The Coronary Artery Entrapment

The Coronary Artery Entrapment

Bernard Lown, MD

 

Essay 31

What propelled the transformation of medicine from a humanitarian profession to a costly technocracy? It has seemingly happened in a single lifetime, and I witnessed much of it. Let me relate what transpired. Be forewarned, however: history is more accurately perceived as a Rashomon experience than garnered from near-deathbed confessionals.

In the metamorphosis to medical modernity cardiologists led the charge. The focus of their concern was the epidemic prevalence of coronary artery disease (CAD). For the past fifty or more years CAD has been the leading cause of death. It kills and disables people during the most productive period of their lives. Women lag about ten years behind, with CAD manifesting usually after the menopause. By age 70 about a fifth of Americans of both sexes are afflicted with some form of heart disease.

The overwhelming power — nay, seductive charm or even stranglehold — of technology in medicine was manifested first in relation to CAD. The Faustian bargain was as insidious as it was all-consuming. The devil’s emissary promised wealth, scientific pretensions of unimpeachable verisimilitude, leadership in the cutting edge of medical innovation, and most irresistibly, the transformation of work into child’s play, with novel, unimaginably versatile toys. In return the doctor promised adherence to the demands of workplace industrialization, thereby augmenting both efficiency and profitability. While the cardiologists were triumphant, something vital was leached from doctoring. It meant spending less time with patients and abandoning the ancient skills of listening as well as the consummate art of the physical examination. Some doctors felt an ache like the passing of a dear friend. Most, though, never experienced even a quiver of loss. These humanitarian skills, not being taught in medical schools or mentored in hospitals, were never acquired, thus never lost.

March of Technological Progress

This Faustian pact did not go into high gear in one fell swoop. Its implementation came in driblets of small advances over more than a century. The objective challenge was how to improve blood flow through obstructed coronary arteries. The options were essentially two: either bypassing the narrowed segments or widening a vessel’s obstructed lumen. Before being able to deal with the lesion, one had to locate its exact site. This was no mean accomplishment. The arteries, having the diameter of a shoelace, embrace the heart like a coiled fishnet. The challenge was to look within these diminutive vessels, locate the blockages, and assess their extent.

It began in the 1860s, when the great French physiologist Claude Bernard put a thin rubber tube into a beating animal heart. Nearly seventy years later the German physician Werner Forssmann performed a catheterization in a living human being. On several scores this was a first in the annals of eccentric medical lore. The experimental subject was none other than Forssmann himself. He anesthetized his forearm and then treaded a long urinary catheter into his ante-cubital vein until it lodged in a right heart chamber. Forssmann then marched to the X-ray department and took radiograms showing that the tip of the catheter was indeed located in his heart. There were no untoward effects other than Forssmann being dismissed from his medical appointment. Eventually he was vindicated and much honored, receiving a Nobel Prize in medicine.

Transforming catheterization from an oddity to an indispensable tool is associated with the names of two American physicians, André Cournand and Dickinson Richards, from the Bellevue and Presbyterian hospitals, respectively, in New York City. Being primarily interested in lung function, they needed to sample blood gas concentrations, such as oxygen and carbon dioxide, from the heart. Cournand was familiar with Forssmann’s unorthodox method and adapted the technique to studying cardiac function. They rapidly confirmed safety of the method, standardized the procedure of cardiac catheterization, and established its great utility in diagnosing congenital as well as rheumatic valvular heart disease. Cournand and Richards thereby opened a new frontier in medicine and established a new discipline in cardiology. For these achievements they shared a Nobel Prize for physiology and medicine with Forssmann in 1956.

