Risk Stratification in Acute Coronary Syndrome Using Cardiac Troponin I (Editorial‪)‬

The interest in risk stratification of patients with acute coronary syndrome (ACS), i.e., acute myocardial infarction (MI) and unstable angina pectoris (AP), has increased considerably within recent years because of improved knowledge of pathology, progress in immunoassays of already existing biochemical markers, introduction of new biochemical markers [especially cardiac troponin I (cTnI) and T (cTnT)], and new methods of treatments. Coronary artery disease may present clinically as stable AP or ACS. In cases of stable AP, myocardial ischemia commonly results from increases in myocardial oxygen demand that outstrip the ability of stenosed coronary arteries to increase oxygen delivery (1). In ACS, the accepted cause of acute MI is a plaque disruption, or fissuring, leading to coronary thrombosis with or without vasospasm, and thereby intermittent or persistent coronary occlusion. In patients with unstable AP, pathological postmortem investigations have documented that unstable AP leading to MI or cardiac death frequently is preceded by microinfarctions (2). This is important because patients with non-Q-wave MI tend to have smaller infarcts on presentation and rarely have total occlusion of the infarct-related vessel; it therefore is considered a relatively unstable condition associated with a lower initial mortality but a higher risk of later MI or cardiac death (3).