Correlation of Antemortem Serum Creatine Kinase, Creatine Kinase-Mb, Troponin I, and Troponin T with Cardiac Pathology (Enzymes and Protein Markers)
In recent years, serum troponins have been increasingly used in the diagnosis of acute coronary syndromes as studies have shown their greater clinical sensitivity over creatine kinase-MB (CK-MB)  (1, 2). In patients with non-Q-wave myocardial infarction (MI) or unstable angina, serum troponins can provide risk stratification for short-term (3-9) and long-term (9,10) cardiac events and mortality. This has been attributed mainly to the ability of serum troponins to detect microinfarcts, areas of necrosis too small to produce electrocardiographic changes or increased serum cardiac enzymes. Whereas increased short-term complications and mortality may understandably be explained by these microinfarcts, long-term events have also been attributed to complications of ischemia. Additionally, a high percentage of end-stage renal failure patients show increased cardiac troponin T (cTnT) in the absence of acute cardiac ischemia (11,12). There have been suggestions that these represent spurious increases arising from re-expression of the cardiac isoform, the fetal form, in skeletal muscles of these patients (13). We have observed a threefold increase in 1-year mortality in 172 hemodialysis patients with increased cTnT (14), and although increases in cTnT may result from silent MIs that occur frequently in these patients, the temporal pattern of increases was not in keeping with acute ischemic events. This raised the possibility that increased cTnT in this group of patients was indicative of chronic disease processes that compromise survival.