Unstable angina - an overview.

Unstable angina pectoris is an intermediate syndrome between classic exercise-induced angina pectoris and acute myocardial infarction characterized by the appearance of new ischemic pain, the development of more intense pain, often at rest, or intermittent ischemic attacks complicating the early recovery phase of established acute myocardial infarction. The major risk of unstable angina pectoris is acute myocardial infarction which may occur in about 25% of the patients during the three months following onset of symptoms. Physiologically, ECG changes and hemodynamic alterations generally precede the onset of pain. In unstable angina, the accompanying hemodynamic change and increased oxygen demand in the already-ischemic heart represents positive feedback creating further instability. The hemodynamic alterations may be the result of an abnormal response to stress or to inappropriately high chemoceptor discharge. While coronary spasm may play a definite role in the pathogenesis of unstable angina, other factors such as hemorrhage into the wall of an atherosclerotic plaque, peripheral embolization in the coronary tree from a proximal soft cholesterol "abscess", changes in platelet adherence and aggregability or altered vascular responsiveness must be taken into consideration. Treatment is directed toward inducing coronary and peripheral vasodilatation and reducing cardiac work with medications such as nitrates, calcium antagonists and, with reservations, beta-adrenergic blockers. In patients unresponsive to medical therapy, treatment with the aortic counter-pulsating balloon has been recommended. Surgery should be performed on an elective and not an emergency basis. The full clinical and pathologic significance of unstable angina pectoris is still being uncovered. Problems for the future lie in further exploration of the mechanism, treatment and prevention of the entity.