The major cause of morbidity and mortality associated with coronary atherosclerosis is plaque rupture, which often results in one of the acute coronary syndromes: unstable angina, non-Q-wave myocardial infarction (MI), or Q-wave MI. Plaque rupture may be attributable to the thickness of the overlying fibrous cap; thinner plaques are more likely to rupture. It appears that the presence of inflammation is a significant contributor to rupture. Acute-phase treatments are highly efficacious, but secondary prevention, often overlooked, also is life-saving. Diet, exercise, and medications are the interventions available for secondary prevention. Four classes of medications--aspirin, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins)--are also used in this setting with a high degree of success in reducing mortality and morbidity. Numerous studies have demonstrated a 30-50% reduction in mortality with aspirin. The reduction in mortality achieved with beta blockers in studies of patients after myocardial infarction are 15-50%. ACE inhibitors significantly reduce the risk of death from myocardial infarction in patients with coronary artery disease with or without myocardial infarction. Statins are beneficial even in patients whose cholesterol level is low to normal. Patients who were discharged on a statin showed a 50% reduction in mortality over those who did not receive statin therapy independent of lipid level. C-reactive protein, a marker of inflammation, is predictive of mortality, as are age and ejection fraction. Statins may be anti-inflammatory in addition to their lipid-lowering effect. Secondary-prevention strategies such as case management, electronic discharge prompting, better communication between referring physicians and cardiologists, and patient education may also have positive effects on after-discharge morbidity and mortality.