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(Circulation. 2000;102:IV-2.)
© 2000 American Heart Association, Inc.

Special Anniversary Issue

Progress in the Treatment of Acute Coronary Syndromes

A 50-Year Perspective (1950–2000)

Pierre Théroux, MD; James T. Willerson, MD; Paul W. Armstrong, MD

From the University of Montreal/Montreal Heart Institute, Montreal, Quebec, Canada; the Department of Internal Medicine, University of Texas–Houston Medical School, and Texas Heart Institute; and the Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.

Correspondence to James T. Willerson, MD, Circulation, SLEH/THI, 6720 Bertner, Room B524, MC 1-267, Houston, TX 77030.

Early in the past century, skillful physicians observed that prodromal symptoms often precede acute myocardial infarction,^{1 2 3} an observation that was prospectively validated in mid-century in cohorts of patients presenting with a changing pattern of chest pain.^{4 5 6} In the 1960s, the new syndrome was in search of a semiology and a natural history and was variously identified by symptoms (crescendo angina, status anginosus, accelerated angina), by presumed pathophysiology (coronary failure, acute coronary insufficiency), or by its prognostic significance (impending myocardial infarction, preinfarction angina). The term unstable angina proposed by Fowler was eventually adopted.⁷ The modern era was introduced by an early trial by Paul Wood with an oral antivitamin K prematurely discontinued because of excess events in the absence of treatment,⁸ and in the 1970s and 1980s and accelerating to the present, by the definition of risk strata^{9 10} and the pioneer works on pathophysiology and treatment (Table 1).^{11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56} Constantinides described fissuring of atherosclerotic plaques leading to coronary artery thrombosis in 1966.¹¹ Willerson et al, in the late 1970s, postulated that "an alteration in atherosclerotic plaque morphology led to platelet adhesion, thromboxane A₂ accumulation, growth of thrombus and dynamic vasoconstriction" and that this sequence of events caused the conversion from a stable to an unstable coronary syndrome.¹² Davies et al¹³ and Falk¹⁴ showed at postmortem studies that patients with unstable angina and myocardial infarction almost always have atherosclerotic plaque fissuring or ulceration. The vulnerable plaques have thin fibrous caps, an adjacent lipid core, and a large number of inflammatory cells, primarily . . . [Full Text of this Article]