This could be explained by the kinetics of cardiac troponins in myocardial infarction, where hs-c-TnI slightly increases initially, indicating either an ischemia-induced release of the “early-release pool” or micronecrosis, followed by a significant increase within 2–6 h, reflecting extensive myocardial necrosis and degradation of myofibrillar proteins (16). This evidence concerns the gene TNNI3 and myocardial infarction.