Left main coronary artery stenosis: Clinical spectrum, pathophysiology, and management

Abstract

Atherosclerosis is the major cause of LMCAS. Isolated LMCAS occurs only rarely. Marked narrowing of the LMCA is usually indicative of severe, diffuse coronary atherosclerosis. Physiologically significant LMCAS is present in less than 15% of patients with symptomatic ischemic heart disease. Angina pectoris is the most common symptom in patients with LMCAS. The incidence of unstable angina is higher in these patients when compared to patients without LMCAS. Stress testing may help identify patients with LMCAS if the following criteria are met: (1) greater than 2 mm ST segment depression. (2) prolonged duration of ST segment change after exercise, (3) blunted or decreased heart rate response to exercise, and (4) ST segment change suggesting ischemia at a low heart rate. Coronary angiography provides definitive anatomic description of the location, length, and severity of LMCAS. The procedure can be performed at low risk if proper precautions are taken. Experimentally, 85% reduction in diameter of the LMCA is required to reduce resting coronary blood flow. Parameters of LV function begin to deteriorate at this level and progress as the degree of narrowing increases. General principles of good medical therapy for patients with ischemic heart disease also apply to patients with LMCAS. However, it is important to exercise caution when using agents that lower blood pressure. Patients with LMCAS who are in an unstable state should be hospitalized, monitored, and treated vigorously with pharmacologic agents. If pain persists, intraaortic balloon counterpulsation can be tried as a temporizing measure. Prognosis of medically treated patients with LMCAS is influenced adversely by poor ventricular function, coexistent disease of the right coronary artery, and severity of the narrowing in the left main coronary artery. When surgery is being considered, intraaortic balloon counterpulsation can be useful adjunct in patients with continuing chest pain. However, in the usual patient with LMCAS who is responsive to pharmacologic agents, intraaortic balloon counterpulsation is not necessary. Survival of patients with LMCAS treated surgically is better than that of comparable medically treated patients. However, there are subsets of high- and low-risk patients related to ventricular function, degree of narrowing of the LMCA, and associated disease of other coronary vessels. We conclude that current aggressive medical therapy has eliminated the need for emergency or urgent coronary artery surgery in all but a few patients with LMCAS and persistent symptoms. However, despite the initial success of medical management, the long-term prognosis in these patients is poor. At the present time, surgery should be considered in all symptomatic patients with ≥50% LMCAS.