illustrative purposes only.
THE COURT: Court will receive 300013, 300014, 300009.
MS. NELSON: Let me just say that again, Your Honor, I think I may have misread them.
THE COURT: Okay.
MS. NELSON: It's 30003, 30014, and 30009.
THE COURT: All right.
BY MS. NELSON:
Q. Dr. Graham, can you describe the angioplasty procedure again for the jury?
A. Again, we spent years doing cardiology fellowships to learn how to do this procedure, and I don't expect to -- to teach each of you about the procedure. But I would just advance this wire, which we placed through the angioplasty catheter, and then the end of this wire, you'll see, has a very small J tip on it, and we -- we dance that artery -- we dance that down inside that artery that's smaller than a pencil, and then --
Oh, once we have the wire down, we then advance this balloon over that wire. And when we are just across the blockage, watching again under the radiation of the fluoroscope, we blow up the balloon and we measure the pressure anywhere from just a couple all the way up to 20 atmospheres of pressure, and the balloon crimps open the artery at that point.
Now that's how big the artery is. I mean the picture makes it look much better. But that's the small space that we're working in.
Q. Doctor, are there risks to this procedure?
A. There are risks any time -- and that's why we take --
Even doing an angiogram, the diagnostic procedure itself has a one in 300 to one in 500 chance of having a heart attack or stroke, about a one in 1,000 chance of dying from the procedure. And when we do an angioplasty there's about -- at the Minneapolis Heart Institute we're about 90 to 95 percent successful with the initial balloon. In about one to two percent of cases, when we blow up the artery -- again, think we're working about an arm's length away -- the artery can tear, and if we can't fix it, the patient needs to go to the operating room for an emergency bypass surgery.
So again these -- these are lifelong diseases that have taken many, many years to manifest themselves. None of these are cures. In the appropriately selected patients they are very, very good treatments, but they're not cures.
Q. Doctor, do you find that patients who have had an angioplastic procedure come back and the condition that they originally presented with has reoccurred?
A. Yes. And angioplasty is an injury, just like smoking is an injury, to the artery. But it pushes it open very, very wide. About 30 percent of people form a scar between two and six months after that initial injury where the artery comes back and narrows in, and they re-present with symptoms again. And then we either have to decide at that point whether we're going to stretch the artery again -- there's only about a 50/50 chance of success -- or whether the patient at that time will need bypass surgery.
So again, the Achilles heel of angioplasty has been something called restenosis or rescarring of the artery back in.
Q. Doctor, what is the typical cost of a coronary angioplasty?
A. The typical cost of a -- of a coronary angioplasty is about 16,000 dollars.
Q. Doctor, then turning your attention to the stent procedure for a moment, if you would look in your book at Trial Exhibit 30025.
Does that depiction accurately depict a stent procedure?
A. Yes.
MS. NELSON: Your Honor, we would offer 30025 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30025 for illustrative purposes.
BY MS. NELSON:
Q. And doctor, looking at 30002 and 30006, are those both examples of stents?
A. Two and four.
Q. 30002 and 30004.
A. Yes.
MS. NELSON: Your Honor, we would offer 30002 and 30004 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30002 and 30004 for illustrative purposes.
BY MS. NELSON:
Q. Now Dr. Graham, looking at the procedure on the screen and utilizing the stents themselves, can you describe to the jury what a stent procedure involves.
A. Stent --
Angioplasty is about 12 to 14 years old now. Stents have been the first real improvement over angioplasty in that when we place a stent, it -- it's actually like a little scaffold. It's deployed over a balloon, and the balloon is -- the stent is crimped on the balloon. The balloon, just as the angioplasty balloon that you're holding now, is delivered across the blockage, but what happens is it scaffolds the artery open. So when we finish an angioplasty, by the time the patient leaves the room, being it is living tissue, there is some elastic recoil, and then if you get that scarring restenosis, it closes down tight. In the stent when you leave the room, the artery remains scaffolded open by a piece of steel. And when that happens, even if it scars back in, we tend to still have an adequate blood flow down the artery.
The benefit of stents is that it has decreased the restenosis rate, or that scarring back in, from about 30 percent down to about 10 percent.
I have a couple of stents here. Again, this is a -- a stent that is working to show you somewhat of the magnitude of the sizes that we work with. That's the stent that's expanded that would go in the coronary artery. This is a stent that's a little larger that is placed in the coronary artery. The company made a magnifying glass so you can actually see it. But it's a little piece of woven wire that goes in the artery, holds that artery open, and that has been a very major benefit for us in the catheterization laboratory.
