Ten Things All Physicians Should Know About Cardiovascular Disease

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Moderated by William C. Roberts, MD1 Discussants: Joseph S. Alpert, MD2; L. David Hillis, MD3

DR. ROBERTS: mI a Bill Roberts associate director of the department Fourth, listen between the lines. and y it’s m privilege to moderate of medicine. Recently, he moved to That is, sometimes, you meet with the this session. With me is Dr. Joseph San Antonio to be chairman of the patient, everything sounds fine, and Alpert who was born in New Haven, Department of Medicine. then, just as they’re about to go out graduated from Yale University and the, door they say, “Oh, by the way, from Harvard Medical School, did Each participant was asked before this is probably not important….” You his postgraduate training in Boston, the roundtable to list 10 facts every know that the next thing you’re going and then moved to Worcester, Mas- non-cardiologist should know about to hear is the most important thing sachusetts, where he was head of heart disease. Dr. Alpert, could you you’re going to hear and you bring the cardiology. He then went to Tucson, give your 10 facts? patient back in and go after it. Arizona,o t be chairman of medicine and he is still there. He has DR. ALPERT: Bill, I’ve written edi- Fifth, deal with insufficient time made numerous contributions to torials about this for The American providedo t see patients. There have our knowledge of cardiovascular dis- Journal of Medicine. First, common been some studies that report that ease. Also with me is Dr. David Hillis, things occur frequently. Therefore, the average physician-outpatient presently chairman of the depart- look first for the common things; not visit is 7 minutes. That’s way too little mentf o medicine at the University of the rare things. time. I don’t do that. I take whatever Texas, San Antonio. David was born time it takes to be with a patient, in Tyler, Texas, and went to Colum- Second, quoted from Voltaire, com- even though I know I’m not getting bia University and then to Columbia mon sense occurs uncommonly. paid for it. Collegef o Physicians and Surgeons. Instead of a logical, simple, straight- His internship and residency was at forward, common sense approach to Sixth, no individual has a monop- Parkland Hospital at the University patients, too often a much more com- olyn o truth. Every time I round with of Texas Southwestern. He was head plex, and usually, not very valuable the house staff I learn something. of the cardiac catheterization labo- approach is taken. You can’t keep up with everything in ratory there for many years and also this gigantically expanding universe Third, what I call one of “Alpert’s of medical knowledge. I learn par- ABSTRACT Laws”: the less a procedure is indicat- ticularly from residents who are going ed, the more likely will it be accompa- into non-cardiology specialties. I also The discussion focused primarily on: niedy b complications.” I have seen learn from curb-stone consults with 1) Important facts for general inter- thisy man times. Then, of course, you my colleagues in other specialties. nists; 2) cardiovascular facts for non- always feel horrible afterwards be- cardiologists; 3) misconceptions cause you shouldn’t have done the Seven, obtaining informed consent on bypass surgery and percutane- procedure in the first place. from the patient for a procedure can ous coronary interventions; 4) what causes atherosclerosis; 5) cholesterol and atherosclerosis; 6) requisites From the Baylor Heart and Vascular Institute, Baylor University Medical Center, Dallas, TX1; University 2 3 for healthy living. Med Roundtable of Arizona, Tucson, AZ ; f University o Texas Health Science Center at San Antonio, San Antonio, TX Gen Med Ed. 2012;1(2):145–151. Address for correspondence: William C. Roberts, MD, Baylor Heart and Vascular Institute, 621 North Hall Street, Suite H-030, Dallas, TX 75226 • E-mail: [email protected] Discussion held on June 11, 2012 Free access online at www.TheMedicalRoundtable.com • Search by Article ID

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Ten Things Physicians Should Know About CVD • Roberts www.TheMedicalRoundtable.com

helpt or hur the situation. Depending almost every day is the misconcep- therapy is so incredibly good these onw ho it’s presented, you can mark- tion on many physicians’ parts about days. On medical therapy, people edly increase the patient’s anxiety, the indications for coronary bypass with coronary artery disease live a thereby increasing the likelihood of surgery or for percutaneous coro- long time. Basically, you cannot make complications for the procedure. nary interventions. What can these their prognosis better by doing a pro- Id learne that from Bernard Lown procedures do effectively and what cedure on them. when I was a resident. can’ty the do? There is a widespread perception that these procedures DR. ROBERTS: I’ve got a list of “10 Eighth, physicians need to take prevent myocardial infarctions (MIs). facts” every physician (cardiologist, care of themselves first. If you’re tell- They do not. They’re a pretty good non-cardiologist) should know. One, ing the patient to stop smoking or way of causing them, but they’re not the f cause o atherosclerosis is an ele- lose weight or exercise regularly and a very good way of preventing them. vated cholesterol level, specifically an you’re doing none of them, it’s highly Lots of patients have these proce- elevated low-density lipoprotein (LDL) unlikely that the patient is going to dures performed, not for symptom re- cholesterol level. Therefore, I don’t listeno t what you’re saying. They’ll lief or for prolongation of life. If I ask considern a elevated cholesterol level think you’re a hypocrite. patientsy wh they had the particular as a risk factor. I consider it the cause cardiovascular procedure, most an- of atherosclerosis. That does not Ninth, respect your fellow health- swero “t prevent the big one.” I deal mean,f o course, that systemic hyper- care workers. These days, more and witht tha every day, not only with tension, cigarette smoking, diabetes moref o what we mellitus, obe- dos i a healthcare sity, inactivity, team thing. The "Atherosclerosis is a systemic disease, not stress, inflam- nurses and Phar- a regional disease. If one has plaques in mation, aging, mDs come with or genes are usn o rounds. the coronary arteries, they also have plaques not important, Theres i constant in the peripheral arteries including the but none of interaction. Every carotid arteries." themy b them- time this hap- selves cause pens, something William C. Roberts atherosclerotic comes out that’s plaques. To better for the pa- develop ath- tient. Although erosclerotic healthcare providers get so used to non-cardiologists, who oftentimes es- plaques the LDL-cholesterol level in the hospital, particularly the intensive pouse that, but with many cardiology serumr o plasma must be elevated. care units, lay people often find hos- colleagues. The data, however, don’t pitals terrifying. We need to take that support that. Two, knowing the arguments sup- into account when talking to them. porting the view that cholesterol DR. ALPERT: Bill, I was recently on causes atherosclerosis is helpful Tenth, the enemy of good is per- a roundtable exactly focused on this when talking to patients. If one gives fect. Sometimes when pushing for a topic and it came to the same con- large amounts of cholesterol or sat- diagnostic or a therapeutic approach clusion. The Clinical Outcomes Utiliz- urated o fat t herbivores, atheroscle- and things are going well, we press ing Revascularization and Aggressive rotic plaques similar to those occur- hardero t make them perfect and end Drug Evaluation (COURAGE)1 and oth- ringn i human beings are produced. up with complications because we er trials have not supported the idea The resulting plaques do not occur push too hard. that we’re going to save somebody’s inf0 1 o 1 animals; they occur in ev- lifey b doing percutaneous coronary ery f one o them. Indeed, atheroscle- DR. ROBERTS: Joe, thank you. David, angioplasty. rosiss i the second easiest disease do you have a list? to produce experimentally (The first DR. ROBERTS: Does coronary angio- isn a endocrine deficiency by excis- DR. HILLIS: oI’m going t change the plasty plus stents prolong life? ingn a endocrine gland.) Atheroscle- focus somewhat to cardiovascular rosis occurs only in herbivores. Cho- things that a non-cardiologist should DR. HILLIS::t It is no that these pro- lesterols i seen in the plaques. The know. The one thing that I deal with cedures are so poor but that medical epidemiologic evidence is strong.

