International heart journal
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Randomized Controlled Trial
Effect of ischemic postconditioning in correction of tetralogy of Fallot.
Inappropriate myocardial protection is considered one of the main causes of mortality and morbidity in the correction of tetralogy of Fallot (TOF). Results of previous reports about the effects of ischemic postconditioning on myocardial protection in animals and humans are very encouraging. This randomized and controlled trial aimed to assess the effect of ischemic postconditioning on protection against myocardial ischemia reperfusion injury in TOF patients receiving cardioplegia. ⋯ As a result, ischemic postconditioning reduced postoperative peak release by 45% for cTnI compared with the control group (0.43 ± 0.18 ng/mL versus 0.78 ± 0.15 ng/mL, P < 0.0001). Ischemic postconditioned patients had a lower peak inotropic score during the first postoperative 24 hours (5.6 ± 2.2 µg/kg/minute versus 8.6 ± 3.6 µg/kg/minute, P < 0.0001), extubation time (21.5 ± 7.3 hours versus 30.2 ± 12.4 hours, P = 0.0002) and length of ICU stay (43.4 ± 12.6 hours versus 56.3 ± 17.8 hours, P = 0.0003), while they had a higher cardiac output on the first postoperative day (1.41 ± 0.26 L/minute versus 1.28 ± 0.25 L/minute, P = 0.0255) as compared to the control group. In conclusion, ischemic postconditioning may to some extent provide myocardial protection in children undergoing correction of tetralogy of Fallot.
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Nemaline myopathy is a representative form of congenital myopathy, and is characterized by nemaline bodies in muscle fibers. Here we report a 47-year-old man with congenital nemaline myopathy complicated with dilated cardiomyopathy-related heart failure, and restrictive respiratory failure. ⋯ The patient responded to the combination of conventional therapy for heart failure including β-blocker and noninvasive continuous positive-pressure ventilation for respiratory failure. His general condition has been stable during a 10-month follow up period.
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The right ventricular outflow tract (RVOT) is considered the arrhythmogenic region that gives rise to Brugada syndrome. To obtain a better understanding of this substrate, we performed electroanatomic mapping of the right ventricle (RV) in patients with Brugada syndrome. ⋯ The low voltage zone area (< 1.5 mV) was larger (16.1% versus 7.8%, P < 0.01) and the bipolar electrogram duration was greater (81.6 ± 7.8 ms versus 53.4 ± 5.6 ms, P < 0.01) in the patients with Brugada syndrome versus the control patients; the bipolar electrogram duration was greater in the septal portion and free wall of the RVOT. Our data suggest that regional endocardial conduction slowing based on structural abnormalities exists at the RVOT in Brugada syndrome.
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High mobility group box 1 (HMGB1), which has properties similar to those of proinflammatory cytokines, is released from activated immune cells and necrotic cells. It is known that cardiopulmonary bypass (CPB) induces systemic inflammation and aortic cross-clamping induces myocardial ischemia. This study was conducted to clarify whether HMGB1 is released in CPB-supported cardiac surgery in comparison to off-pump coronary artery bypass grafting (OPCAB) where CPB is not used. ⋯ IL-6 and IL-10 increased after aortic declamping in the CPB group and after coronary revascularizations in the OPCAB group. Based on these results, we conclude that the major factor involved in the increase in HMGB1 level might be myocardial ischemia/reperfusion during cardiac surgery. Activation of immune cells, altered tissue perfusion, and pulmonary ischemia and reperfusion could be additional factors that increase the HMGB1 level in CPB-supported cardiac surgery.