Q. Now turning your attention to another procedure calls extraction atherectomy, would you look in your book to Exhibit 30024.
A. Yes.
Q. Is that an accurate portrayal of extraction atherectomy?
A. Yes.
MS. NELSON: Your Honor, we would offer 30024 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30024 for illustrative purposes.
BY MS. NELSON:
Q. Now Dr. Graham, can you describe this procedure for attempting to remove blockage.
A. Yes. The -- the atherectomy chamber has a cutting-head gear and a rotating blade that, as it goes across a blockage, actually then traps the debris here and we actually take it out of the body. One of the angiograms I'll show you, we actually used an atherectomy catheter such as this.
It's a big device. We can't use it on a bend over here, it has to be used on a straight. And we need even a bigger tube than I showed you there to place it in the groin. So it -- it's a tool that we use, and -- and what is happening in the catheritization laboratory, we're kind of like a carpenter where we used to only have a hammer, and that's an angioplasty balloon, we now have stent, atherectomy devices, Roto-Rooters and things like that, so we have plyers and screwdrivers and the rest of the things too.
Q. Now this rotating cutting blade, is that like a knife that you're putting into the artery?
A. It's exactly like a knife.
Q. Okay. What does that procedure cost, doctor?
A. This procedure, because of the enhanced equipment, it actually uses a mechanical cutter, costs about 18,000 dollars.
Q. And are there risks to this procedure?
A. The biggest risk from this procedure, in about one percent of cases, that you would cut the wall of the artery, and then you would -- the patient would need to go to the operating room. Again, that's why we've learned not to do it on bends, we just do it on straightaways so that the cutter doesn't go out into the -- into the wall of the artery.
Q. Turning your attention now to coronary rotoblade procedure, Trial Exhibit 30027, is that an accurate portrayal of that procedure, doctor?
A. Two seven?
Q. There you go.
A. Yes.
MS. NELSON: We would offer, Your Honor, 30027 for demonstrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30027 for illustrative purposes.
BY MS. NELSON:
Q. Can you explain what the coronary rotoblade procedure is, doctor.
A. This is the rotoblader that many patients think that they should have, but again when -- when the burr comes through here, it twirls a diamond bit here. Each of these bits cost about seven to eight hundred dollars. Goes across the lesion, and it works well in people who have heavy calcified lesions, where the lesions are like rocks, "lesions" meaning blockages.
Again the problem with the rotoblader is when we chop some of this up, some of it goes downstream. It can cause muscle damage downstream in the heart and you need big arteries to do this in. Because of that, again, this has been kind of a niche player. Again, we select the right tool that's appropriate for the right job.
Q. And doctor, what is the typical cost of this procedure?
A. Also about 18,000 dollars.
Q. Turning your attention then to coronary bypass surgery, if you would look at the model 30016, could you explain to the jury what coronary bypass surgery is.
MS. NELSON: Your Honor, we offer 30016 for demonstrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30016 for illustrative purposes.
A. If there are blockages in many vessels, and there -- we will sometimes, and unfortunately too often, do coronary artery bypass surgery. And if there's a blockage in the right coronary, the left anterior descending and the circumflex, where there is just too many to do balloons on and the patient has on going symptoms or is at risk, we think, of dying from his or her disease, the surgeon will then open the chest and then place -- and stop the heart, the patient will be placed on an oxygenated heart/ lung machine to bypass the heart to give the surgeon time to work on that, and then we'll take a vein from the leg and bypass around the most serious blockages.
We'll oftentimes use what we have call the left internal mammary artery to bypass the LAD. It's not depicted on this model. But a bypass is a detour around the blockages.
We know in post-bypass stage that if patients do not address their causative agents and they continue to smoke, if they have high cholesterol, that these grafts, nearly 60 percent of them will be gone by 10 years after they -- after the surgery. And we take a vein, which is a very low pressure system, and put it under that arterial pressures, remember that left ventricle is pumping very hard and it pounds that, and if there are injuries to the vein, the vein can then close and the patient would have a heart attack.
Q. Dr. Graham, what is the most frequent major surgery in the United States?
A. Unfortunately, coronary bypass surgery has become the most common procedure, major surgical procedure in the United States. Over 400,000 performed last year.
Q. And what are the risks of this procedure?
A. If you have a good pump going in, your surgical risks are usually one to two percent. Depending on how well the heart pumps going in, your risks go up as high as 20 to 30 percent mortality.
