Analytic Review: Thrombolytic Therapy in Acute Myocardial Infarction

Abstract

The salvage of myocardium in the setting of acute myocardial infarction has long been a goal of physicians involved in the care of patients with coronary artery disease. Understanding the role of thrombosis in the pathogenesis of acute myocardial infarction has led the way to an entirely new approach to the treatment of this entity. Thrombolytic therapy has now become a widely used form of treatment with encouraging results. Both intravenous and intracoronary administration of thrombolytic agents have been shown to promote recanalization of acutely occluded coronary arteries. Results of studies using the clot-specific agent, tissue plasminogen activator, intravenously have been most encouraging; successful reperfusion has been obtained in approximately 70% of patients treated. In addition, a recent large-scale trial has shown a reduction in morbidity and mortality with the early use of thrombolytic agents.Ongoing trials should help delineate the precise role and timing of these agents as the initial form of therapy for acute myocardial infarction. Other issues that remain unresolved are the frequency of restenosis and the role of percutaneous transluminal coronary angioplasty in addition to thrombolytic therapy in the treatment of acute myocardial infarction.Coronary heart disease is the leading cause of death in the United States; over one-half million individuals die from it each year. Between 5 and 6 million Americans have chronic, symptomatic coronary artery disease. In 1983, over 680,000 individuals were hospitalized with myocardial infarction [1]. J.The medical management of myocardial infarction has evolved gradually over the past 30 years, from a strategy of permitting the heart to heal by putting the patient and the heart to rest to increasingly more active monitoring in coronary care units with aggressive treatment of identified abnormalities. It is uncommon for a patient with myocardial infarction to die of a primary rhythm disturbance in the acute phases of infarction [2]. Today, extensive myocardial injury is the most common cause of death and morbidity among patients hospitalized with acute myocardial infarction (AMI) [1]. Massive myocardial ischemia produces pump failure and serious ventricular arrhythmias [3]. Thus, shortterm survival is intimately related to the size of myocardial infarction; loss of more than 40% of the left ventricular (LV) myocardium almost always results in death. The risk of death appears to decrease with decreasing infarct size.Methods to reduce the extent and severity of myocardial damage have therefore been sought. Myocardial damage results from the disparity between oxygen demand and delivery in ischemic tissue. To limit infarct size, one can attempt to reduce myocardial oxygen demands or improve myocardial oxygen supply. Attempts to limit infarct size and improve early survival in AMI by pharmacologically decreasing myocardial oxygen demands have been disappointing [4][5][6]. Beta blockers have been shown to improve long-term survival when used prophylactically [7,8], a...

Thrombolysis in Acute Myocardial Infarction

“…and Gore on the use of thrombolytic therapy in patients with acute myocardial infarction [1]. The authors note the history and vicissitudes of the notion that myocardial infarction is caused by coronary thrombosis and set forth the concept of the limitation of infarct size.…”