 A major next step was taken by Mason Sones of the Cleveland Clinic. The date is worth noting, as it marks the galloping takeoff for cardiac interventions. On October 30, 1958, Sones was catheterizing the heart of a young man with rheumatic valvular disease. He aimed to visualize a diseased aortic valve by injecting contrast dye into the left ventricle. Sones was dismayed that the catheter tip had inadvertently slipped into the right coronary artery. Before he could stop the intended injection, a massive amount of dye was infused into the small artery. The heart stopped and after a few minutes resumed its normal beating. This accident, which could have proved fatal, was a transforming experience. Sones, unperturbed, forged ahead, introducing modern coronary artery imaging.(1)

Not at all surprisingly, the next advance also took place at the Cleveland Clinic. In 1967, Sones’s colleague, Dr. René Favaloro, performed the world’s first coronary artery bypass operation to promote myocardial revascularization. He used a leg vein (saphenous) as the conduit for bypassing the coronary obstruction. This could not have happened without coronary angiography.

A word of confession is in order. I was remotely implicated in these developments. The direct current (DC) defibrillator and the cardioverter that I introduced facilitated cardiac revascularization. Coronary artery surgery is best accomplished in a quiescent nonbeating heart. The way to stop the heartbeat is to induce ventricular fibrillation.(2) But how is one to restore a normal heart rhythm? Paul Zoll’s alternating current (AC) defibrillator was already available. The pulse wave of Zoll’s defibrillator, however, is injurious to heart muscle and fails in a large number to restore a normal rhythm. Its use resulted in an unacceptable operative mortality. DC defibrillation, being comparatively innocuous, facilitated the new era of cardiac surgery.

I failed to realize this association until it was brought to my attention in a curious manner. One day I received a telephone call from Dr. Don Effler, the director of cardiac surgery at the Cleveland Clinic. It was in his department that the revolution had been wrought. He was lecturing in Boston and wondered if he could stop by to say hello. Never having met the man, I was perplexed. This very tall gent showed up, and before saying a word, lifted me into the air in a tight bear hug, announcing in a booming voice with a surgeon’s not uncommon swagger, “Thanks, Bernard, for making modern cardiac surgery possible.”

Revascularization of the Heart

Bypass surgery was a substantial advance for managing patients with severe symptomatic coronary artery disease. Yet, in the United States as well as in the rest of the developed world and for rich patients in the third world, it rapidly became a theological fixation for treating patients with CAD. While the virtues of revascularization were invariably overpraised, the grief at times provoked by these operations was commonly underreported.

Because a procedure is possible, is it unexceptionally necessary? And if necessary, who gains and who loses? Invariably there is a human cost, consisting of injury, at times long-lasting or irreversible, and sometimes even death. I have encountered many who were severely damaged as the result of a bypass operation, yet the surgeons appraised the outcomes as successful. Far more numerous victims come to mind than I wish to remember.

For some fifteen years I had followed HW, who had significant three-vessel coronary artery disease.(3) I referred him for revascularization because of intensifying angina not readily responsive to a bevy of medications. The operation went well. However, after six months angina recurred. He was additionally troubled with sternotomy pain.(4) Far more disabling was the unrelenting discomfort in his left upper leg at the site where the vein graft had been harvested. He would plaintively beg, “Dr. Lown, can’t you remove the tourniquet around my thigh?”

I still tremble with remorse recalling MK, a gaunt, introspective man with chiseled Lincolnesque features. Compelling was his uncomplaining dignity in the face of angina of a severity I had never before or have since encountered. He was unable to walk any distance at all. Paralyzing chest discomfort forced him to stop dead in his tracks. Nitroglycerine by the fistful afforded scant relief. Leaning forward and bearing down somewhat assuaged the anguish. Raising a fork to his mouth sufficed to bring on a bout of distress. His wife spoon-fed him. With each episode of angina he felt life itself ebbing away. Cold sweat was so marked that he soon stood in a puddle of water. With the onset of angina, time stopped. Yet his work as an artist, doing oil paintings and watercolors, never provoked angina. He indicated that art enabled him to survive day by day and kept him from suicide.

