Circulation
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Coronary bypass surgery in women is associated with lower survival than in men. We need to know whether this is because of patient-related factors and whether the lower survival is present in all subgroups of patients and for all time periods during which the surgery was performed. ⋯ Women have a higher operative mortality and lower long-term survival than men after coronary bypass surgery for angina. However, the differences are small, even if statistically significant. Importantly, patient-related factors and not sex are independent predictors of poorer survival. Therefore, coronary bypass surgery should not be delayed or denied to women who have the usual indications for surgery.
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Left ventricular outflow tract obstruction (LVOTO) occurs in 4% to 5% of patients after prosthetic ring mitral valve repair. Major anatomic factors incriminated in the genesis of LVOTO include degenerative mitral valve insufficiency with excess leaflet tissue, nondilated left ventricular cavity, and narrow mitro-aortic angle. We have previously reported a 14% incidence of LVOTO after prosthetic ring mitral valve repair in this high-risk group of patients. Serial echo Doppler studies demonstrated an overlapping and/or inversion of the left ventricular functional compartments generating systolic anterior motion of the posterior leaflet and paradoxical opening (eversion) of the anterior leaflet. In an attempt to eliminate LVOTO after mitral valve repair, a new surgical procedure was developed in 1988 by Carpentier: the sliding leaflet technique, which reduces the height of the posterior leaflet. The purpose of this study was to analyze the results of the new technique in terms of the occurrence of LVOTO: ⋯ This study was not done on a concomitant series of patients but on patients with the same type of pathology. It demonstrates that (1) the sliding leaflet technique eliminates significant LVOTO in the high-risk patients; (2) the sliding leaflet technique is associated with a low mortality; and (3) no reoperations for mitral insufficiency were required in this series.
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Randomized Controlled Trial Comparative Study Clinical Trial
Nafamostat mesilate reduces blood loss during open heart surgery.
Nafamostat mesilate (FUT-175) is a protease inhibitor inactivating coagulation, fibrinolysis, and platelet aggregation. A prospective, randomized trial was performed to assess the efficacy of FUT-175 in the reduction of postoperative bleeding tendency. ⋯ FUT-175 inhibits fibrinolysis and preserves platelet counts and function during CPB and reduces blood loss during open heart surgery.
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Heparin rebound, the reappearance of anticoagulant activity after adequate neutralization with protamine, can lead to excessive postoperative bleeding after cardiac surgery. We investigated the mechanism of heparin rebound by using chemically modified heparin that lacks anticoagulant activity (low-affinity heparin) but that is able to displace protein-bound anticoagulantly active heparin. ⋯ Our findings demonstrate that heparin anticoagulant activity persists for up to 6 hours after surgery despite apparent protamine neutralization. The observation of the marked increase in plasma anti-factor Xa activity after the addition of low-affinity heparin suggests that after its administration, a large proportion of the heparin binds to plasma proteins and is incompletely removed by protamine. After protamine is cleared, the protein-bound heparin dissociates slowly and binds to anti-thrombin III to produce an anticoagulant effect.
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Mounting evidence suggests a protective effect of exogenous adenosine in myocardial ischemia and reperfusion. We tested the hypothesis that augmentation of endogenous adenosine levels, achieved by inhibiting adenosine catabolism and washout, is beneficial in postischemic myocardial dysfunction ("stunning"). ⋯ This study demonstrates that (1) administration of an adenosine deaminase inhibitor plus a nucleoside transport blocker is remarkably effective in augmenting myocardial adenosine levels during regional ischemia and subsequent reperfusion in vivo, (2) this augmentation of adenosine results in a significant and sustained attenuation of myocardial stunning, and (3) the attenuation of stunning is not due to ATP repletion or to nonspecific actions on hemodynamic variables or coronary flow. These findings suggest that endogenous adenosine production during ischemia serves as an important pathophysiological mechanism that protects against myocardial stunning. The results also suggest that augmentation of endogenous adenosine (without exogenous adenosine administration) represents an effective therapeutic approach to the alleviation of reversible postischemic dysfunction.