Heparin and Aspirin in the Treatment of Unstable Angina

Abstract

Since the recognition of unstable angina as a clinical syndrome often leading to acute myocardial infarction, its pathogenesis has remained uncertain. In recent years, however, several lines of investigation have provided evidence for the role of plaque rupture leading to platelet activation and thrombus formation. Visualization of thrombus in the coronary arteries of patients with unstable angina by coronary angiography has been reported by Holmes et al. [1], Zack et al. [2], and Ambrose et al. [3]. Similarly, intracoronary deposits of thrombus material have been observed by means of angioscopy [4]. Plaque fissuring and thrombus formation have been documented at necropsy in patients who died with unstable angina by Falk [5] and Davies and Thomas [6]. Biochemical evidence that platelet activation is important has been provided by Fitzgerald et al. [7] and Hamm et al. [8]. Theroux et al. [9] and Kruskal et al. [10] have reported detection of fibrin and fibrinogen breakdown products in patients with unstable angina implicating ongoing thrombus formation.