Without a moment’s hesitation I urged him to undergo bypass surgery. The operation was straightforward. A few days later his cardiac surgeon was ecstatic. “It is a miracle. This guy is totally free of angina. We had him climb two flights and he didn’t even blink.” When three months later he revisited for a postoperative assessment, he appeared more gaunt and more depressed. Angina had not recurred. However, intraoperatively he suffered what the surgeon called a “minor” stroke that paralyzed part of his right arm and hand. He no longer could paint. He would have preferred the angina, he stated categorically. Resigned and without a patina of anger in his voice, he said, “Doctor, I wish I had not met you or been carried away by your enthusiasm.” I asked if he had talked with his surgeon about what transpired. MK responded, “He would not have understood. He was even more enthusiastic than you!”

I began this discussion with the need for caution because all procedures carry risks. But this is an illogical place to begin. After all, what we do is actuated by the anticipation of benefit, not by its association with a low titer of harm. The paramount issue is whether a new treatment will afford more benefit at the same level of risk as existing therapies. In relation to coronary artery disease the first question is therefore whether CAD can be diagnosed without angiography. A second question is whether medical therapy can afford a normal lifestyle without a shorter survival than an intervention. To both questions the answer is a categorical YES!

But this type of discourse is not possible when both doctor and patient believe that coronary angiography is the sine qua non for diagnosing coronary artery disease.(5,6) When one begins with coronary angiography as the indispensable first measure in diagnosis, one is already on a toboggan ride hurtling downhill. The inexorable destination is to repair whatever coronary artery obstruction is encountered. Such a journey results in costly overtreatment,(7) a fact even acknowledged among some interventionist cardiologists. The temptation to intervene with a procedure once a coronary narrowing has been identified has been dubbed the “oculostenotic reflex.” “Even if you get a good result, you don’t seem to have an improved clinical outcome. So when you are weighing risk and benefit, there is a bit of risk and not much benefit. While the cost overruns of such an approach preoccupy our political discourse, the ethical bankruptcy of modern doctoring rarely gets a whisper”.(8)

About thirty-five years ago leaders of Blue Cross of Massachusetts invited my associate Dr. Thomas Graboys and me to consult on how to stem the tide of coronary interventions. Our advice was straightforward: Instead of constantly mopping up the puddle from an overflowing sink, shut off the spigot of coronary angiography. Translated: Instead of starting with visualizing obstructed vessels, demand a second opinion on whether the patient needs a therapeutic intervention. Without an angiogram the judgment will necessarily be more conservative. If the doctor rendering the second opinion is not an interventionist cardiologist, the flood of overtreatment will be reduced to a trickle.

There were huzzahs for our great wisdom. Yet nothing transpired. We turned out to be the wise men of Chelm. Encountering one of the executives years later, I probed why our advice was ignored when initially greeted with so much enthusiasm. His answer was blunt. In essence, had they followed our counsel, the leading teaching hospitals in Boston would have gone bankrupt. Their failure would in turn have undermined the bottom line of the medical insurance industry. Then with a laugh, he said, “Doctor, I would have had to exchange my Mercedes for a Ford.” In fact the health insurance industry, the hospitals, and the interventionist cardiologists shared an economic interest.

There are several substantial arguments against the rush to interventions other than their prodigious cost. First is the clinical fact, as discussed in an earlier essay,(9) that the majority of narrowed coronary vessels are quiescent. Their progress is a function of risk factors such as psychological stress, increased blood pressure, elevated blood cholesterol, a sedentary lifestyle, the presence of diabetes, and smoking. These are controllable with sound medical management. Second is the patho-physiological observation that the main dreaded complications of coronary artery disease result from seemingly innocuous plaques.(9) These may provoke a heart attack or, far worse, a malignant arrhythmia such as ventricular fibrillation, which, if not instantly reversed, results in sudden cardiac death. But the inflamed threatening plaque may occur in a modestly obstructed or even in a totally unobstructed vessel.(10) In fact, the threatening plaque is not identifiable by any current technological tools. Coronary angiography is useless in locating unstable plaques. Third, and trumping all else, is the growing body of evidence that current medical treatment yields outcomes every bit as good as far more costly and more complication-prone interventionist procedures.