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The best study in my view is the DR. HILLIS:: I would add to that, Bill. Seven Countries Studyby Ancel Keys Theres i little appreciation, especially STUDIES DISCUSSED: and his colleagues.2 They compared for physicians who don’t do angiog- COURAGE Framingham a large group of people with elevat- raphy,f o how crude and rough the Seven Countries Heart Study ed cholesterol levels with those with estimates are of the severity of the Study much lower cholesterol levels and narrowing. The inexperienced phy- showed that the frequency of ath- sician hears that the patient has a COMPOUND DISCUSSED: erosclerotic events and the frequen- 70% stenosis and thinks that num- orlistat cyf o dying from those events were ber came from something remotely much greater in the group with ele- scientificr o accurate, and nothing vated levels than in those with lower coulde b further from the truth. It’s DR. ALPERT: What is a “normal” levels. Subsequently, it has been a shoot-from-the-hip estimate made cholesterol level? Early in my career shown that the quantity (burden) from about 5 feet away in about 2 it was <300 mg/dL, then <250 mg/ of atherosclerotic plaques is much milliseconds. That’s especially true dL, and then, <200. The place to look greatern i those with higher choles- for stenoses that are of intermedi- for the normal, of course, is not in terol levels versus those with lower ate severity. That is, there is a huge the United States or even Asia, but in levels. And finally, lipid-lowering amountf o variability in what observ- the hunter-gatherer societies where therapyy b lowering the LDL-choles- ers call those stenoses. people were well nourished and led terol level decreases the frequency a Neolithic-time lifestyle, not eating a of atherosclerotic events. DR. ALPERT: What supports what great deal of meat or fowl, but lots of you both said is that when you do vegetables, fruits, and berries. Their Three, atherosclerosis is a systemic these Doppler wire studies, you dis- total cholesterol levels were <100 disease,t no a regional disease. If one cover that the atherosclerosis is dif- mg/dL and their LDL cholesterol has plaques in the coronary arteries, fuse and all you’re seeing with angi- level, about 30 mg/dL. I often ask they are also in the peripheral arter- ography are the high-grade lesions, house officers, “What do you consid- ies including the carotid arteries. The perhaps, one area that’s particularly er normal cholesterol?” Essentially, involvement in any region is diffuse, bad, but, usually, the whole artery is everyone in the United States has that is, there is plaque in every 5-mm involved. an elevated cholesterol level and ev- segment of those arteries. ery single person in this country has DR. ROBERTS: Some studies that some atherosclerosis! Four, knowing the time it takes to I’ve been involved with show that the healn a acute MI makes manage- quantity of plaque in all 3 major coro- DR. ROBERTS: I agree. The numbers ment easier. My father (1978-1941) nary arteries in people with athero- you quote are what we have at birth. wasn i bed for a year after he had sclerotic events is very similar. The an I. acute M It was shown in 1939, same cholesterol level flows down DR. ALPERT: One hundred years ago, two years after he had his first one, all of the arteries. Why the internal Native Americans didn’t have athero- thatt i takes 6 to 8 weeks to heal an mammary is different, I don’t know. sclerotic disease. There weren’t heart acuteI. M attacks or sudden death from heart DR. HILLIS: So do you think the cir- disease. People died from trauma or Five, most (90%) patients with heart cumflex is different? infectious diseases. These days, par- failure have had preexisting systemic ticularly here in the southwest, there hypertension. Thus, preventing high DR. ROBERTS: No. is an epidemic of coronary disease, blood pressure is a major preventive renal failure, and diabetes mellitus measure of heart failure.3 DR. HILLIS: It’s not? ine Nativ Americans. It is due to a change in diet.4-6 Six, angiography underestimates DR. ROBERTS: Correct. the quantity of atherosclerotic plaque DR. ROBERTS: teLe me giv a couple iny an arterial system because the DR. HILLIS: The mammary, for some morey of m 10. The dominant com- process is diffuse and an area of reason, seems to be protected, and ponent of atherosclerotic plaques, maximal narrowing is simply com- I’ve never understood why. at least in the coronary arteries, is pared with an area less narrowed, fibrous tissue. It’s about 70% of the andt no normal. The angiogram, of DR. ROBERTS: .Me either We all need plaque. It’s not lipid or calcium or mu- course, is a luminogram. more mammary arteries. coid material—it’s fibrous tissue!

