Unstable angina pectoris

The pathophysiology of unstable angina has been better elucidated in the past five years and has led to more rational therapy. Coronary arteries in patients with unstable angina have atherosclerotic plaques which are often complex and are the site of platelet activation and fibrin deposition. Nitrates, one of the oldest therapies, are efficacious and act not only by dilating coronary vessels but by reducing preload and afterload. Beta blockers have a salutary effect by decreasing myocardial oxygen demand. Calcium channel blockers attenuate smooth muscle contraction and thereby act to decrease coronary artery spasm. Beta blockers and calcium channel blockers are equally efficacious in unstable angina. The antiplatelet agent, aspirin, has been shown to reduce fatal or non-fatal myocardial infarction and probably overall mortality. The use of heparin acutely for unstable angina has been demonstrated to decrease refractory angina and myocardial infarction, and acutely is probably better than aspirin. For patients with reduced ejection fractions (0.30-0.49), a prospective randomized trial has shown that coronary artery bypass graft surgery offers an improved three-year survival compared with medical therapy; however, surgery does not prevent myocardial infarction. Percutaneous transluminal coronary angioplasty may be a reasonable therapeutic alternative for some patients with single-vessel disease who are refractory to medical therapy but there are as yet no controlled trials of this question. To date a clinical benefit from thrombolytic therapy has not been demonstrated.