Why do patients then acquiesce to procedures that are adverse to their well-being and possibly even threatening to their health? The sad truth is that patients are flooded with misinformation and simplistic ideas spewed out 24/7 by the entertainment-oriented mass media. These tend to medicalize every aspect of life. The paradigm communicated about CAD is that of a plumbing problem, equivalent to a kinked garden hose, for which cardiologists have devised brilliant technological solutions. Unkinking the hose provides a lifelong solution that can be achieved during an overnight stay in a hospital. Such a course of action is enormously inviting, as it is in lockstep with the zeitgeist of our culture. We are increasingly incapable of tolerating uncertainty. We are thus ready customers for instant cures.

And herein lies a seeming oddity. In my experience, interventionist cardiologists almost never directly assure patients that a prescribed procedure — whether bypass surgery, angioplasty, or stenting — will prolong their lives. A different approach is pursued. Patients are led to believe that inaction is likely to have threatening consequences to their very survival. The ensuing fear assures a docile acceptance of the interventionist course of action.

Data amassed over the past forty years has shown no survival advantage for those undergoing intervention. Yet if anything ,the practice has grown. The current supporting argument is specious. Proponents maintain that interventions improve the quality of life by eliminating the troublesome symptoms of CAD. What are these symptoms? There are none except for angina pectoris, namely, an oppressive discomfort behind the breastbone provoked by exertion or psychological stress. As much depends on the cogency of this claim, it deserves focused examination.

Angina Pectoris

Cardiologists commonly encounter one of two types of presentations in relation to the oft-occurring problem of coronary heart disease. First is the patient with chest discomfort. Second is the middle-aged asymptomatic male who comes for reassurance that he does not have silent CAD.(11) In considering the patient with chest discomfort, the primary concern is determining the presence of angina pectoris. AP is a unique discomfort reflecting a diseased coronary circulation.

The British physician William Heberden first described this syndrome to the Royal College of Physicians in 1768. His classic description went as follows: “But there is a disorder of the breast marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare. … The seat of it, and sense of strangling, and anxiety with which it is attended, may make it not improperly be called angina pectoris.

“They who are afflicted with it, are seized while they are walking, (more especially if it be up hill, and soon after eating) with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life, if it were to increase or continue; but the moment they stand still, all this uneasiness vanishes.”

Angina pectoris is caused by temporarily reduced blood flow to heart muscle. It is not a heart attack. It does not cause heart damage. The diagnosis of AP relies exclusively on a careful history. Coronary angiography does not prove or disprove the presence or absence of AP. The reason for such a seemingly categorical statement is that AP can occur without any significant coronary obstructions and may be never experienced among those with advanced disease involving all coronary vessels. As in Heberden’s time, the most rewarding avenue in reaching a correct diagnosis remains an unhurried interview with a patient.

In more than 90 percent of patients, this distinctive syndrome can be diagnosed or dismissed merely by attentive listening to the story. A patient may be at a loss for words to explain the sensation. Even a highbrow intellectual may stutter with uncertainty, “Doctor, I find it hard to explain.” For angina is not experienced as a pain, neither sharp, nor throbbing, nor stinging, nor knife-like, nor piercing. It is more like a tightening, an oppressive weight, a heaviness, “an elephant sitting on my chest.” When asked to point with a finger where it hurts, the patient will place hand or fist on the breastbone. In any one person recurring episodes are remarkably consistent with regard to location, quality, severity, and provocative factors. AP is more likely to occur in the morning hours, when the patient is feeling robust rather than fatigued, when he or she is going to work rather than returning, and outdoors rather than indoors. It is of brief duration, lasting minutes rather than lingering for hours. It is singular rather than oft recurring. Recumbency aggravates the discomfort. AP is more commonly provoked when the patient is under time pressure, when hurrying or running, and especially when the weather is cold or humid. It is more likely in the hardworking than the loafing. Not uncommonly one may suspect subclinical depression. Interestingly, when the discomfort abates, unlike with other bodily afflictions, the patient experiences a prompt return of vigor, ready to charge ahead rather than craving to disconnect and rest.

