[Troponin T, Troponin I and CK-MB (mass) in the detection of periprocedural myocardial damage after coronary angioplasty].

The development of methods for the detection of circulating CK-MB mass, cardiac troponin T (cTn-T) and troponin I (cTn-I) has increased the diagnostic potential in the identification of myocardial damage. Coronary angioplasty (PTCA) represents a widely accepted revascularization procedure and a clinical model of induced ischemia. Using these new biochemical markers, we evaluated the incidence and the clinico-procedural correlates of minor myocardial damage (MMD) in a series of patients treated with PTCA in our Department. In 57 consecutive patients (75% males; mean age 58 years; range 35-80) undergoing elective PTCA from March 1 to June 30, 1995, serum levels of CK-MB mass, cTn-T and cTn-I were measured at baseline and at 6, 12 and 24 hours after the procedure. Seventy-eight coronary stenoses were dilated (mean 1.4 lesion/patient), 17 of these were in infarct-related vessels; 8 were total occlusions and 2 were located in saphenous vein grafts. Twenty-two procedures were completed by coronary stenting (17 elective). cTn-T and cTn-I were considered abnormal when serum levels were > 0.2 ng/ml and > 0.6 ng/ml, respectively. CK-MB mass was also determined in all patients (abnormal > 5 ng/ml). No patients had clinical or electrocardiographic evidence of myocardial infarction after the procedure. Overall, 16 patients (28%) developed biochemical evidence of post-procedural MMD (defined as the presence of at least one abnormal sample of any among the three markers tested). Four (7%) had abnormal CK-MB mass (at least one sample), 9 (16%) abnormal cTn-T, and 15 (26%) abnormal cTn-I. When CK-MB mass was elevated, both cardiac troponins were also elevated. In patients positive for MMD and abnormal CK-MB mass, peak cTn-I was significantly higher than in patients with normal CK-MB (3.02 +/- 1.07 vs 1.02 +/- 0.11 ng/ml; p = 0.009). The difference was not evident when comparing the same groups of patients for cTn-T (0.26 +/- 0.04 vs 0.18 +/- 0.10 ng/ml; p = 0.16). Also, peak cTn-I but not peak cTn-T had a positive correlation with peak CK-MB mass (r = 0.89; p < 0.0001 and r = 0.23; p = 0.40). The elevation of either marker of MMD was not related to clinical, angiographic or procedural variables. A possible interpretation for MMD was found in 2/3 of cases: bail-out (2); late occlusion (1); minor side branch occlusion (3); distal embolization from saphenous vein grafts (2) or total occlusions (2). In our series, MMD after PTCA occurs in 28% of cases and is unrelated to clinical, angiographic and procedural variables. Both cTn-T and cTn-I increase the sensitivity of CK-MB mass in the detection of MMD after PTCA, cTn-I being the most sensitive marker. In about 1/3 of cases, the presence of MMD remains unexplained. The prognostic implications of MMD are as yet undefined.