Abstract
Modern methods of cardiac troponin determination have enabled early diagnosis of acute myocardial infarction (AMI) and selection of optimal treatment tactics for patients early from admission. It has markedly improved the further prognosis of these patients. Unfortunately, there are a number of problems arising from the use of high-sensitivity cardiac troponins: frequent and unexplained increases in serum troponin levels in a number of pathological conditions not associated with AMI; insufficient study of mechanisms of release and increase, features of circulation and elimination of cardiac troponins; inconsistent data on the influence of several factors (circadian, gender and age characteristics), on cardiac troponin levels. All this may be accompanied by difficulties and errors in differential diagnosis as well as insufficient use of the diagnostic potential of cardiac troponins. In general, these problems are due to our insufficient understanding of the metabolic pathway of cardiac troponins. This review briefly discusses the main stages of the metabolic pathway of cardiac troponins and focuses in detail on the first stage of metabolism (the release of cardiac troponins).