I am reminded of an experience of nearly fifty years ago. FB, a medical editor of a leading national business magazine, interviewed me on the risk factors for CAD, then a novel subject. He was extraordinarily compulsive and comprehensively read numerous cardiovascular journals and textbooks. We spent many hours together. I was taken aback when some months later he consulted me professionally about himself, convinced that he was experiencing AP. This seemed unlikely. FB was barely 40, tall, thin, and very athletic. There was no heart disease in the family. I knew he was filled with textbook lore about AP.

My questions were therefore aimed at determining whether I could mislead him into textbook-based answers. For example, I asked him to point where the pain was. He placed an index finger on his upper belly below the breastbone. Clearly he misinterpreted the textbook description of the pain being beneath the sternum as below it. He affirmed that it was a severe pain that lasted for hours, and that he felt drained and had to rest when an episode ended. The pain was eased when lying down. The so-called angina was more likely indoors and occurred at the end of a workday.

Certainly these episodes had nothing to do with the heart. Further examination or tests were not warranted. I nonetheless carried out a meticulous physical examination. I then announced triumphantly that there was not a scintilla of evidence of any heart problem, that it was all in his head. The arrogant locution indicated my ineptitude as a clinician, eager to flaunt diagnostic brilliance rather than tuning in to a patient’s sensibilities. I was blinded to the deeper question of why these symptoms occurred in the first place. Rather than being satisfied that he was free of heart disease, FB bristled with anger, responding that my opinion was not based on hard evidence. He demanded some objective test to affirm the exclusion of coronary heart disease. This was before the days of coronary angiography. FB underwent exercise stress-testing on a motorized treadmill. He walked a remarkable 16 minutes without pain or electrocardiographic changes. At last he was satisfied that he was free of CAD. Though we had communicated often over the preceding months and struck up a friendship during the time of his writing the series of articles on heart disease, I never heard from him again after this last visit.

My errors were several. Primarily, I rushed to judgment but left the underlying psychopathology unexplored. I could have involved him in a shared conclusion that he did not have AP by having him try nitroglycerine (TNG). For those with AP, the chest pressure almost immediately abates as this small pill melts under the tongue. Alas, doctors currently undervalue this drug.

TNG is a powerful therapeutic agent. When used properly, it circumvents the need for invasive cures. My great teacher and mentor, Dr. S. A. Levine, maintained that the free use of TNG enables patients with angina to outlive their doctors. This matter deserves some elaboration.

Nitroglycerine

TNG is truly a wonder drug. When properly used, it enables patients to live a normal life free of angina. The drug dilates coronary arteries and decreases the workload of the heart, two factors responsible for the discomfort. Yet a majority of anginal patients use the drug sparingly if at all. The reasons are several. Mostly these relate to hurried and improper instruction by the physician. When I asked one patient why he never used nitroglycerin, he related that when complaining to his doctor that the TNG invariably resulted in a throbbing headache, the cardiologist responded, “You are lucky the pill didn’t blow off your head.” He added, “Don’t you know that nitroglycerine is the explosive substance in dynamite?” Patients are cautioned to use TNG sparingly and urged to alert their physician when resorting to more than their norm, since they would then have to undergo prompt revascularization to prevent a heart attack or worse. With such instructions, is there any wonder patients avoid using nitroglycerine?

Early in my medical practice, some fifty or more years ago, I was dismayed to learn that a majority of my patients did not take TNG despite my careful counseling. They failed to use it prophylactically or even with chest discomfort. In many conversations, I learned that patients had to overcome a number of psychological hurdles. These included an uncertainty about when exactly to take it, a hope that an episode would rapidly abate spontaneously, the fear of a throbbing headache, anxiety that if TNG worked it was proof of a cardiac problem, an unwillingness to acknowledge having a heart condition that could cripple or kill, an unreadiness to become dependent on or habituated to pills. I realized it also reflected my poor doctoring due to a immature clinical imagination. Bear with me.

Consider a Bostonian rushing for a bus in midwinter. It is cold with snow on the ground. He develops chest discomfort and stops. Dutifully, following his doctor’s instructions, he carries a small unopened bottle of nitroglycerine. He twists off the cap, finding a plastic seal that cannot be pushed in with a fingertip as the bottle opening is too small. Finally he breaks through with a fingernail. At this point he realizes that a glob of cotton batting has been squeezed down beyond reach. There is no way on God’s earth to get it out with a frozen ungloved hand. So he furiously shakes the bottle. The cotton batting falls out together with some pills. He picks up one from the snow and puts it under his tongue. By this time the nitro is half melted. Nonetheless, he develops an intense throbbing headache, far worse than the chest discomfort. He forswears ever using nitro again and tosses away the half-emptied bottle.

The above is not an invention. Listening carefully to dribs and drabs of stories from patients I imagined the real.(12) It led to a drastic change in how I prescribed nitroglycerine. At the end of an initial visit with patients having angina, I would offer a nitroglycerine pill. The response would be, “But, doctor, I do not have any discomfort.” I indicated that it was important to determine whether any adverse effects would ensue. The patient placed the pill under the tongue. I started a stopwatch and began an explanation that went somewhat as follows: “This small pill dissolves almost instantly. When it does, you have a tingling sensation under the tongue. You may experience a nice fullness and a very nice throbbing sensation in the head. These are due to a rush of blood confirming that your heart, like your head, is receiving more sorely needed oxygen. As a dividend you also get more oxygen delivered to your brain; most of us can profit from a little clearer thinking.”

At this point I would begin a conversation related to some pleasant aspects of the history I had just obtained. For example, if the patient had a son who was graduating from a university, a daughter who had just won an academic prize or had a grandchild, I would question the patient about such proud matters. After three minutes, I would inquire whether the patient had a throbbing sensation in the head. The invariable answer was either, “No, I experienced nothing” or “Yes, I had a fullness,” but a headache was almost never mentioned.

I would then encourage the free use of TNG, urging that it be taken at the very onset of discomfort. One cannot be certain whether a minor chest pressure will abate or increase in severity and injure the heart. Taken early, TNG protects the heart from possible injury. When chest discomfort is promptly relieved, there is no need to interrupt activities except perhaps to slow their tempo. Better still is to take a pill in anticipation of discomfort. One rapidly learns when angina is likely to occur. Under such circumstances of increased exertion, excitement, or anxiety it is worthwhile to take a nitroglycerine prophylactically, thereby preventing angina’s very occurrence.

I continued this mini-lecture by informing the patient that the drug was not habit forming, as it was not a narcotic or a pain killer. It is permissible to take TNG numerous times a day without adverse effects. These instructions took about ten minutes. Thereupon I would evince deep satisfaction that the pill worked so remarkably well, and wrote the prescription. Patients so instructed experienced no untoward effects from this medication and used TNG freely.

Additionally we drafted a pamphlet of about fifteen paragraphs with precise affirmative instructions.(13) Later we developed an interactive computer program relating to nitroglycerin. This consisted of a series of questions and answers that led through a tree of responses. Patients could take as long as they wished. If they failed to answer some questions appropriately, the computer would automatically go back to an earlier point in the dialogue with somewhat altered content. When the program was over, and this was watched by both patient and spouse, they were given the pamphlet that recapitulated and reinforced these essentials. These three measures have enhanced enormously the use of nitroglycerin.

