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Reaffirms plaque disruption and thrombosis as central to ACS; confirms foundational mechanisms for therapy and future mechanistic studies.
Acute coronary syndromes (ACS), including unstable angina, non-Q-wave myocardial infarction, and ST-elevation myocardial infarction, are the most commonly encountered conditions facing clinical cardiologists today, accounting for more than 650,000 hospitalizations annually (1). The pathophysiology of ACS is now well described, beginning with disruption of an atheromatous plaque, with subsequent platelet aggregation and thrombus formation. The resulting clinical syndromes vary, and depend upon multiple related factors.
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Tolleson et al. (1999) studied this question.
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