Cardiac Troponin T and Cardiac Troponin I: Relative Values in Short-Term Risk Stratification of Patients with Acute Coronary Syndromes (Enzymes and Protein Markers‪)‬

Investigating use of biochemical markers for risk stratification of patients who present within the spectrum of acute coronary syndromes, from unstable angina to acute myocardial infarction (MI), has been an active area of research [1-6].(6) These investigations have been driven, in part, because biochemical markers are minimally invasive and clinical indicators such as the frequency, timing, and duration of ischemic symptoms, along with the electrocardiogram (ECG), can often differentiate unstable angina from acute MI [7, 8], but these indicators are not useful in stratifying patients in the short term. A further role for biochemical markers may be as a guide for intervention. Although no appropriate trials addressing these issues have been completed to date, Lindahl et al. reported that cardiac troponin T (cTnT) identifies unstable coronary artery disease patients who benefited from long-term treatment with antithrombotic therapy [9]. Troponin T and troponin I function together as essential components of the contractile apparatus in striated muscle [10]. Although the troponin complex functions similarly in all striated muscle, isoforms of both troponin T and troponin I differ in cardiac vs skeletal muscle because these proteins are coded by separate genes in these tissues [11]. Both the myocardial and skeletal isoforms of troponins T and I show striking differences that include biological function, amino acid sequences, and molecular weight. Further, the proportion of total troponins T and I representing the "cytosolic pool" available for rapid release and time of increase after myocardial necrosis differ [12, 13]. Therefore, the characteristics of these proteins may differ with regard to risk stratification. Antibodies specific to the cardiac isoforms are the basis for sensitive cTnT and cTnI assays [14, 15].