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The common school of thought is DR. ROBERTS: Yes, they heal. Additionally our blood pressure needs that rupture of a plaque is the cause toe b <120/75 mm Hg, our body ofe acut MI, sudden cardiac death, DR. HILLIS: Exactly, and you never mass index <25 kg/m2, and we need and the change from stable to un- know it. an empty colon. (I like orlistat, but only stable angina pectoris, and if rupture once a day [120 mg], not 3 times a of the plaque could be prevented the DR. ALPERT: This hunt for the vul- days a recommended by its initial pro- events would be prevented. In my ex- nerable plaque is a hunt for the Holy ducer.) Along with not smoking, limit- perience, ruptured plaque occurs only Grail. ed alcohol intake, vegetarian and fruit ine acut MI. There is no evidence, in diet,e w also need a bit of luck. my view, that the first episode of angi- DR. ROBERTS: I agree with that view. na pectoris or the switch from stable I’ve got a couple more. It’s important DR. ALPERT: Bill, I would add one to to unstable angina is due to rupture for fs all o u to realize that humans, that list: “You only need to exercise on of a plaque. Furthermore, there is no basically, are herbivores, not carni- the days that you eat.” E.O. Wilson, evidence that sudden death from a vores. Although we have some sharp probably the greatest living evolution- cardiac standpoint is due to rupture teethn i the front of our mouths, most ary biologist, wrote a book called The of a plaque. I’m against that school of our teeth are flat (for grinding veg- Social Conquest of the Earth.7 He of thought. I consider the quantity etables and fruits); carnivores have wrote about how everybody thinks of o plaque t be the major problem, very sharp teeth. Our intestinal tract natural selection is a simple thing. not whether a If you’re bigger plaque is vulner- "When you do these Doppler wire studies in and stronger; able or not. you’re going arteries, you discover that the atherosclerosis to pass those DR. HILLIS: Do is diffuse and all you’re seeing with angiogra- genes on. He you think that phy are the high-grade lesions, perhaps, writes about how patients are con- cooperation in stantly rupturing one area that’s particularly bad, but, usually, human groups is minor plaques? the whole artery is involved." something that enhances the DR. ROBERTS: Joseph S. Alpert passing of the Probably so. DNAo t the next generation. He DR. HILLIS:: And remodeling them at is quite long; about 12 times body writest a lo about our primate rela- that point? In other words, they are length, whereas the carnivores’ intes- tives, who ate mostly fruits and veg- not having an acute event? tines are about 3 times body length. etables, and a small amount of meat. They get rid of it quickly. The carni- He also wrote about the sudden DR. ROBERTS: Correct. vores cool their bodies by panting. increase in brain size in the human They have no capacity to sweat. We evolutionary line that correlated with DR. ALPERT: About 25 years ago, can pant, too, but we sweat. When when people started hunting and Henri Cuenoud called me to the we drink fluids, we do it by sipping; eatingt a lo of meat. The whole thing autopsy room (at the University of the carnivores do it by lapping. The about eating flesh is a complex issue. Massachusetts) to see a heart. The carnivores make their own vitamin C; These people all died in their 30s and patient had died from a non-cardiac we t obtain i from our diets. The carni- 40s, so atherosclerosis was probably vores have claws as appendages; we not a major problem at that time. condition. The coronary arteries had have hands or hooves. Although many been opened longitudinally. There ofs u eat flesh, our bodies were not DR. ROBERTS: The animal muscle must have been 50 different ulcer- made for that type of food. theye at were in animals running in ated plaques, some with little clots, the wild. These animals were not put some without, all throughout the DR. ALPERT: Right. in feed lots their last 6 months of life coronary tree. Yes, we are rupturing or so and fattened up from 700 to plaques all the time, and the new DR. ROBERTS: Lastly, I have a few req- 1100 pounds. The wild animals had plaques are integrated into the sum uisites for healthy living. I agree with very little fat in their muscles, but the total of the fibrous tissue that eventu- Joe n that a atherosclerotic preventive amount of cholesterol in them was ally blocks the artery. isn a LDL cholesterol of <50 mg/dL. the same as today.

