Lower socioeconomic classes are not the only ones susceptible to stress-induced heart problems. In the mid-1950s, Meyer Friedman and Ray Rosenman, two American cardiologists working at Mount Zion Hospital in San Francisco, created the idea of a high-achieving personality, which they called type A, that was particularly susceptible to heart disease and was disproportionately found in higher socioeconomic groups. “The type-A person is invariably punctual and greatly annoyed if kept waiting,” they wrote. “He rarely finds time to indulge in hobbies, and when he does, he makes them as competitive as his vocation. He dislikes helping at home in routine jobs because he feels that his time can be spent more profitably. He walks rapidly, eats rapidly, and rarely remains long at the dinner table. He often tries to do several things at once.” They described a characteristic physiognomy of this personality type. “[The type A man] tends to look you straight and quite unflinchingly in the eye. His face looks extraordinarily alert; that is, his eyes are very much alive, quickly seeking to take in the situation at a glance. He may employ a tense teeth-clenching and jaw-grinding posture. His smile has a lateral extension, and his laughter is rarely a ‘belly-laugh.’” In short, they said, the type A person is “aggressively involved in a chronic, incessant struggle to achieve more and more in less and less time.”
Friedman and Rosenman’s research was girded by the idea “that a person’s feelings and thoughts have an influence on the development of coronary heart disease.” They wrote, “Too many finely executed studies suggested that neither cholesterol nor the fat content of various diets could always explain coronary heart disease. Other factors just had to be playing a part.” In one of their studies, men who fit the type A pattern were seven times more likely to develop arterial disease than was a cohort of (presumably more mellow) municipal union workers and professional embalmers, as well as a group of forty-six unemployed blind men who were assumed to exhibit “little ambition, drive, or desire to compete” because of their lack of sight. The wife of one of the type A subjects told the cardiologists, “If you really want to know what’s giving our husbands heart attacks, I’ll tell you. It’s stress, the stress they receive in their work, that’s what’s doing it.”
The idea of a stressed but high-achieving subset of American society especially prone to heart disease captured the American imagination. In 1968, the surgeon Donald Effler wrote in Scientific American, “The heart attack is so common among professional people, executives, and men in public office that it has become almost a status symbol. If all the men in these groups who have had coronary attacks were forced to retire…, the shortage of manpower at the top levels of government, industry, and the professions in the U.S. would cripple the nation.”
The type A link to heart disease has not stood up to modern investigation and is now generally considered an artifact of its time. More recent research has focused on the association of “negative affectivity” traits, such as depression, anxiety, and anger, with heart disease. The strongest evidence has emerged for depression, which seems to be an independent risk factor for coronary artery disease and increases the risk of poor outcomes, including death, after a heart attack. How does depression affect heart health? Possible mechanisms include elevating blood pressure, causing vascular inflammation, disturbing autonomic nervous system function, and increasing blood clotting. Also probably playing a role are unhealthy behaviors associated with depression, such as physical inactivity, smoking, and failure to take medications or adhere to medical advice.
Today a massive amount of epidemiological data associates heart disease with chronic emotional disorder—or disruption of the metaphorical heart. For example, individuals in unhappy marriages are at a much higher risk for heart disease than those in more joyous unions. The risk of myocardial infarction and death increases dramatically in the year following a broken romance.
These associations hold true even for animals we would not consider needing social connection. For example, in a study in the journal Science, researchers fed caged rabbits a high-cholesterol diet to study its effect on heart disease. Surprisingly, they found that animals in high cages got much more cardiovascular disease than ones in cages near the floor. The scientists investigated air circulation and other possible factors, without success. Then they discovered that the technician who delivered food played more often with the animals in the lower cages than with the ones near the ceiling. So they repeated the study, randomly dividing the rabbits into two groups: one group that was removed from their cages and petted, held, talked to, and played with, and another that remained in their cages and was ignored. The first group had 60 percent less aortic atherosclerotic surface area on autopsy than the second, despite having comparable cholesterol levels, heart rate, and blood pressure.
Socially stressed laboratory monkeys also develop more heart disease than matched controls. In another study in Science, male monkeys that had stranger monkeys introduced into their cages, often in the presence of an estrogen-laden female monkey, resulting in fights for dominance and less social huddling, developed more coronary artery disease than a control group of monkeys that was not stressed, even though cholesterol levels, blood pressure, blood sugar, and body weight were similar between the two groups. “Psychosocial factors,” the authors concluded, “thus may help explain the presence of coronary artery disease (occasionally severe) in people with low or normal serum [cholesterol] and normal values for the other ‘traditional’ risk factors.”
We paid little attention to “psychosocial” factors during fellowship. The focus of our seminars was on pressure-volume loops, cardiac work cycles, resistance of fluid-filled pipes, and capacitance of fluid-filled chambers. We concentrated on clinical trial design, biological mechanisms, and understanding the heart as a machine. As with most academic training programs, the fact that there was an emotional world that could damage (or heal) this pump was largely ignored.
