Right ventricular failure after left ventricular assist device placement is the major concern on weaning from cardiopulmonary bypass and it is one of the most serious complications in the postoperative period. This complication has a poor prognosis and is generally unpredictable. The identification of pre-operative risk factor for this serious complication is incomplete yet. In order to determine pre-operative risk for severe right ventricular failure after left ventricular assist device support we analyzed preoperative hemodynamics, laboratory data and characteristics of 48 patients who received Novacor (World Heart Corp., Ottawa, ON, Canada). We compared the data from the patients who developed right ventricular failure and the patients who did not. Right ventricular failure occurred in 16% of the patients. There was no significant difference between the groups in demographic characteristics. We identified as preoperative risk factors the pre-operative low mean pulmonary artery and the impairment of hepatic and renal function on laboratory data. Our results confirm in part the findings of the few previous studies. This information may be useful for the patient selection for isolated left ventricular assist device implantation, but other studies are necessary before establishing criteria for patient selection for univentricular support universally accepted.
The findings confirm that plateau waves are caused by vasodilation and show that indomethacin, by constricting the cerebral arteries, is effective in extinguishing plateau waves, ultimately restoring cerebral perfusion and oxygenation.
Brugada syndrome is characterized by a distinctive electrocardiographic pattern (right bundle branch block and ST segment elevation in precordial leads) and a high risk of cardiac arrest for malignant dysrhythmia. The genetic basis is a molecular defect of the cardiac sodium channel and the pattern of inheritance is autosomal dominant. Many factors during general anesthesia (medications, bradycardia, temperature changes) could precipitate malignant dysrhythmia in these patients. Because criteria to identify the surgical patient at high risk for developing malignant dysrhythmia are lacking, we can only speculate about the available studies on nonsurgical patients. We describe four patients during general anesthesia and propose intraoperative and postoperative monitoring (the first 36 h).
The aim of the study was to examine the cardioprotective effect of morphine and Delta 2 opioid D-Ala2-Leu5 enkephalin(DADLE) administered, at early reoxygenation, in isolated human myocardium exposed to hypoxia–reoxygenation. Then,we tested the involvement of mitochondrial permeability transition pore in morphine and DADLE-induced postconditioning.Human right atrial trabeculae were obtained during cardiac surgery (coronary artery bypass and aortic valve replacement).Isometrically contracting isolated human right atrial trabeculae were exposed to 30-min hypoxia and 60-min reoxygenation(control group). In treatment groups, morphine 0.5 mmol, DADLE 10 nmol, DADLE 50 nmol and DADLE 100 nmol were administered during the first 15 min of reoxygenation. In two additional groups, morphine and DADLE 100 nmol were administered in the presence of atractyloside 50 mmol, the mitochondrial permeability transition pore opener. The force of contraction at the end of 60-min reoxygenation period (FoC60 expressed as % of baseline) was compared (mean+standard deviation) between the groups by an analysis of variance. Morphine (FoC60: 81+9% of baseline), DADLE50 nmol (FoC60: 76+11% of baseline) and DADLE 100 nmol (FoC60: 81+4% of baseline) increased significantly (P,0.001) the FoC60 as compared with the control group (FoC60: 53+3% of baseline). DADLE 10 nmol did not modify the FoC60 (50+9% of baseline; P ¼ 0.60 versus control group). The enhanced recovery of FoC60 induced by morphine and DADLE 100 nmol were abolished in the presence of atractyloside (FoC60: respectively 57+6% and 44+7% of baseline;P, 0.001). In conclusion, the administration of morphine and DADLE, in early reoxygenation period, protected human myocardium, in vitro, against hypoxia–reoxygenation injury, at least in part, by the inhibition of mitochondrial permeability transition pore opening.
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