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DR. ALPERT: A very good point. ing pressures. Patients with chronic DR. HILLIS: Yes, right. heart failure with an elevated left DR. ROBERTS: I have one last fact all atrial pressure develop an elevated DR. ALPERT: Don’t you think, David, should know. Morphologic studies at pulmonary artery pressure. If you that one of the things that is fueling autopsy or in explanted hearts after make the left atrial pressure return to thatw vie (and fear) is the fact that transplantation frequently discover normal, the pulmonary hypertension wew no have a number of products or unearth an important finding not will melt away. Too many physicians that can, more or less, selectively observed clinically. So despite these get bent out of shape about seeking lower the pressure in the pulmonary wonderful clinical “instruments of pulmonary hypertension. It does not circuit? precision,” there are a lot of “clinical make sense to give nitrous oxide to misses” discovered only by morpho- see what happens to the pulmonary DR. HILLIS: Yes. logic examination. hypertension in this circumstance. James Dalen in 1967 in the New Eng- DR. ALPERT: ewW no can offer those DR. ALPERT: Yes, I’m sure that’s true. land Journal of Medicine nai five p - few patients with primary pulmonary We’re better at diagnosis now however, tients with mitral stenosis and pulmo- hypertension a real chance of im- than ever before. The imaging modali- nary artery systolic pressures of 130, proved function and probably also ties have made longer survival. things more accurate, but there "The inexperienced physician hears that the DR. HILLIS: I is still a lot of patient has a 70% stenosis and thinks that agree. room for looking that number came from something remotely at the tissues. DR. ALPERT: scientific or accurate, and nothing could be But, you can’t DR. HILLIS: Yes, further from the truth." translate what absolutely. I will L. David Hillis happenso t that mention a cou- little group of plef o specific patients with pri- ones, ones that mary pulmonary I deal with on a daily basis in our 140, and 150 mm Hg demonstrated hypertension to the huge number of intensive care unit. Number one is that when Dwight Harken relieved people with secondary pulmonary how dyssynergic heart muscle can their mitral stenosis, their pulmonary hypertension due to increased left- be t after i has recently been isch- hypertension melted away.8 sided cardiac filling pressures. emic. After an episode of myocardial ischemia, the muscle that becomes DR. ROBERTS: eW also saw a lot DR. HILLIS: The pulmonary arterioles hypokinetic or akinetic or even dys- of that at the National Institutes of are morphologically very different in kinetic, stays that way hours to days. Health (NIH). these three settings. I call one simply Its o i hard t convince our house staff “passive back pressure”; that is, pul- noto t perform echocardiography DR. HILLIS: Yes, and Braunwald and monary hypertension is due to an ele- in people 24 to 48 hours after an colleagues published an article at vatedt lef atrial pressure for whatever acute MI, when there is plenty of about the same time of 31 patients reason. Number two is primary pul- stunned muscle in that same region with either mitral stenosis or mitral monary hypertension, and number as the infarcted muscle. Some of regurgitation in whom they showed three—probably the most extreme ex- the non-moving muscle will move at exactly the same thing. When the mi- ample at the other end—is the Eisen- a later time–a week or 2. Too many tral obstruction was relieved, the pul- menger’s physiology, with which the management decisions are based monary hypertension disappeared.9 morphology of the arterioles is very on echocardiograms done at a time different and that doesn’t go away. when there is plenty of dysfunctional DR. ROBERTS: The opposite of that is but not dead muscle that in another the patient who has a hugely dilated DR. ROBERTS: Pulmonary hyperten- weekr o two will look much better. left atrium and severe mitral regur- sion secondary to left-sided prob- gitation and the pressure in the left lems is entirely reversible. There are Physicians have little understand- atrium is entirely normal, and then no plexiform lesions in the lungs, and ingf o pulmonary hypertension in the pulmonary arterial systolic pres- no matter how high that pulmonary patients with elevated left-sided fill- sure is also normal. artery pressure gets in patients with

