Unstable angina pectoris is a clinical syndrome between chronic stable angina pectoris and acute myocardial infarction. In many respects it is a heterogeneous entity, as attested to by the anatomic findings in this study of 50 patients of whom 74% had significant obstructive disease of one or more coronary arteries, 16% had at least 50% luminal diameter narrowing of the left main coronary artery and 10% had no evidence of arteriosclerotic narrowing. For patients in the latter group with normal anatomic findings, coronary vasospasm and enhanced platelet aggregability may be important contributary factors for which therapeutic modalities aimed at their control should be considered. Medical therapy of unstable angina pectoris, which has evolved rapidly in the past 5 to 10 years includes: nitrates, short and long-acting, administered sublingually, orally, topically or intravenously. Since the intravenous route may lead to a marked reduction in left ventricular filling pressure, monitoring of the pulmonary capillary wedge pressure is warranted. Aggressive nitrate therapy is especially rational for those patients in whom vasospasm plays an etiologic role. Beta-receptor blocking agents are generally given in increasins dosages until either symptoms are controlled or side effects intervene. In vasospastic angina pectoris, beta-adrenergic blockade may actually unmask coronary artery vasoconstriction and conceivably aggravate myocardial ischemia. Calcium antagonists exert a vasodilatory action independent of and complimentary to that of the nitrate preparations. They are also effective at preventing ergonovine-induced coronary vasospasm in patients with variant angina. Intra-aortic balloon counterpulsation cannot be utilized in all patients and, in those in whom it is inserted successfully, complications are substantial. Its utilization should be considered for patients with unstable angina pectoris only if medical therapy (including intravenous nitrates) is ineffective. Coronary artery bypass surgery is generally not performed as an emergency in patients with unstable angina pectoris. It is preferable to stabilize the patient with intensive medical therapy, including intra-aortic balloon counterpulsation if necessary, before proceeding to coronary arteriography and surgery. In any case, acute myocardial infarction must first be ruled out. Comparison of medical with surgical therapy can only be considered for the group with fixed coronary artery disease, with the exception of those with disease of the left main coronary artery in whom it may be unethical to withhold surgical therapy. Although the comparison is never strictly between pure surgical and medical therapy alone, the results of several studies suggest that surgery provides better relief of angina than medical therapy. Initial relief of angina pectoris, however salutary it may be, does not imply permanent relief of angina and a combination of graft attrition and progression of disease in the native circulation may lead to reappearance of symptoms in approximately 5% of patients per annum following initial relief of angina by aortocoronary bypass surgery. When the cost of treating all patients originally randomized to medical therapy is compared to that of surgical treatment, the patients randomized to medical therapy incurred higher cost during the first two years than patients initially randomized to surgical therapy due to late cross-over. It appears that surgical therapy does not prevent myocardial infarction or death in patients with unstable angina pectoris. In fact, the in-hospital rate of myocardial infarction for patients treated surgically may be higher than for those treated medically, although the rate of late myocardial infarction is similar.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine