Use of cardiac troponin I to diagnose perioperative myocardial infarction in coronary artery bypass grafting

Abstract

Abstract Cardiac troponin I (cTnI) is a regulatory protein unique to myocardium. We used a cardiospecific 30-min ELISA to measure cTnI in EDTA-plasma samples serially drawn from 28 patients before and after coronary artery bypass grafting (CABG)--26 elective and 2 salvage cases. The cTnI increase in 22 of the elective CABG patients, who did not have perioperative myocardial infarction (not-PMI), reflected the inevitable myocardial damage caused by cannulation and cardioplegic arrest, with peak values of 1.7 +/- 1.0 microgram/L (mean + 2 SD = 3.7 micrograms/L), the peaks occurring on average 8 h (range 4-24) after aortic unclamping. Two of the 22 not-PMI, elective CABG patients showed cTnI peaks > 3.0 micrograms/L (3.9 and 3.4 micrograms/L), indicating more extensive perioperative myocardial damage than the other 20, as confirmed by clinical and electrocardiographic or echocardiographic signs, although creatine kinase isoenzyme MB (CKMB) activity was below our PMI decision limit of 20 U/L (25 degrees C). As classified by electrocardiography, echocardiography, and increased CKMB activity, four of the 26 elective CABG patients did have a PMI. One patient with Q-wave PMI had peak cTnI approximately 30 micrograms/L, and three with non-Q-wave PMI had lower peak values (approximately 5 micrograms/L). The two salvage CABG cases had increased cTnI before surgery. One developed a Q-wave acute myocardial infarction with a 3-h cTnI peak of approximately 35 micrograms/L. We conclude that, after elective CABG, cTnI peaks > 3.7 micrograms/L and concentrations > 3.1 micrograms/L at 12 h or 2.5 micrograms/L at 24 h indicate PMI with high probability.