The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Randomized Controlled Trial Clinical TrialPrevention of bleeding after cardiopulmonary bypass with high-dose tranexamic acid. Double-blind, randomized clinical trial.
This prospective, double-blind, randomized trial assessed the effectiveness of high-dose tranexamic acid given in the preoperative period on blood loss in patients undergoing cardiopulmonary bypass. One hundred fifty patients scheduled to undergo cardiac operations with cardiopulmonary bypass were randomized into three groups of equal size. The first group received 10 gm of tranexamic acid intravenously over 20 minutes before sternotomy and a placebo infusion over 5 hours. ⋯ Continued tranexamic acid infusion (10 gm over 5 hours) did not reduce bleeding further. There was no difference in the coagulation profile before operation between patients with and without excessive bleeding. However, coagulation tests done in the postoperative period indicated ongoing fibrinolysis and platelet dysfunction in patients with excessive bleeding.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Randomized Controlled Trial Clinical TrialHemostatic function of aspirin-treated platelets vulnerable to cardiopulmonary bypass. Altered shear-induced pathway.
The impaired hemostasis of aspirin-treated patients is an annoying problem during and after cardiopulmonary bypass. The hemostatic function of platelets comprises two mechanisms: the shear-induced and the cyclooxygenase pathways. Because the latter is inhibited in aspirin-treated patients, the hemostatic function depends mainly on the former pathway. ⋯ The inhibitory effects of aspirin on thromboxane production and on collagen-induced platelet aggregation remained throughout the operation. In aspirin-treated platelets, the aggregation capacity induced by adenosine diphosphate was inhibited before the operation (p < 0.05) and showed substantial recovery during the operation (p < 0.05). These results suggest that the shear-induced pathway of aspirin-treated platelets is more vulnerable to cardiopulmonary bypass than the pathway in normal platelets and causes severe impairment of hemostasis afterward.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Clinical TrialExtracorporeal membrane oxygenation as an adjunct treatment for primary graft failure in adult lung transplant recipients.
Primary graft failure is a catastrophic event in lung transplantation. Failure is characterized by profound abnormalities of gas exchange that are frequently unresponsive to alterations in mechanical ventilation. This condition can be fatal and, if less severe, is usually associated with significant permanent damage to the allograft. ⋯ In comparison, there were no survivors among six recipients placed on extracorporeal membrane oxygenation for late (> or = 7 days) graft dysfunction. Extracorporeal membrane oxygenation is a lifesaving adjunct in recipients with acute graft failure after lung transplantation. Ischemia-reperfusion injury and acute graft dysfunction after lung transplantation can be successfully reversed with early aggressive intervention.
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Comparative StudyComparative results with the St. Jude Medical and Medtronic Hall mechanical valves.
This study compared the clinical performance of the St. Jude Medical and Medtronic Hall mechanical valves in isolated aortic or mitral valve replacement. From 1984 to 1993, 349 St. ⋯ The 5-year actuarial estimate of freedom from reoperation therefore for aortic valve replacement was 99% +/- 1% with the St. Jude Medical valve and 96% +/- 2% with the Medtronic Hall valve (p = 0.09) and for mitral valve replacement was 98% +/- 2% with the St. Jude Medical valve and 95% +/- 3% with the Medtronic Hall valve (p = 0.40).(ABSTRACT TRUNCATED AT 400 WORDS)
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J. Thorac. Cardiovasc. Surg. · Sep 1995
Desensitization of myocardial beta-adrenergic receptors and deterioration of left ventricular function after brain death.
Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. ⋯ Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.