If somebody comes in on a helicopter, we do an emergency angiogram, we see that many vessels are blocked, and their ejection fraction is 20 percent, normal being 60 percent, meaning how much blood the heart ejects with each squeeze, and then we rush them to the operating room in order to try and save their lives, you know, we may lose two or three out of 10 of those patients. We save seven or eight of them, but we still lose patients. And we try to do everything we can, but, you know, this isn't tiddlediwinks. We -- patients, even when we do everything as best we can, the crime is those patients die right in front of our face, and we have to deal with them.
Q. Doctor, what are the major risk factors for a poor outcome of coronary bypass surgery?
A. In the short term, as I just mentioned, the worst outcome is left main coronary artery disease, the main artery going into the heart and the ejection fraction. Long term, the two things that have been closely related to lack of survival of these bypass grafts or closing of them, which are now the patient's lifeline, are smoking and high cholesterol.
Q. What happens when a patient comes to you, a smoker comes to you with COPD and requires coronary bypass surgery?
A. Again, as we talked about the risk of -- of bypass surgery and as we talked about the causative agents of why smoking was bad, if you have somebody now who is in the midst of an unstable situation and they have lung disease, like Dr. Davies outlined, even if it has not been a clinical problem to their life, they have an organ system that is on the blink, they need lung reserve like they've never had before. Patients who have scarred their lungs, even if it hasn't been a problem to that time, are now -- their risk of bypass surgery goes up two to three times because of their lungs. They tend not to be extubated or get the tube out after they've had bypass as quickly. The longer that they are kept on the breathing machine, the more chance they have of pneumonia. There are just many, many risk factors that go along with smoking. And what may be subclinical, which means it has not presented as to the doctor's saying I have COPD, but with the stresses and the need for the extra reserve of their lungs, it isn't there.
Q. Doctor, what is a typical cost of coronary bypass surgery?
A. Typical cost in the Twin Cities area of bypass surgery is approximately 30,000 dollars.
Q. Thank you, doctor. You can return to the witness stand.
Now you have a patient who has recovered from one of these life-saving procedures, the angioplasty or the rotoblade or coronary bypass, and has stabilized. At this point what interventions are available?
A. Once a patient's life has been saved and -- and -- and I would stress that, you know, it's -- it's often a life and death situation, the long-term prognosis of that patient is to keep their blockages that they have now in their coronary arteries from progressing. Somebody who has had a heart attack and was in the lucky 70 percent to make it to the hospital the first time, if they have a second heart attack, their out-of-hospital mortality rises not from 30 percent but to 50 percent. Okay. So we do everything we can to keep that patient out of a crisis, which is both medically expensive and life threatening to the patient.
So if the patient smokes, we do everything in our power to try and get them to quit smoking. If a patient has high cholesterol, we educate them in diet, in exercise to increase HCL, the good cholesterol, and they may not pharmacologic or drug treatment to lower their cholesterol. If a patient has diabetes, we very aggressively treat their diabetes to normalize the blood glucose or the blood sugar. If there are certain drugs, again, that have been shown if a patient has heart disease to keep them alive, the patient will be on aspirin the rest of their lives, a class of drugs call beta blockers which has been shown to decrease the incidence of death after a heart attack, a classic drug called an ace inhibitor, which makes -- decreases the strain on the heart and makes it easier for it to push forward, especially in those patients who are prone to what we call congestive heart failure. So the patient now becomes a high-maintenance patient.
What we want to do for a number of reasons is to keep that patient out of, again, another crisis of medicine.
Q. Are those long-term drug therapies costly?
A. They can be very costly.
Q. Now a patient who has bypass surgery, does that patient need cardiac rehabilitation?
A. The standard of care in Minnesota -- and we are very strong believers in working with our primary care counterparts throughout the state -- is to have an aggressive cardiac rehab program. We are very efficient in getting patients in and out of the hospital, so efficient that sometimes they -- they don't remember what we tell them because they are still under the effects of some of our medications when they -- by the time they leave, but then working through cardiac rehab, the messages of stopping smoking, of treating cholesterol, of exercise, are reinforced in a structured fashion that has been become standardized and is very beneficial to the patient.
Q. And is cardiac rehabilitation costly, doctor?
A. Yes. Most patients will undergo anywhere from 18 to 36 sessions.
Q. Now doctor, once the patient has suffered a heart attack, and as a consequent death of a portion of the heart muscle that you showed us before, is that patient at increased risk for other diseases?
A. The heart muscle once it dies -- in its living state it conducted electricity in a very regular way, and that's how the heart beats. There's an electrical wave that crosses the heart that causes the muscle to twitch, just like a nerve in our hand, it really is an electrical wave that causes the muscles to twitch.
