Broken Hearts: The Tangled History of Cardiac Care

3. The Case against Plaque Rupture

Paris Constantinides and Meyer Friedman had great confidence that their methods had produced definitive evidence in support of the plaque rupture hypothesis. The three other groups who employed comparably rigorous techniques converged on plaque rupture as the most likely cause of heart attacks . One might expect that the results of such methodical scientific research would speak for themselves. In practice, however, this does not always happen. Almost any phenomenon in science or medicine is open to multiple interpretations .1 Nature is complicated, scientists are creative, and many factors influence how scientists resolve debates. The search for the cause of heart attacks demonstrates this well. When Timothy Leary and others first made serious attempts to decipher the cause in the 1930s, they proposed a series of theories, from progressive obstruction to intramural hemorrhage, spasm, plaque rupture, and others. But they could not produce evidence for any one theory that convinced everyone. A similar story played out in the 1960s. Even as Constantinides and Friedman developed one line of evidence—autopsy analyses—to a high state of refinement, other scientists introduced other ways of studying and visualizing the pathochapter three The Case against Plaque Rupture The Case against Plaque Rupture 49 genesis of heart attacks. These competing methods supported different theories and prevented closure of the heart attack debate in the 1960s and 1970s. Even as bypass surgery became more and more popular in the 1970s, physicians remained uncertain about the cause of the problem that bypass hoped to prevent. The challenges to the plaque rupture hypothesis came from many directions. The primary challenge arose from old doubts about the relevance of coronary thrombosis. Even if Friedman and Constantinides had produced compelling evidence that a plaque rupture was at the root of every coronary thrombosis, they had not convinced their colleagues that a coronary thrombosis caused every heart attack. The rigor of their method proved to be an obstacle here. Because it took so long to study the hundreds or thousands of cross-sections from a single patient, the researchers could examine only a small number of patients. Did their small samples fairly represent the entire population of people who suffered heart attacks? Did thromboses cause the attacks in all of them? Those questions lingered for decades. Many of the competing theories from the 1930s remained ongoing concerns in the 1960s. Although Leary came to favor the plaque rupture hypothesis , he had also described cases in which spasm appeared to play the dominant role. Remember the violinist’s father who dropped dead from excitement before his son’s recital, or the bookie who died after a reprimand at work? When Leary dissected their bodies, he found no remarkable disease in their coronary arteries and concluded that the emotional arousal had triggered coronary spasm. He acknowledged that his evidence was circumstantial: “The clinical and pathological material here presented can be, of course, only suggestive as to the possible role of coronary spasm leading to attacks of angina or in producing sudden death.”2 In the absence of positive evidence that spasm had occurred, the idea gained little traction. Coronary spasm hypotheses made a comeback in the 1950s. In 1959 Los Angeles cardiologist Myron Prinzmetal described what he called “variant angina .” Unlike classic angina, it was not triggered by exertion and relieved by rest. It occurred and resolved spontaneously. Having seen spasms in the arteries of rabbits’ ears, he suggested that spontaneous changes in vascular tone could cause angina and even infarction. This fit well with popular notions— ironically made popular by Meyer Friedman’s type A personality hypothesis— that linked stress to coronary disease. Supportive evidence came in the 1960s 50 Theory and Therapy as doctors described good clinical results using nitrates and other drugs that relaxed the muscle cells in artery walls and relieved vascular spasms.3 In one remarkable case doctors realized that the spasm theory could explain an outbreak of angina and heart attacks among workers at a Wisconsin munitions factory. In 1966 a factory near Milwaukee reopened to make nitroglyercin -cellulose fuel, used as a solid rocket propellant. Although employees wore gloves and aprons to minimize their contact with the chemicals, some exposure occurred. Workers suffered from headaches, weakness, dizziness, and nausea, all symptoms of nitroglycerin poisoning. Many had to quit their work at the factory. Others acclimated to the exposure: their bodies increased their vascular tone to balance the vasodilating effects of the chemical. This adaptation...