Serotonin and Acute Ischemic Heart Disease

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Abstract
Over the past 10 to 15 years, we have gained considerable insight into the pathophysiology of acute ischemic heart disease, and as a result our therapeutic approach has changed substantially. In the 1960s and early 1970s, Prinzmetal's variant angina, an uncommon entity, was shown to result from transient reductions in myocardial oxygen supply, which were due to vasospasm (often superimposed on a fixed stenosis) of an epicardial coronary artery.1 In contrast, the more common forms of acute ischemic heart disease, such as unstable angina and myocardial infarction, were thought to result from excessive myocardial oxygen demand in the setting of . . .