Biochemical advances in detection of the acute coronary syndromes: Implications for therapeutic decisions

Abstract

In this paper, I have attempted to place the evolving insights of the pathophysiology of coronary atherosclerosis in the context of the conventional perspective of clinical medicine. We strive to prevent death and to relieve suffering. Our clinical tools are critical but limited. Troponin, a biomarker of unprecedented organ specificity, in the context of the appropriate setting of new chest pain (or its equivalent syndrome), is an extraordinary aid to clinical diagnosis. Highly effective therapy is evolving which reduces loss of myocardium, undoubtedly reducing not only acute death but progression to congestive heart failure. Even if the newer therapies of the GpIIb/IIIa platelet antagonists and antithrombins are not yet widely employed, or may not be available to some physicians, the convincing demonstration of myocardial injury by troponin presents objective evidence to both the patient and the attending physician that serious compliance with a program of risk reduction must be urgently considered. Hoeg has described the mosaic of risk factors beyond the conventional and often ignored basic ones (JAMA, 1997, 277, 1387–1390). He provides thoughtful hope and encouragement for both patient and physician to do more in prevention of the subsequent predictable progression. We should look on a troponin positive vague unstable angina event as similar to a tremor which preceeds a subsequent earthquake. Although the mass of myocardium lost in such an episode may be small, it is a warning of the major acute myocardial infarction which can be predicted to follow at a later time if the course of the individual patient is not altered. Troponin is the objective evidence.