Southwestern Internal Medicine Conference: Unstable Angina Pectoris: The First Half Century: Natural History Pathophysiology, and Treatment

Unstable angina pectoris as a distinct syndrome intermediate between chronic stable angina and acute myocardial infarction was first described about a half century ago. The incidence of death or myocardial infarction rises in the first few months after destabilization of angina. Hemodynamic, scintigraphic, and arteriographic studies in the last 15 years have shown that unstable angina is chiefly due to “dynamic” coronary stenoses, transient reversible limitations in coronary blood flow caused by a complex interaction between coronary vasoconstriction, transient platelet plugging, and transient thrombosis. The trigger for the onset of dynamic coronary stenoses is probably acute changes in coronary arterial morphology in or near atherosclerotic plaques making those areas more thrombogenic. A large fraction of patients with unstable angina restabilize initially with medical management. The role of beta blockers is unclear, but they may protect against development of coronary events for patients with unstable angina similar to that reported for patients with myocardial infarction. Nitrates and calcium blockers are probably superior to beta blockers in restabilization of angina, but protection against coronary events has not yet been demonstrated clearly. Further investigation is needed to distinguish the relative benefits of a two-drug (heart rate-limiting calcium blocker plus nitrates) regimen vs. a three-drug regimen including beta blocker. There is no basis for emergency coronary bypass surgery to prevent myocardial infarction or death. Urgent surgery should be limited to patients who do not stabilize readily with medical therapy. One third or more of the patients who initially restabilize with medical therapy will require coronary revascularization in the year after unstable angina because of severe angina. An antithrombotic regimen of aspirin (or possibly heparin) reduces the incidence of progression to death or myocardial infarction. Two important future directions for research should be promising: (1) development of better antithrombotic regimens other than aspirin alone for protection against coronary events; and (2) improved ability to distinguish the patients who initially respond to medical therapy who are at low risk for later severe angina from those at higher risk