When the muscle dies, the conduction through that becomes irregular, and if the beat happens at the right time, the patient's heart can start beating chaotically. If the pumping chamber of the heart does not beat, the blood pressure falls to zero and within six seconds the patient would pass out. So there is a considerable number of patients who have had heart attacks who then go out and die suddenly, what's called sudden cardiac death, many of you may know people who died in their sleep, it's not usually of a heart attack that they die, it's usually of an arrythmia, which means a chaotic beating of the heart muscle so that it does not pump blood efficiently.
Q. And are there medical devices available today to lessen the risk of patients suffering from these misfired electrical impulses?
A. We know now that there -- if -- if this life-threatening arrythmia is to happen, that there is no medication that can really save the patient, so because of that, in patients who we risk-stratify, that we think are the highest risk of that, patients again who have poor pumps, ejection fractions less than 40 percent, 60 percent being normal, we will then sometimes undergo what we call electrophysiologic testing. If we create what we believe is a life-threatening arrythmia in a controlled circumstance, again in a somewhat of a cardiac catheterization laboratory, we will then implant what we call a cardiac defibrillator that has leads into the heart that will shock the heart with electricity if the patient has a life-threatening chaotic rhythm. This is what's been shown to be the only effective thing if the patient has a lethal arrythmia.
Q. And do you also have available to you pacemakers?
A. In certain patients, after a heart attack -- again the conduction system of the heart is a very regular, as we think of just electrical circuits going from the top to the bottom of the heart. If the conduction system or if one of those wires that is going through the muscle is damaged after a heart attack, the patients may not conduct electricity from the top to the bottom of the heart. We have then available electronic pacemakers threaded in to the right side of the heart that then causes the heart to beat in a regular fashion and keep a kind of a safety net so the heart doesn't go too slow. Very fortunate in Minnesota to have the three largest pacemaker companies in the world located here in Minnesota.
Q. Dr. Graham, have you brought an example of a real pacemaker and a real defibrillator to the court today?
A. I have.
Q. Could you step down a moment, with the court's permission.
MS. NELSON: Your Honor, we would offer 30000 and 30001 for illustrative purposes only.
MR. MARTIN: No objection, Your Honor.
THE COURT: Court will receive 30000, 30001 for illustrative purposes.
BY MS. NELSON:
Q. Dr. Graham, would you describe both the pacemaker and the defibrillator to the jury.
A. The pacemaker is a marvel of modern electronics. The -- this is made by Medtronic, a Minnesota company. That the leads then are -- this is placed below the skin. We place a needle in a vein and then we thread these leads down into the heart, and this then resides under the skin here. This can be programmed to go faster, slower, to speed up when you walk, things like that. And the electronic engineers are marvelous people.
The leads -- there's two leads. The pacemaker itself costs about 10,000 dollars. Each lead -- there should be two leads on this -- about 600 dollars.
Q. And the defibrillator.
A. This is what some people would call a shock box. It can either deliver a fast burst of electricity or a committed shock to the heart. This is hooked to a series of leads also that are threaded through the venous side into the right side of the heart, and then it's placed under the skin here. It also can be interrogated to see what it's done over the past time. This is made by CPI, again another Minnesota company. This device costs about 25,000 dollars. And with that, leads -- there's four leads in here -- they cost about 600 dollars each.
Q. Take a look at 30020 again, please. Doctor, what is --
Is congestive heart failure another risk posed to a patient who has already suffered a heart attack?
A. As we discussed previously, after somebody has a heart attack there's a critical amount of muscle mass that we all need to push blood forward. If we lose that muscle mass, the heart becomes an inefficient pump, and then we have to give medications and all in order to try to compensate for the heart not pumping well.
Q. What is the most common reason for admission of an adult to an American hospital?
A. The most common reason for admission of adult population in the United States is congestive heart failure.
Q. Doctor, can the treatment of congestive heart failure be complicated by COPD?
A. When people are short of breath, again as I mentioned before, it's often a question: Is it the heart or is it the lung? If somebody has baseline mild shortness of breath from mild lung disease, although they had never presented to the doctor for it, then they come in and have had also the question of heart failure, it becomes oftentimes a diagnostic dilemma. Is it -- is it COPD causing the shortness of breath, or is it heart failure? And sometimes in those patients we place what's called a Swan-Ganz catheter that measures the pressures on the right and indirectly the left side of the heart, so that we know whether to give those patients more or less fluid and helps us make the diagnostic decision whether this is heart failure or whether the lungs are the problem.
