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Ann Thorac Surg 2000;70:2087-2090
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

Cardiac troponin I release after open heart surgery: a marker of myocardial protection?

^a Service de Chirurgie Thoracique et Cardiovasculaire, Service de Biochimie, CNRS UPRES A 7054, Association Claude Bernard, Hôpital Henri Mondor, Créteil, France

Accepted for publication May 8, 2000.

Address reprint requests to Dr Vermès, Service de Chirurgie Thoracique et Cardiovasculaire, Hôpital Henri Mondor, 51, avenue du Maréchal De Lattre de Tassigny, 94010 Créteil, France
e-mail: loisance{at}univ-paris12.fr

Background. Unlike creatine kinase MB isoenzyme, cardiac troponin I (cTnI) is a highly specific marker of myocardial injury. Its release has recently been studied after coronary artery bypass grafting operation. However, its significance after open heart surgery (OHS) remains to be determined. This protein release could be a marker of myocardial protection. We sought to study cTnI release after OHS in patients with normal coronary arteries and to compare it with cTnI release in patients after coronary artery bypass graft (CABG) surgery.

Methods. Eighty-five patients undergoing OHS and 86 patients undergoing CABG were enrolled in the study. CTnI concentrations were measured in serial venous blood samples drawn before surgery and immediately, 12 hours, 24 hours, 48 hours, and 5 days after aortic unclamping.

Results. In the OHS group and in the CABG group without acute myocardial infarction (AMI), cTnI peaked at 12 hours postoperatively (6.35 ± 6.5 and 5.38 ± 8.55 ng/mL, respectively) and normalized on day 5 postoperatively (0.57 ± 2 and 0.72 ± 1.62 ng/mL, respectively). CTnI concentration did not differ significantly between the OHS group and the CABG group in the absence of AMI for any samples considered. In the CABG group, 2 patients had AMI. In the OHS group, cTnI levels at 12 hours postoperatively were found to correlate closely with CPB and aortic cross-clamping (ACC) times, contrary to the CABG group, which correlated only with occurrence of AMI. CTnI release was independent of age and ejection fraction in either group.

Conclusions. cTnI release in patients after OHS with normal coronary arteries has the same profile as cTnI release in patients after CABG in the absence of AMI. However, its peak at 12 hours postoperatively is only correlated to ACC and CPB times, which is contrary to cTnI release after CABG surgery. This observation suggests that cTnI could be a marker of myocardial ischemia after OHS.

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