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Am Fam Physician. 2000;62(5):1174

The morbidity and mortality associated with atherosclerotic coronary artery disease are mainly due to rupture of plaque, which often results in one of the acute coronary syndromes: unstable angina, non–Q-wave myocardial infarction or Q-wave myocardial infarction. Muhlestein reviews the principles of posthospitalization management of high-risk patients.
One study revealed that 50 percent of patients who required hospital readmission within one year after an acute coronary syndrome had new disease progression or plaque destabilization. Three percent had subacute vessel closure, and 47 percent had target-lesion restenosis. Instability of plaque is probably directly related to the thickness of the fibrous caps, with rupture of thick caps less likely than rupture of thin caps. Interventions to prevent plaque instability include dietary modification, exercise and drug therapy (see the accompanying table).
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The benefits of dietary measures and exercise in stabilizing the plaques have not been assessed, and studies have not yet documented that either of these interventions by themselves actually saves lives. Four drug therapies have been demonstrated to save lives: aspirin, beta blockers, angiotensin-converting enzyme (ACE) inhibitors and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins).
Placebo-controlled trials have shown that aspirin, in patients who have sustained a myocardial infarction or have unstable or stable angina, reduces mortality by 30 to 50 percent. In addition to decreased platelet aggregation, beta blockers may also have specific intrinsic antiarrhythmic effects and may decrease the hemodynamic responsiveness of blood vessels, thereby helping to reduce the risk of plaque rupture. The reduction in mortality imparted by beta blockers is not altered by the ejection fraction. The most significant benefits have been noted to occur in patients with ejection fractions less than 50 percent. ACE inhibitors reduce afterload and delay progression of congestive heart failure and death. Studies have also demonstrated that ACE inhibitors reduce the risk of myocardial infarction and death in patients with diabetes or coronary artery disease. Lipid-lowering agents, specifically HMG-CoA reductase inhibitors, have been demonstrated to reduce mortality in persons with known coronary artery disease.
The author concludes that secondary prevention by means of appropriate drug therapy is required in every patient with a diagnosis of coronary artery disease who presents to the hospital with an acute coronary syndrome.

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