Release of creatine kinase, troponin-T, and tissue plasminogen activator in arterial and coronary venous blood during coronary artery bypass surgery

Abstract

Tissue plasminogen activator (t-PA) as a possible marker of endothelial injury during elective coronary artery bypass surgery was studied. T-PA antigen and activity were measured in arterial and coronary venous plasma in 14 patients, and compared to the markers of myocyte injury creatine kinase (CK-MB) and troponin-T (TnT). Cardiopulmonary bypass (CPB) lasted 86 (55–107) min, and aortic cross-clamping (cold, crystalloid cardioplegia) lasted 41 (25–62) min (median (central 90% percentile)). Blood flow in the great cardiac vein was measured by retrograde thermodilution, and increased from 49 (27–90) m1/min before CPB to a maximum of 92 (55–125) ml/min 40 min after declamping (not significant). CK-MB, TnT, and t-PA antigen and activity all increased during CPB, and were significantly higher in coronary sinus than arterial plasma after declamping the aorta. Net cardiac release ([coronary sinus—arterial concentration] x coronary flow) of TnT increased after the aorta was declamped, and was higher in the seven patients with the longest cross-clamping time than in the seven with the shortest time (p<0.01). Cardiac release of CK-MB and t-PA antigen also increased after declamping, but with no significant difference between long and short cross-clamp times. t-PA activity, however, increased more in the patients with the longest cross-clamp times (p<0.008). In conclusion, CK-MB, TnT and t-PA were released from the postcardioplegic heart. Release of t-PA indicates that postcardioplegic coronary endothelial activation or injury occurred. t-PA activity as well as TnT increased more in patients with long times of cross-clamping, indicating that t-PA activity may be a possible marker of postcardioplegic endothelial injury or activation.

Key Words:

• Cardioplegia
• endothelial injury
• myocardial injury
• tissue plasminogen activator
• troponin-T