On one visit a patient said, “Dr. Lown, I hope you will not be hurt by what I’m about to say.” After a momentary hesitation he blurted out, “You know, the computer is far superior to you in explaining when to use a nitro.” I realized that this was true, though the computer program was my brainchild. The computer is unhurried; the patient is unflustered and can go back and relearn the obvious. I am always pressed for time. Notwithstanding all good intentions, I no doubt convey impatience, even irritation and annoyance, when besieged with many questions. Thereby a host of uncertainties that a patient harbors are left unaddressed. Unasked questions are a basis for anxiety, which I believe adversely affects outcome.

Survival

Over the past several decades, possibly due to a dearth of evidence that interventions improve survival, the argument has shifted. Two major lines of reasoning are advanced to justify the widespread practice of revascularization. First, that it is being used to treat intractable or unstable angina, which augurs life-threatening heart attacks or sudden death. Second, that it improves the patient’s lifestyle by obviating all angina. My medical group and I are apparently living in a far more benign parallel universe. We, in fact, rarely encounter anginal patients who do not respond to the highly effective available medical measures. Only about 5 percent of patients seeking a second opinion in our clinic have unstable angina! Since they have already been urged to undergo revascularization, they are a skewed sample with far more advanced disease than the CAD population at large. It stands to reason that the prevalence of unstable AP in the community is much less than what we encounter. My clinical guess is that it may be around 0.5 percent. Namely, one in 200 patients with angina pectoris is refractory to modern medical treatment. If this is even a distant approximation, we are compelled to an absurd conclusion that nearly the entire adult American population has advanced coronary artery disease. Otherwise, how is one to account for the fact that about a million patients undergo revascularization annually?

With the availability of a bevy of effective drugs to address angina (such as beta blockers, calcium channel blockers, long-acting coronary vasodilators), and especially the much underused nitroglycerine, lifestyle improvement by costly interventions should be a nonissue. Uppermost in the mind of patients is the issue of survival. A minuscule fraction would agree to undergo any intervention if the result were not a longer hold on life. Over the past decades the Lown Group has been preoccupied with this salient issue.

Thirty years ago we published our first article in the New England Journal of Medicine describing our management of severe CAD. Since then we have published three additional reports.(14-17) These deal with more than a thousand patients who were treated medically and followed for an average of about five years. The large majority of these patients would have been deemed suitable candidates for revascularization. The annual cardiac mortality as well as hospitalization rate for heart attacks in our population of CAD patients was no different from the best outcomes being reported for revascularized patients.

Our group conducts quarterly mortality conferences. Over the past decade we have examined about 1,200 fatalities. I have been fixated on a single numeric. This relates to the age of death. Remarkably, the average age has consistently been 83 years. Since a majority of heart disease patients we follow are males, this is seven years better than the life expectancy for males in the US. I have commented in an earlier essay that the most hard-nosed persuasive evidence of the validity of our data, in this litigious country, is the fact that we have not had a single malpractice suit for mismanaging a coronary patient in the past forty years.

How to account for our results? The answer is highlighted by a single patient experience. DF had been a longtime patient of Dr. S. A. Levine. He was in his mid-80s when he sought my counsel. From the amount of nitroglycerine he was consuming, one would conclude that he had severe angina. He took about three to five pills daily. This had been his practice for the past thirty years. Incredulous, I inquired with that much angina, why he had not undergone coronary revascularization. His startling response was that in all these years he did not have even a single episode. I was at a loss for words. He explained that when he first encountered Dr. Levine he was having numerous angina episodes daily. But the instruction he received was to take a nitro in anticipation of chest discomfort. This he did religiously. In fact as Levine predicted, DF outlived him by twenty years.

