In a canine model of acute myocardial infarction, the depletion of cTnT in ischemic tissue correlates with infarct size at 3 weeks, mirroring the increase in serum troponin levels.
Tissue cTnT depletion may track chronic infarct size in canine AMI; leaves open isoform-specific biomarker utility in patients.
We studied the distribution of cardiac troponins I (cTnI) and T (cTnT) in ischemic left ventricular (LV) tissue in 7 infarct zones, 7 remote nonischemic LV areas, and 7 nonischemic areas each from the right ventricle and circumflex in an acute coronary artery occlusion dog model to correlate myocardial loss of troponins with infarct size 3 weeks after the infarction and to determine whether the decrease of troponins in ischemic myocardium can be used to assess the infarct size in dogs after coronary occlusion. The serum profiles for time vs mean cTnI and cTnT concentrations in 6 dogs after occlusion showed peak concentrations at 1 day and 5 days, respectively. The concentrations of troponins were similar in all nonischemic zones. However, cTnI and cTnT decreased significantly in the LV ischemic tissues. Loss of cTnT, but not cTnI, in ischemic LV tissues correlated significantly with infarct size 3 weeks after the infarction. Biochemical alterations suggest that the increases in serum troponins after the infarction parallel the decreases in tissue concentrations of troponins.
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Ricchiuti et al. (1998) studied this question.
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