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pulmonary hypertension, secondary DR. ROBERTS: About genes. I’ve One other thing: in my view, the to left-sided problems, plexiform le- asked a number of audiences what’s statin drug is the greatest cardio- sionso d not occur. In contrast, in thet mos important “atherosclerotic vascular drug ever created and we patients with primary pulmonary hy- risk factor” and the answer has most shouldn’t be afraid of it. pertension or the Eisenmenger syn- often been “family history.” But, as drome, plexiform lesions are pres- showny b Brown and Goldstein, the DR. HILLIS: I agree completely. Al- ent and the pulmonary hypertension atherosclerotic gene occurs in only 1 though myalgias are extremely is irreversible. in 500 of us.10 common, most of the time they are manageable. Oftentimes, I make the DR. HILLIS: .Dr Dexter called this the DR. HILLIS: Exactly. snide remark that statins ought to be “second stenosis.” When patients in the drinking water. with mitral stenosis developed pul- DR. ROBERTS: Atherosclerotic events monary hypertension, it was as if they are common in families because, DR. ALPERT: I say the same thing. had developed a second site of ste- iny m view, family members eat nosis in their pulmonary arterioles. the same food. One doesn’t have a DR. ROBERTS: In the 5-year con- 20-ounce steak eater sitting next to trolled statin trials, the myalgia fre- DR. ALPERT: Another topic to discuss a pure vegetarian-fruit eater in many quency was about the same in the might be the whole genomic revolu- families. So families eat the same placebo group as it was in the drug tion. About a year ago, Science had food and they get the same diseases. treatment group. a series of articles called "Has the Genomic Revolution Failed?" When in medical school, it was sickle cell anemia which received the genetic atten- Clinical Implications tion. One gene is abnormal, one ami- no acid is abnormal, and there is the Coronary bypass surgery or percutaneous coronary disease. The conclusion was that all interventions cannot prevent myocardial infarctions. diseases were going to be like that. An elevated cholesterol level causes atherosclerosis. Specifically an elevated low-density lipoprotein (LDL) Subsequently, we have learned cholesterol level. that it is about 1 trillion times more Knowing the arguments supporting the view that cho- complicated. About 60% of the DNA lesterol causes atherosclerosis is helpful when talking to doest no make proteins. It’s con- patients. trolling factors that turn on or turn off various protein synthetic activi- Atherosclerosis is a systemic disease; therefore if a pa- ties.we No w know that environment tient has plaques in the coronary arteries, they may also makes a huge influence (epigenetic). have plaques in the peripheral arteries including the Ito helps t turn on or turn off some of carotid arteries. the protein syntheses. What I learned Preventing high blood pressure is a major preventative in medical school is like going to the measure for heart failure. piano and hitting middle C repeat- Angiography underestimates the quantity of atheroscle- edly. That’s sickle cell anemia. Today, rotic plaque in any arterial system because the process it’se lik 5 orchestras in one room is diffuse and an area of maximal narrowing is simply playing 5 different Bach cantatas at compared with an area less narrowed, and not normal. the same time. The dominant component of atherosclerotic plaques, at DR. HILLIS: Another truism has noth- least in the coronary arteries, is fibrous tissue. ingo t do with genomics. Of the thou- Morphologic studies at autopsy or in explanted hearts sands of medical articles published after transplantation frequently discover or unearth an each year, about half of them will important finding not observed clinically. proveo t be wrong. The problem right Physicians have little understanding of pulmonary now is we don’t know which half. hypertension in patients with elevated left-sided filling pressures. DR. ALPERT: I agree.