The secret of this odd tale is that there is no secret. We subscribe to the dictum of the great American physician Oliver Wendell Holmes Sr. that the key to longevity is to have a chronic incurable disease and know how to take good care of it. In fact, our patients are largely in control, knowing that when in doubt they can readily turn to a physician who is minimalist in disordering a normal lifestyle and maximalist in understanding and empathy. This brings us to a core issue in clinical practice, namely, the role of higher nervous activity in shaping the course and outcomes of illness. This charged topic will be addressed in future essays.

Endnotes and Bibliography

1. Mason Sones invited me to lecture at the Cleveland Clinic. Mason was full of exuberant conviction. He sounded more like a daring Spanish buccaneer explorer discovering new territories than a caring physician. Before I ever met him he telephoned, saying something to the effect of, “Bernie, this is Mason from Cleveland Clinic. I have been using your contraption (defibrillator) for several weeks. It is a godsend. When a patient fibrillates we do not anesthetize. We instantly give him a shock while he still awake. As the anesthetist is retracting the chin he gets a jolt as well. It wakes him up!” Followed by a burst of hilarious laughter.

2. Ventricular fibrillation is a rhythm disorganization of the heartbeat. Instead of orderly sequential electrical activation of heart muscle to contract, there are rivulets of electrical wavelets running helter-skelter. The heart is paralyzed into inactivity and resembles a wriggling can of worms.

3. The heart is nurtured by three coronary vessels and their tributaries, referred to as the left descending, the circumflex, and the right.

 4. In order to reach the heart, one needs to split the sternum, a sternotomy in medical jargon, or cutting the breastbone. Rarely a patient may experience discomfort from the slight movement of the two sutured halves of the sternum.

5. Angiography is indispensable once the decision has been reached for a coronary intervention. No intervention is possible without locating the site of the obstruction and the magnitude of the vessel narrowing.

6. The patient believes this largely because the doctor has so informed him and usually frightened him to think that no other diagnostic venue exists.

7. The cost is not only in dollars; it also may inflict discomfort, lifelong complications, and even death.

8. Angioplaster from Cleveland Clinic Foundation, Dr. Stephen G. Ellis in Circulation 86:1400, 1992.

9. See Essay 28, “A Maverick’s Lonely Path in Cardiology,” posted on March 10, 2012.

10. When investigators carried out two coronary angiograms before and after a heart attack, the culprit vessel responsible for the heart attack invariably was in a vessel not severely obstructed in the first visualization. It is not unreasonable to conclude that coronary bypass or angioplasty would not protect against heart attacks, since the arteries in which the obstructions are widened or grafted are not the ones that cause later mischief.

11.The asymptomatic male with anxieties will be considered in a future essay.

12. From Martin Buber, an Israeli philosopher and promoter of “Hebrew humanism” who maintained the reason for our doing wrong and evil deeds relates to “our inability to imagine the real.”

13. The pamphlet was labeled “Guidelines for the Proper Use of Nitroglycerine,” authored by myself and Dr. Stephen H. Rabinowitz , at the time a postdoctoral research fellow in my laboratory. The pamphlet was so popular that it was translated into Russian, Yiddish, Spanish, and Portuguese.

14. Podrid PJ, Graboys TB, Lown B: Prognosis of medically treated patients with coronary‑artery disease with profound ST‑segment depression during exercise testing. N Engl J Med 305: 1111‑1116, 1981.

15. Graboys TB, Headley A, Lown B, Lampert S, Blatt CM: Results of a second‑opinion program for coronary artery bypass graft surgery. JAMA 258 (12): 1611‑1614, 1987.

16. Graboys TB, Biegelsen B, Lampert S, Blatt CM, Lown B: Results of a second-opinion trial among patients recommended for coronary angiography. JAMA 268 (18):2537-2540, 1992.

 17. Jabbour Jabbour S,Young-Xu Y, Graboys TB, Blatt CM, Goldberg RJ, Bedell SE, Bilchik BZ, Lown B, Ravid S: Long-term outcomes of optimized medical management of outpatients with stable coronary artery disease. Am J Cardiol. 2004;93:294-299.