The Annals of thoracic surgery
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A growing body of evidence relates the release during cardiopulmonary bypass (CPB) of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, to the postoperative systemic inflammatory response syndrome. Antiinflammatory cytokines, such as IL-10, however, may also play an important role in limiting these complications. ⋯ The improved knowledge of cytokine responses to CPB may help to develop interventions aimed at reducing postoperative morbidity and mortality.
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Randomized Controlled Trial Comparative Study Clinical Trial
Attenuation of changes in leukocyte surface markers and complement activation with heparin-coated cardiopulmonary bypass.
The inflammatory response induced by cardiopulmonary bypass can result in severe organ dysfunction in some patients. This postperfusion response is caused mainly by contact between blood and the foreign surface of the cardiopulmonary bypass equipment and includes adhesion of leukocytes to vascular endothelium, which precedes a series of events that mediate inflammatory damage to tissues. ⋯ We conclude that heparin coating reduces complement activation and attenuates the leukocyte integrin and selectin response that occurs when uncoated circuits are used.
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Case Reports
Anomalous papillary muscle as a cause of left ventricular outflow tract obstruction in an adult.
Left ventricular outflow tract obstruction may be caused by abnormalities of the various structures comprised by the outflow tract. Hypertrophic cardiomyopathy is one of the more common causes, but many are rare anomalies, a collection of which we have compiled. We present a case of left ventricular outflow tract obstruction mimicking aortic stenosis in an adult. This was found to be due to abnormal insertion of a hypertrophied papillary muscle, successfully corrected by mitral valve replacement.
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Randomized Controlled Trial Comparative Study Clinical Trial
Preoperative platelet dysfunction increases the benefit of aprotinin in cardiopulmonary bypass.
This study was designed to determine the benefit of aprotinin therapy in reducing bleeding during and after cardiopulmonary bypass in patients with preoperative platelet dysfunction. Platelet function involvement in the mechanism by which aprotinin acts was also investigated. ⋯ The mechanism by which aprotinin reduced bleeding was independent of any effect on platelet function. However, aprotinin produced a greater reduction in bleeding among patients whose condition was hemostatically compromised by preoperative platelet dysfunction.