Ironically, the view that heart disease results from unfulfilled social or psychological needs was widely accepted in primitive societies. That is almost certainly how people thought about heart disease in rural Punjab in the 1950s. Doctors at the hospital where my grandfather was pronounced dead did not know about the damaging effects of cholesterol and hypertension (Framingham results had not yet been broadly disseminated). They would have explained my grandfather’s heart attack as the result of a sudden emotional shock (as when your neighbors bring a dead cobra into your home while you are having lunch with your family), or the years of social and financial struggle he endured after the Partition of India, or the loss of social connectivity that resulted from the fracturing and large-scale displacement of communities that had lived together for centuries, and in a sense they would have been right. Stress-induced surges of adrenaline can cause a stable atherosclerotic plaque to fissure and rupture, forming a thrombosis that can acutely block the artery and stop blood flow, thus causing a heart attack. Starved for oxygen, tissue begins to die. Irreversible cellular injury occurs within twenty minutes. And then, frequently, death.
Medicine today conceptualizes the heart as a machine. With advances in technology, perhaps this was inevitable. Drugs and devices have been responsible for much of the improvement in cardiovascular mortality over the past fifty years.
However, this narrow focus on biological mechanisms has hurt patients. We have overused stents and pacemakers. We have moved away from the emotional heart to a narrow focus on the biomechanical pump. The American Heart Association still does not list emotional stress among the key modifiable risk factors for heart disease—perhaps in part because serum cholesterol is so much easier to reduce than emotional and social disruption. We need a better way, one that recognizes the power and importance of emotions that the heart—the metaphorical heart—was believed to house for millennia. Though we know today that the heart is not the repository of the affections, it nevertheless remains the physiological canvas upon which our emotions are most easily written.
8
Pipes
<
br /> The tragedies of life are largely arterial.
—Sir William Osler, Diseases of the Circulatory System (1908)
The morning call was from the emergency room. A young man—an intern, in fact, who had been on rounds—had been admitted with chest pains. Could I come to evaluate him?
Such calls about hospital staff were dispensed with some regularity, and they rarely amounted to anything serious. Nevertheless, I hurried downstairs. The ER that morning was its customary mix of drunks and drug addicts. Nurses were just coming in for their day shifts. Stretchers were arranged like latticework in the corridors. There were the usual pressured announcements overhead (“Linda, stat to the trauma bay … Linda”). When I found the intern, Zahid Talwar, he was sitting on the side of a gurney, legs dangling, looking bored. He was about thirty, a Pakistani man with a long face and a long white coat who straightened up respectfully when I arrived. I introduced myself and asked him about the chest pain. It had started after dinner the night before, lasting about ten minutes. He had slept comfortably, but the pain recurred while he was walking to the bus stop that morning, persisting almost an hour. It was a dense pressure in the center of his chest that even he, a psychiatry intern, knew should be checked out. So he had decided to leave rounds and go to the ER.
I wasn’t too concerned. Zahid was young, and his blood tests and electrocardiogram were normal. He had none of the usual Framingham risk factors for heart disease, such as diabetes, hypertension, or a regular smoking habit. I suspected he was suffering from acute pericarditis, a usually benign inflammation of the membrane around the heart often treated with over-the-counter anti-inflammatory drugs. Characteristic of pericarditis, the pain worsened when he took a deep breath. I told Zahid that if blood tests in six hours were normal, we would send him home. I joked there were easier ways to get out of internship duty.
Later that morning, I got a call from an ER physician informing me that Zahid’s pain had resolved completely after he took ibuprofen, further confirming the diagnosis of pericarditis. For a moment I considered sending him home right then, but I decided to wait until the next set of blood tests was complete.
Just before leaving the hospital that evening, I ran into a physician assistant who told me that Zahid’s subsequent blood tests showed abnormal enzyme levels, evidence of minor cardiac muscle damage. This took me by surprise. Pericarditis usually does not result in cardiac damage. I explained that the problem was probably myopericarditis, in which inflammation of the surrounding membrane can partially involve the heart muscle. This, too, was relatively benign. The physician assistant asked me whether the young doctor should have a cardiac catheterization to rule out coronary blockages. I assured him that a thirty-year-old with no coronary risk factors did not have coronary artery disease. I instructed him to draw more blood, and to order an echocardiogram and call me at home if there were problems.
Zahid had chest pains through the night. Doctors who were called to see him attributed them to myopericarditis, the diagnosis written in the chart. At 2:00 a.m., he asked for more ibuprofen. “I told them, if it’s pericarditis, give me more medication,” he told me later. “Means, do whatever it takes to make the pain go away.”
When I saw him in the morning, the pain had subsided. However, further blood tests showed evidence of continuing heart muscle injury, and an EKG now showed new, though nonspecific, abnormalities. Though I still doubted that he had coronary artery disease, I sent him to the cardiac catheterization lab for an angiogram.
