Release of macromolecular cardiac troponin I complex after successful percutaneous transluminal coronary angioplasty in acute myocardial infarction.

Abstract

Cardiac troponin I (cTnI) has been proposed for use in early assessment of reperfusion therapy (1)(2)(3)(4). However, commercial cTnI assays may react differently depending on the circulating forms of cTnI (5). Numerous reports have focused on the existence of troponin I complexes with the two other troponin components in the bloodstream of patients with myocardial infarction (6)(7). Independent of cTnI proteolysis occurring in the bloodstream related to the existence of covalent complexes of cTnI with cardiac troponin C (cTnI-cTnC) and T (cTnT-cTnI-cTnC) (8), cTnI degradation products also occur within human myocardium (9). To our knowledge however, no report has identified the cTnI forms released in patients with acute myocardial infarction (AMI) undergoing reperfusion therapy. Our purpose was to study cTnI release in patients undergoing successful (TIMI 3) reperfusion by primary percutaneous transluminal coronary angioplasty (PTCA) with stenting to ascertain and visualize rapid restoration of the coronary flow. We first established the release characteristics of cTnI and creatine kinase MB (CK-MB) in 11 AMI patients [9 males and 2 females; age range, 51–80 years; 4 with an occluded right coronary artery (RCA), and 7 with an occluded left anterior descending artery (LAD)] undergoing PTCA who presented within 6 h after onset of chest pain (2–6h). All patients received standardized adjunctive therapy consisting in abciximab, heparin, clopidogrel, and aspirin. Plasma (heparin) cTnI (10) and CK-MB concentrations were measured on the DPC Immulite [upper reference limit (URLs): cTnI, 1 μg/L (ROC curve); CK-MB, 4.8 μg/L (99th percentile)]. Samples were taken before PTCA (0 min) and 30, …