**2. Clinical utility of cardiac troponin in myocardial damage**

Cardiac-specific isoforms of the contractile protein complex troponin, namely cTnT and cTnI, are released into the bloodstream following damage to cardiomyocytes. The mechanism by which these structural proteins are released into the circulation has been debated significantly over many years. Initially, it was thought that cTn could only be released following overt cellular necrosis; however, recently it has been suggested that release can occur in ischemia without necrosis [3]. A review of the subject by Ragusa and colleagues suggest release mechanisms, including apoptosis, necroptosis, physiological cardiomyocyte renewal, and cellular wounding can contribute to cTn release as well as necrosis [4]. An immunohistochemical study using a canine model of coronary occlusion ranging from 30 minutes to 6 hours demonstrated variable loss of both cTnT and cTnI in paraffin-embedded left ventricular myocardial sections [5]. Loss was variable but more so for cTnT than for cTnI, and loss was greater at the periphery of the infarct area rather than the centralised region (**Figure 1**).

#### **Figure 1.**

*Canine left ventricular myocardial tissue following 6 h of coronary artery occlusion. Immunohistochemical staining of (A) cTnI demonstrating decreased but non-uniform staining in the central necrotic area (asterisk); (B) cTnT demonstrating loss at edge of infarct zone (arrows) and (C) canine left ventricular myocardial tissue following 45 min of coronary artery occlusion demonstrating loss of cTnI in the zone of necrosis (asterisk) (source: Adapted from [5]).*