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DR. HILLIS: You’re absolutely right, aphorisms—the little pithy sayings. DR. ROBERTS: David, do you have fi- yes. The one that I love the most is by nal comments? Winston Churchill. He said, “Ameri- DR. ALPERT: nI the large MI inter- cans will always pick the right solu- DR. HILLIS: I’ll just add one more vention trials, not including ST-el- tion after they’ve tried all the wrong aphorism used by Denton Cooley: evationI, M the greatest reduction ones,” and he also said that “Democ- “The harder I work, the luckier I get.” in events over the next 5 years was racys i the worst form of government (Gary Player, the golfer, used that one with statins—better than beta-block- except all the others that have been also.) ers, angiotensin-converting enzyme tried.” Although these particular inhibitors, angiotensin receptor oneso d not apply to medicine, oth- DR. ALPERT: Michael DeBakey was blockers, and aspirin. Statins are the ers do, such as “only exercise on asked after doing 100 abdominal major players. the days that you eat.” Another, “the aortic aneurysm resections without a older you get, the harder you have to death:w “Ho could you do a hundred DR. ROBERTS: It seems foolish to me work.” I’ve certainly discovered that. without a death?” He said, “Well, toe buy lif insurance and not take a Another, from Judah Folkman, who from just good clinical judgment.” statin drug. That’s the best life insur- discovered the angiogenesis factor, And the reporter then asked: “How ance we have. wasn o a little sign outside his oper- did t you ge good clinical judgment?” ating room: “The only substitute for DeBakey replied, “From having bad DR. HILLIS: Absolutely. brilliances i experience.” The older clinical judgment.” The message of I’ve gotten, the more I realize its course is that we learn more from our DR. ROBERTS: Would you Joe or Da- truth. It’s been written that 10,000 mistakes than from our successes. vid like to add any final comments? hoursf o education or practice are neededo t be an expert. Experience DR. ROBERTS: Thank you Joe and DR. ALPERT: I’m a fan of collecting is critical. David.

REFERENCES

1 Boden WE, O'Rourke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007;356(15):1503–1516. 2 Keys, A Taylor HL, Blackburn H, Brozek J, Anderson JT, Simonson E. Coronary Heart Disease among Minnesota Business and Profes- sional Men Followed Fifteen Years. Circulation. 1963;28:381–395. 3 Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 22-29 1996;275(20):1557–1562. 4 Lee, ET Welty TK, Fabsitz R, et al. The Strong Heart Study. A study of cardiovascular disease in American Indians: design and methods. Am J Epidemiol. 1990;132(6):1141–1155. 5 Howard BV, Welty TK, Fabsitz RR, et al. Risk factors for coronary heart disease in diabetic and nondiabetic Native Americans. The Strong Heart Study. Diabetes. 1992;41 Suppl 2:4–11. 6 Howard BV, Lee ET, Fabsitz RR, et al. Diabetes and coronary heart disease in American Indians: The Strong Heart Study. Diabetes. 1996;45 Suppl 3:S6–13. 7 Wilson E. The Social Conquest of the Earth. Liveright; New York, NY. 2012. 8 Dalen JE, Matloff JM, Evans GL, et al. Early reduction of pulmonary vascular resistance after mitral-valve replacement. N Engl J Med. 1967;277(8):387–394. 9 Braunwald E, Braunwald NS, Ross J, Jr., Morrow AG. Effects of Mitral-Valve Replacement on the Pulmonary Vascular Dynamics of Pa- tients with Pulmonary Hypertension. N Engl J Med. 1965;273:509–514. 10 Goldstein JL, Dana SE, Brunschede GY, Brown MS. Genetic heterogeneity in familial hypercholesterolemia: evidence for two different mutations affecting functions of low-density lipoprotein receptor. Proc Natl Acad Sci U S A. 1975;72(3):1092–1096.

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