The major cause of morbidity and mortality associated with coronary atheros
clerosis is plaque rupture, which often results in one of the acute coronar
y syndromes: unstable angina, non-Q-wave myocardial infarction (MI), or Q-w
ave MI. Plaque rupture may be attributable to the thickness of the overlyin
g 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 o
verlooked, also is lifesaving. Diet, exercise, and medications are the inte
rventions available for secondary prevention. Four classes of medications-a
spirin, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (stati
ns)-are also used in this setting with a high degree of success in reducing
mortality and morbidity. Numerous studies have demonstrated a 30-50% reduc
tion in mortality with aspirin. The reduction in mortality achieved with be
ta blockers in studies of patients after myocardial infarction are 15-50%.
ACE inhibitors significantly reduce the risk of death from myocardial infar
ction in patients with coronary artery disease with or without myocardial i
nfarction. Statins are beneficial even in patients whose cholesterol level
is low to normal. Patients who were discharged on a statin showed a 50% red
uction in mortality over those who did not receive statin therapy independe
nt of lipid level. C-reactive protein, a marker of inflammation, is predict
ive of mortality, as are age and ejection fraction. Statins may be antiinfl
ammatory in addition to their lipid-lowering effect. Secondary-prevention s
trategies such as case management, electronic discharge prompting, better c
ommunication between referring physicians and cardiologists, and patient ed
ucation may also have positive effects on after-discharge morbidity and mor
tality. (C)2000 by Excerpta Medica, Inc.