Acute Coronary Syndromes

Ischemic heart disease includes a wide spectrum of conditions, ranging from silent ischemia and exertion-induced angina, through unstable angina, to acute MI. Unstable angina occupies the center of this spectrum, causing disability and risk greater than that of chronic stable angina but less than that of acute MI (Fig 1). Although non–Q-wave MI for many years was considered prognostically similar to unstable angina, recent longitudinal studies indicate that it is similar to Q-wave infarction (Fig 2). The concept of unstable angina has emerged from observations of frequent symptoms preceding acute MI, followed by prospective documentation that unstable symptoms frequently culminated in acute MI. The syndrome was rapidly accepted as a well-defined clinical entity as specific clinical manifestations, pathophysiological mechanisms, laboratory findings, and treatment became better characterized. Unstable angina is currently one of the leading causes of hospital admission for CAD, and non–Q-wave MI accounts for .30% of admissions for acute MI. Yet, the diagnosis of unstable angina remains clinical, based on symptom recognition. The physician caring for patients with unstable angina is in a privileged position of recognizing rapidly evolving CAD and being able to intervene to prevent irreversible left ventricular damage and progression of CAD. Unstable angina is classically described as a heterogeneous disease, referring to a wide spectrum of clinical manifestations from stable angina to MI, of disease processes from coronary vasospasm to thrombus formation, and of extent of CAD from no significant stenosis to severe three-vessel disease. Not surprisingly, therefore, the prognosis of unstable angina is quite variable. Despite all these heterogeneous features, the recent progress made in knowledge and management of unstable angina and acute MI has driven the acute coronary syndromes to the forefront of modern cardiology, helping shape future research and development. The new concepts are active coronary plaque and triggers and promoters of inflammation and of thrombus formation. The new therapeutic goals are plaque stabilization and prevention of accelerated atherosclerosis.