Q. Now doctor, you explained to the jury at the beginning that the Heart Institute also performs heart transplants.
A. Yes.
Q. Could you describe to the jury the process of cardiac transplantation.
A. Cardiac transplantation is something we reserve to patients -- for patients who have no other options. Transplantation, taking immunosuppressive drugs, waiting on a list, waiting for a heart transplant, is no bowl of cherries. And there's always a risk that the body will reject the heart and the immunosuppressive drugs need to be titrated.
We do approximately 25 transplants a year at the Minneapolis Heart Institute. Half of the patients who have a heart transplant have had heart attacks previously; the others have had various other sicknesses of the heart where their heart no longer functions.
With that, you know, the expense of waiting for a heart transplant sometimes can be the -- the biggest -- as big an expense as the actual operation itself. We just yesterday transplanted a man who was waiting 75 days in our coronary care unit for a heart as a status one heart transplant. And it's maintaining that very delicate balance of a -- of a compromised heart. We have another man who is approaching 60 days and is there now. And the problem is the donors, we don't have the donors.
Q. And what is the cost of the typical heart transplant?
A. The yearly cost of a heart transplant would approach, the first year, over a hundred thousand dollars.
Q. Doctor, I want to turn your attention back to 30018. We've been addressing blockages in the coronary arteries of the heart. Are there other ways in which arterial blockages occur in the body?
A. Much the same as the risk factors and causative agents that led to blockages in the heart and what we think is very, very important -- because if the pump doesn't work, nothing works -- atherosclerotic or blockages in the carotid arteries leading to the brain as well as -- which would lead to stroke, the other common cause of strokes is after somebody has had a heart attack, if they form blood clots in the heart from part of the heart not working well, pieces can break off and go north into the head and cause a stroke.
Remember, the brain is the most sensitive organ in the body as far as deprivation of oxygen. Six seconds is all it can stand. So stroke is a -- is a debilitating, terrible disease, and especially in our older population, most of our patients are probably more afraid of stroke than they are of dying.
Q. And what are the treatments available for someone who has had that sort of clot and the consequent stroke?
A. Unfortunately, patients oftentimes, when they presented with stroke, they -- they are far down -- too far out to -- to give much therapy. We have begun giving some patients the same type of clot-dissolving medicine for certain types of stroke, but they need to be rushed to a CAT scanner first to make sure that they have had no bleeding in their head, because if you gave a clot-dissolving medicine and the patient had that type of stroke that was from bleeding, you would make the bleeding worse. And then once that happens, the -- if the patient has not been salvaged from that or has had an incomplete stroke, sometimes they will have a carotid endoterectomy, which is a surgery that essentially peels the plaque out of the carotid artery, with about a 10 percent incidence of stroke just from the procedure itself.
The worst thing about stroke is most patients -- the right side of the brain runs the left side of the body and vice versa. Oftentimes we have a very debilitated patient who, as I said, especially in our older patients who are faced with stroke, are more afraid of that debilitation than actually dying.
Q. And can that debilitation, doctor, often lead to nursing home care?
A. Again, in a -- in a patient who half of his or her body does not work oftentimes needs heavy levels of care. There is usually an acute hospitalization, a transitional-care unit, which is a step down within the hospital or a like unit, and then oftentimes chronic nursing home care of some sort.
Q. And then looking at the lower portion of the body, the aorta and down, do you find that there's blockages in those peripheral vascular locations?
A. Again, peripheral vascular disease -- "peripheral" meaning downstream, especially in the legs -- happens to two groups of people, smokers and diabetics. So people whose blood glucoses are high, blood sugars are high, and smokers, are at risk for developing peripheral vascular disease. While it again is a terribly debilitating disease and tends to be a more diffuse disease all up and down the artery, and so by-passing around those or doing a balloon on those oftentimes is very difficult. Plus the arteries are very small as they go down, especially below the knee. Can then sometimes lead to amputations, multiple surgeries in order -- if the blood supply is there, that the wounds don't heal well. So it's a very, very morbid thing to have.
The other side of the coin is people usually don't die of peripheral vascular disease. But if somebody had symptomatic blockages in their legs, and if they walk in and tell me that they have pains in their legs when they walk a block or two, so it's fairly symptomatic, those patients statistically have a 75 percent 10-year cardiac mortality. Because I know if there's blockages here, there's almost certainly blockages here.
MS. NELSON: Your Honor, this point would be a good time to break for the evening.
THE COURT: All right. We'll recess, reconvene tomorrow morning at 9:30.
THE CLERK: Court stands adjourned until tomorrow at 9:30.
(Court recesses.)
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