Circulation
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Acute occlusion after balloon coronary angioplasty is associated with an increased risk of angina, emergency coronary artery bypass grafting (CABG), myocardial infarction (MI), and death. Stents offer a way of restoring patency and avoiding these complications. ⋯ Coronary artery stenting for acute closure after PTCA relieves myocardial ischemia and provides an alternate means of treatment. This series includes early learning curve experience; 70% (67 of 96) of patients were spared emergency coronary artery bypass graft surgery when this adverse outcome occurred. Certain clinical and angiographic subsets are at increased risk for restenosis and future cardiac events.
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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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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.
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Randomized Controlled Trial Comparative Study Clinical Trial
Cyclosporine-induced hypertension. Efficacy of omega-3 fatty acids in patients after cardiac transplantation.
Cyclosporine-induced hypertension may be related to vasoconstriction of the afferent arterioles in the glomeruli caused by changes in the prostaglandin profile. omega-3 Fatty acids have demonstrated vasodilatory properties related to a favorable effect in the prostaglandin profile. The purpose of this study was to evaluate the antihypertensive effects of oral supplementation with omega-3 fatty acids in cyclosporine-treated cardiac transplant recipients. ⋯ omega-3 Fatty acids (3 g/d) reduce blood pressure by decreasing systemic vascular resistance and, therefore, can be used as an adjuvant for the treatment of hypertension in cyclosporine-treated cardiac transplant recipients. Their vasodilatory effect may be related to a beneficial change in the prostaglandin profile.
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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.