Why medical science needs to return to viewing the heart as an emotional object

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 US 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 behaviours 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 athero-sclerotic 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 neighbours 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 conceptualises 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 recognises 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.

Excerpted with permission from Heart: A History, Sandeep Jauhar, Penguin Random House India.