Circulation
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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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Randomized Controlled Trial Comparative Study Clinical Trial
Comparison of cold versus warm cardioplegia. Crystalloid antegrade or retrograde blood?
To evaluate the efficacy of warm versus cold and antegrade versus retrograde cardioplegia, 163 patients were randomized in sequence in three groups and underwent isolated coronary artery bypasses (mean, 4 grafts/patients) alternating in sequence. ⋯ Continuous warm cardioplegia (group 2) did not provide better myocardial protection despite that no CK-MB isoenzyme leak was demonstrated intraoperatively. Intermittent cold crystalloid cardioplegia and cold retrograde provided a clearer operative field and motionless heart. As long as O2 was adequately supplied, under 90 minutes' cross-clamp time, cold crystalloid cardioplegia and cold retrograde blood cardioplegia is safe under hypothermic conditions, whereas warm cardioplegia requires continuous uninterrupted technique with oxygen delivery.
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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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Multicenter Study
Management of patients with intramural hematoma of the thoracic aorta.
Intramural hematoma of the thoracic aorta (IMH) is a diagnosis of exclusion and represents spontaneous, localized hemorrhage into the wall of the thoracic aorta in the absence of bona fide aortic dissection, intimal tear, or penetrating atherosclerotic ulcer. This process may arise from primary vasa vasorum hemorrhage within the aortic media or rupture of an atherosclerotic plaque. The clinical presentation of patients with IMH mimics that of acute aortic dissection; moreover, considerable diagnostic confusion exists despite the use of many different imaging modalities. The optimal mode of management of patients with IMH (medical versus medical plus surgical) remains problematic because of the paucity of information available. ⋯ IMH is a distinct pathological entity, should not be confused with aortic dissection, and probably will be identified more frequently in the future. All patients with IMH should be monitored carefully and treated with aggressive antihypertensive therapy. Frequent serial assessment is necessary using TEE or MRI/CT scans. Based on this small experience, patients with ascending/arch IMH, ongoing pain, or IMH expansion should probably undergo early graft replacement. Patients with IMH involving the descending thoracic aorta who have no evidence of progression and become pain free can probably be treated conservatively but require antihypertensive therapy and serial aortic imaging surveillance indefinitely.
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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.