Troponin T is a unique cardiac antigen which is continuously released from infarcting myocardium. Its cardiospecificity as a marker protein might be particularly useful in assessing myocardial cell damage in patients undergoing cardiac surgery. Therefore, circulating troponin T was measured in serial blood samples from 56 patients undergoing cardiac surgery and in two control groups--22 patients undergoing minor orthopaedic surgery and 12 patients undergoing lung surgery by median sternotomy. In both control groups no troponin T could be detected, whereas activities of creatine kinase were raised in all 12 lung surgery controls and activities of the MB isoenzyme were raised in five of the 12 patients in the lung surgery group and in four of the 22 patients in the orthopaedic surgery group, respectively. All the patients undergoing coronary artery bypass grafting (n = 47) and cardiac surgery for other reasons (n = 9) had detectable concentrations of troponin T. Five patients had perioperative myocardial infarction detected as new Q waves and R wave reductions. In these five patients troponin T release persisted and serum concentrations (5.5-23 micrograms/l) reached a peak on the fourth postoperative day. In the 51 patients without perioperative myocardial infarction serum concentrations and the release kinetics of troponin T depended on the duration of cardiac arrest. In patients in whom aortic cross clamping was short troponin T increased slightly on the first postoperative days; in patients with longer periods of aortic cross clamping troponin T concentrations were higher and remained so beyond the fifth postoperative day. In patients with non-specific changes on the electrocardiogram troponin T concentrations were significantly higher on days 1 and 4 after operation than in patients with normal postoperative electrocardiograms(11.2 (5) and 4.5 (2.6) v 8.2 (3.4) and 2.9 (1.6) 1microg/l). Serum concentrations of troponin T showed some myocardial cell damage in every patient undergoing cardiac surgery. The persistent increases that were more common in patients with longer periods of cardiac arrest must have been caused by damage to the contractile apparatus. These results suggest that perioperative myocardial cell necrosis may be more common than indicated by changes of the QRS complex on the electrocardiogram.