Circulation
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Systolic anterior motion of the mitral valve causing left ventricular outflow tract obstruction occurs in 1% to 2% of patients having mitral valve repair, in some cases requiring further surgery to relieve the obstruction, but the mechanism and the geometry involved are not certain. ⋯ After mitral repair, left ventricular outflow tract obstruction occurs when the mitral coaptation line is displaced anteriorly. When systolic anterior motion occurs, reduction of the amount of annuloplasty or use of the posterior leaflet sliding procedure may eliminate this problem. Understanding the geometry of this phenomenon may facilitate preoperative echo selection of high-risk patients (those with large redundant posterior leaflets and relatively normal ventricular size) and modification of surgical technique to avoid the problem of outflow tract obstruction after mitral valve repair.
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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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Comparative Study
Comparison of phasic blood flow velocity characteristics of arterial and venous coronary artery bypass conduits.
Coronary artery bypass conduits derived from internal mammary arteries show relative resistance to atherosclerosis and significantly improved long-term patency compared with saphenous vein grafts. Atherothrombotic occlusion of venous conduits has previously been correlated with lower flow rates measured intraoperatively. To quantitate coronary bypass conduit flow velocity, we examined the phasic blood flow velocity patterns by intravascular Doppler spectral analysis in patients during cardiac catheterization to test the hypothesis that resting systolic and diastolic phasic blood flow velocity patterns differ significantly between arterial and venous bypass conduits. ⋯ Patterns of resting phasic blood flow, as well as mean velocity and total velocity integral, differ significantly between internal mammary artery and saphenous vein bypass conduits. These differences may have implications regarding blood-vessel wall interactions, the development of degenerative graft disease, and long-term conduit patency.
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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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Metabolic interventions capable of preventing ventricular dysfunction "stunning" or accelerating its functional recovery have potential clinical importance. Myocardial protection of the stunned myocardium has not been documented when drugs were administered only during postischemic reperfusion. The role of ATP depletion and release of purines in myocardial injury was assessed using the selective nucleoside transport blocker p-nitrobenzylthioinosine (NBMPR) in a combination with specific adenosine deaminase inhibitor erythro-9-[hydroxy-3-nonyl]adenine (EHNA) administered during reperfusion after reversible ischemic injury. ⋯ Selective entrapment of adenine nucleosides during postischemic reperfusion attenuated ventricular dysfunction (stunning) after brief global ischemia. It is concluded that nucleoside transport plays an important role in myocardial stunning, and its blockade augmented myocardial protection against reperfusion injury. Selective entrapment of endogenous inosine, generated during ischemia, represents an attractive therapeutic approach to the alleviation of postischemic dysfunction mediated by reperfusion in a wide spectrum of ischemic syndromes, including percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery.