Knowledge of the pathophysiology of acute coronary syndrome has advanced in parallel with awareness of the significant limitations inherent in clinical and electrocardiographic assessment. In the meantime, biochemical assays, long established as a reliable means of detecting World Health Organization-defined myocardial infarction, have improved significantly. Prior of the late 1980s, diagnostic testing for so-called "cardiac" enzymes was not enough sensitive and cardiac-specific. New immunochemical techniques for measuring the mass rather than the activity of an enzyme permit the detection of smaller amounts of the protein markers, and therefore earlier diagnosis is possible. In addition, new laboratory techniques now allow rapid measurement of a wide variety of markers of myocardial cell death. Several serum proteins have recently been introduced and evaluated to determine sensitivity and specificity for detection of acute myocardial damage, including creatine kinase-MB mass measurements, myoglobin, cardiac troponin I, and cardiac troponin T. Cardiac troponin measurement is probably the most clinically effective test, also offering prognostic information to the clinician unavailable by other methods. The diagnostic superiority of these proteins has been established by clinical studies and rigorous statistical comparison with other markers. Furthermore, there is interesting evidence that minor myocardial cell injury revealed by these markers is strictly associated with a high risk of developing major cardiac events during follow-up. This means that these markers should replace existing traditional strategies to guide patient management. Obviously, there will also be financial benefits in terms of reduction in patient episode cost and improvement in decision-making.