The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Determinants of operative mortality in reoperative coronary artery bypass grafting.
Previously suggested risk factors for operative mortality in reoperative coronary artery bypass grafting are contradictory. Therefore, we analyzed our data of 622 patients who underwent reoperative bypass grafting from January 1986 through June 1993. Among these patients, 258 had saphenous vein grafts alone and 364 had internal mammary artery grafting, including unilateral (342 patients) and bilateral (22 patients) mammary artery grafting with or without additional saphenous vein grafting. ⋯ The logistic regressions demonstrate that preoperative variables (low ejection fraction [p = 0.0002], old age [p = 0.003], female gender [p = 0.011], and history of arrhythmia [p = 0.023]), intraoperative variables (emergency operation [p = 0.0001] and long perfusion time [p = 0.0001]), and postoperative variables (complications) are independently associated with higher mortality. Unlike previously described results, aortic crossclamp time, route of cardioplegia, use of internal mammary artery, number of grafts, and year of operation are not associated with operative mortality. The identification of these risk factors may have important implications in further improvement of the results of reoperative coronary artery bypass grafting.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Adenosine triphosphate-sensitive K+ channels mediate postcardioplegia coronary hyperemia.
The purpose of the present study was to examine the role of adenosine triphosphate-sensitive potassium channels in mediating the coronary hyperemic response after crystalloid cardioplegia. Thirteen pigs were placed on normothermic cardiopulmonary bypass support. Hearts were arrested with cold (4 degrees C) crystalloid ([K+] 25 mmol/L) cardioplegic solution for 60 minutes. ⋯ The response to pinacidil was markedly inhibited by glibenclamide, which confirms these antagonistic effects on K+ adenosine triphosphate channels. Decreased tissue concentrations of adenosine triphosphate in the coronary arterial smooth muscle and myocardium were observed after cardioplegia and persisted for up to 60 minutes of reperfusion (both p < 0.05 versus control). These results suggest that coronary hyperemia associated with postischemic cardioplegia is mediated in part by activation of K+ adenosine triphosphate channels in the coronary microcirculation.
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J. Thorac. Cardiovasc. Surg. · Oct 1995
Constitutive nitric oxide release is impaired after ischemia and reperfusion.
Myocardial ischemia and reperfusion may result in endothelial dysfunction and reduced release of nitric oxide. With the use of an amperometric sensor, the first direct measurements of constitutive nitric oxide release from a beating heart were measured from the coronary effluent of isolated working rat hearts subjected to ischemia and reperfusion. Rats, six to eight per group, were randomly studied as follows: control (no pretreatment) and pretreatment with the nitric oxide donor L-arginine (3 mmol/L), its enantiomer D-arginine (3 mmol/L), nitric oxide inhibitor N omega-nitro-L-arginine methyl ester (100 mumol/L), and combined N omega-nitro-L-arginine methyl ester/L-arginine. ⋯ We conclude that after ischemia/reperfusion, endothelial dysfunction results in decreased nitric oxide release, which can be ameliorated with L-arginine pretreatment. The direct cytoprotective properties of nitric oxide may contribute to improved functional recovery in hearts pretreated with L-arginine. Augmentation of the L-arginine/nitric oxide pathway may provide a new approach for improved recovery after cardiovascular operations.