CARDIAC TROPONIN-I TO DIAGNOSE PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY-RELATED MYOCARDIAL INJURY

The purposes of the present study were to evaluate cardiac troponin I (cTnI) in the diagnosis of percutaneous transluminal coronary angiopla sty (PTCA)-related myocardial injury in comparison with cardiac tropon in T (cTnT) and creatine kinase (CK) MB mass concentration, and to inv estigate the frequency of myocardial injury, as indicated by myocardia l protein release, after clinically symptomless side-branch occlusion (SBO) which may occur in the proximity of the attempted stenosis. The final study population comprised 80 patients undergoing elective, sing le vessel PTCA. Blood samples were drawn before, 6, 24 and 48 h after PTCA. cTnI, cTnT and CKMB mass baseline values were within the referen ce intervals in all patients (cTnI < 0.1 mu g/l, cTnT < 0.2 mu g/l, CK MB < 5 mu g/l). Two patients, presented with primary failure of PTCA, and visually successful PTCA was performed in all remaining patients. Seven patients (four with SBO) subsequently developed acute myocardial infarction (AMI). Symptomless SBO occurred in 16 patients. In control s (n = 55) there were no significant increases in cTnI, cTnT, or CKMB concentrations compared with baseline values, and all markers stayed w ithin their reference intervals. In half the patients with symptomless SBO (n = 8) all markers were slightly to moderately increased, in two additional patients only CKMB was elevated (cTnI: 0.1 - 1.0 mu g/l; c TnT: 0.25 - 0.81 mu g/l and CKMB: 7.9 - 25.6 mu g/l). In the majority of patients with primary failure or AMI we found pronounced increases in all tested markers (cTnI: 0.2 - 12.0 mu g/l; cTnT: 0.44 - 12.10 mu g/l; CKMB: 19.2 - 423.0 mu g/l). The results of this study indicate th at cTnT is comparably useful to cTnT or CKMB mass for diagnosing myoca rdial injury in PTCA patients. From our results a preference for one o f the tested parameters cannot be clearly derived. Post-procedural cTn I, cTnT, and CKMB mass values are not higher than baseline values in u ncomplicated cases, whereas AMI after PTCA leads to pronounced marker increases. SBO, even when symptomless, leads frequently (in about half the patients) to slight marker increases. (C) 1997 Elsevier Science B .V.