I received a call about an hour later asking me to come over to the lab. When I arrived, the angiogram was playing on a computer screen. It showed a complete blockage of the left anterior descending (LAD) artery. The artery looked like a lobster tail, unnaturally terminating after several centimeters. X-rays showed severe dysfunction of the entire anterior portion of Zahid’s left ventricle. My young patient—a doctor—had been having a heart attack for more than twenty-four hours.
* * *
If, as Osler said, the tragedies of life are mostly arterial, then the source of most of mankind’s misery is the fatty plaque. By cutting off blood flow, obstructive arterial plaque is responsible for heart attacks and strokes, the most common ways we die. By the 1960s, the mechanisms underlying this process were being aggressively investigated. In 1961, the Framingham study confirmed that cholesterol is a risk factor for coronary heart disease, but it did not explain why. In the decade following, scientists showed that when the concentration of blood cholesterol gets too high, small cholesterol particles can burrow through the inner lining of blood vessels and take up residence inside the wall. This begins benign, but the cholesterol soon reacts with oxygen to form free radicals that injure nearby cells. As these injured cells release chemical signals—calls for help—white blood cells swarm to the site of injury. There, they transform into cells called macrophages that feed on the oxidized cholesterol. Bloated by this indigestible cholesterol, the macrophages turn into “foam” cells, padding the vessel’s wall. They continue to gobble up cholesterol until they pass the brink of rupture, vomiting a gooey paste into the wall. The domino effect continues as more macrophages are recruited to the site, multiplying, causing the lesion to enlarge. Scar tissue is deposited to form a crust over what is now a malignant soup of fat, digestive enzymes, swarming macrophages, and dead cells—a full-fledged atherosclerotic plaque. In the beginning, the artery expands to compensate for the intrusion of plaque into the space within, but as the lesion gets bigger, the plaque eventually pushes into the vessel, hindering blood flow.1
The physiology of atherosclerotic plaque was mostly understood by the early 1960s, but how to treat it? As with any pipe, the first step is to pinpoint the blockage, not an easy feat in the dark caverns of the human body. On a temperate October day in 1958 in Cleveland, Ohio—just two years after Werner Forssmann received the Nobel Prize—Mason Sones, director of the cardiac catheterization lab at the Cleveland Clinic, came up with a solution to this problem.
Like Forssmann, Sones was a bit of a lunatic. Even in an era when doctors lived and breathed medicine, Sones topped the charts. He routinely worked until midnight, holding his cigarettes with sterile forceps while he smoked in the cath lab. Then, instead of going home to his wife and children, he’d peel off his stained white undershirt and go out for drinks at a nearby hotel. Nurses and secretaries were known to hide from him in the ladies’ bathroom. He’d soon catch on, pounding on the door whenever he had a task that demanded their immediate attention. Like Forssmann, Sones was brash and bullying. Like his great predecessor, he skipped animal studies and went straight to human demonstration. And like the German, he had the brazenness—and perhaps the good fortune—to go first.
Coronary arteries (Courtesy of Scott Weldon)
The coronary arteries take off from the aorta, the main artery in the body, just beyond the aortic valve. In the 1950s, cardiologists, fearful of putting a catheter directly into the coronaries, would inject massive amounts of dye into the aortic root, hoping some of it would trickle into the coronaries so they could be visualized by X-ray. Such “nonselective” injection was a feint, a sort of foreplay, and it provided few useful images.
One October morning, Sones was getting ready to inject dye into the aortic root of a twenty-six-year-old man to image the vessel in preparation for open-heart surgery when, as he was moving the catheter into position, it slipped into the opening of the right coronary. I learned during my fellowship that because of the shape of the aortic arch, it is almost easier to insert a catheter into the right coronary than to avoid it. Sones knew this, too, and whenever the catheter slipped into the orifice, he would withdraw it a few millimeters to disengage it. However, this time, before he could do anything, his assistant stepped on the dye pedal and dumped 50 cc of dye into the artery.
In a letter to a colleague, Sones recounted the fateful episode:
When the injection began I was horrified to see the right coronary artery become heavily opacified and realized th
at the catheter tip was actually inside the orifice … I ran around the table looking for a scalpel to open [the patient’s] chest in order to defibrillate him by direct application of the paddles … Fortunately he was still conscious and responded to my demand that he cough repeatedly. After three or four explosive coughs his heart began to beat again.
He later wrote,
Initially, I could feel only unbelievable relief and gratitude that we had been fortunate enough to avert a grievous disaster. [But] during the ensuing days I began to think that this accident might point the way for the development of a technique, which was exactly what we had been seeking.
Sones’s technique, called coronary angiography, outlined the flow of blood in the coronaries using dye and X-rays, thus pinpointing the location of plaque. “I knew that night that we finally had a tool that would define the anatomic nature of coronary artery disease,” he said. However, as is often true in medicine, diagnosis was only the first step toward a cure. It took almost two decades after Sones’s breakthrough to develop this “cure.”
Heart--A History Page 12