Perioperative myocardial cell damage assessed by immunoradiometric assay of beta-myosin heavy chain serum levels in patients undergoing coronary bypass surgery.

In order to investigate myocardial cell damage in patients undergoing coronary bypass surgery, serum levels of cardiac myosin fragments, using monoclonal antibodies to myosin beta heavy chains, were measured in serial blood samples of 85 patients, 79 male and 6 female, 43-66 years old, after a total of 86 internal mammary artery and 137 saphenous vein graft implants. Eight patients had perioperative acute myocardial infarction (MI), detected by abnormal Q waves and a rise of CK-MB levels. After surgery, beta-myosin levels increased from post-operative day 3 and reached peak values on day 5 in patients without and in day 7 in patients with perioperative MI, in these 8 patients, myosin peak levels were greater as compared to 77 patients without perioperative MI (3452 +/- 1596 vs. 761 +/- 494; P < 0.01). There was a correlation between myosin peak levels and creatine kinase (CK) (r = 0.71; P < 0.05) and CK-MB peak levels (r = 0.74; P < 0.05) only in the patients with perioperative MI, but not in the patients without MI. There was no correlation between myosin peak levels and the times of aortic cross clamping or cardiopulmonary bypass. Peak myosin levels over 75% confidence limits of the mean were found in 23 patients; post-operative low output syndrome occurred in 10 of these 23 patients and in 7 out of 62 patients with peak myosin levels within 75% of the mean (P < 0.005). The increase in beta-myosin heavy chain serum levels observed in almost all patients undergoing coronary surgery suggests lesser perioperative damage of the contractile apparatus, which could be detected by the usual enzyme and ECG criteria. The higher prevalence of low output syndrome in patients with higher increases in myosin levels suggests more pronounced damage to the contractile apparatus in these patients. The higher myosin levels clearly indicate the presence of perioperative MI.