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J Thorac Cardiovasc Surg 2000;120:651-659
© 2000 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Biochemical assessment of myocardial injury after cardiac surgery: Effects of a platelet activating factor antagonist, bilateral internal thoracic artery grafts, and coronary endarterectomy

David P. Taggart, MD, FRCS

From Oxford Heart Centre, John Radcliffe Hospital, Oxford, United Kingdom.

Funded by British Biotech Pharmaceuticals Ltd, Watlington Rd, Oxford, OX4 5LY, United Kingdom.

Address for reprints: D. P. Taggart, MD, FRCS, Consultant Cardiothoracic Surgeon, Oxford Heart Centre, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom (E-mail: david.taggart{at}orh.anglox.nhs.uk).

Objective: Platelet activating factor antagonists reduce ischemia-reperfusion injury in experiments, but there is no supportive clinical evidence.
Methods: A single-center, double-blind, minimized, placebo-controlled, randomized trial of low-dose (10 mg) or high-dose (100 mg) platelet activating factor antagonist was conducted in 150 patients undergoing coronary artery bypass grafting. Myocardial injury was determined by serial measurements of the MB isoenzyme of creatine kinase and cardiac troponin T. The effects of single or bilateral internal thoracic artery grafting and coronary endarterectomy on myocardial injury were also assessed.
Results: The placebo and platelet activating factor antagonist groups were similar with respect to preoperative, intraoperative, and postoperative factors. Four patients (2.7%) died before discharge, 3 from cardiac events. Thirteen patients (9%) had biochemical evidence of myocardial infarction, of whom 3 died. Stepwise multiple regression analysis demonstrated that duration of cardiopulmonary bypass was the most important determinant of elevations in creatine kinase MB isoenzyme and cardiac troponin T up to 6 hours after the operation and that the use of a platelet activating factor antagonist and the number of internal thoracic artery grafts did not influence myocardial injury at any time. Endarterectomy was performed in 11 patients (7%), of whom 6 (55%) had biochemically defined myocardial infarction and of whom 1 died (9%). Endarterectomy was the most important determinant of elevated levels of creatine kinase MB isoenzyme and cardiac troponin T 24 and 48 hours after the operation.
Conclusion: Platelet activating factor antagonists do not reduce perioperative myocardial injury. Bilateral and single internal thoracic artery grafting results in similar levels of myocardial injury, whereas endarterectomy is frequently associated with biochemical evidence of myocardial injury.




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