Left ventricular assist device (LVAD) support has offered many individuals with end-stage heart failure an improved quality of life and enhanced survival. Prolonged mechanical assistance, however, has shown the potential to induce hemodynamic and structural changes in the native heart. One such dismal drawback is the development of de novo aortic valve lesions leading to aortic insufficiency (AI). Significant AI can lead to ineffective LVAD output and end-organ malperfusion, and may hamper the success of recovery attempts. If AI at the time of LVAD implantation can be proactively managed by replacement or closure of the aortic valve, later development of aortic valve dysfunction may pose a difficult management issue.A 53-year-old male patient (height, 190 cm; weight, 90 kg) with end-stage dilated cardiomyopathy was uneventfully implanted with a Thoratec HeartMate II LVAD (Thoratec Corporation, Pleasanton, California) intended as a bridge to transplantation. Ten months postoperatively, he showed progressively worsening AI requiring hospital readmissions for increased exercise intolerance, desaturation, and arrhythmias. In view of the unfavorable anthropometric characteristics, any attempt to anticipate transplantation was unsuccessful for lack of appropriate donors. Ineffective LVAD output, pulmonary edema with desaturation, and arrhythmias ultimately required endotracheal intubation and cardiopulmonary resuscitation. Since neither optimal medical therapy nor LVAD adjustments provided hemodynamic stability, the heart team decided for emergency life-saving aortic valve implantation (Fig. 1, Online Video 1). Transcatheter aortic valve implantation was undertaken with a percutaneous approach through the right femoral artery. Through an 18-F introducer, an extra-stiff guidewire was positioned in the left ventricle, and a 29-mm CoreValve (Medtronic, Milwaukee, Wisconsin) was implanted under fluoroscopy and echo control. Due to a moderate periprosthetic regurgitation (Fig. 2, Online Video 2), a second 29-mm CoreValve was deployed within the previous valve prosthesis From the
Extracorporeal life support (ECLS) to manage acute antiarrhythmic drugs toxicity in neonates has never been reported. Here presented is a case of venoarterial extracorporeal membrane oxygenation support in a newborn with refractory low cardiac output as a result of acute Ca-channel and β-receptor antagonist toxicity for treatment of paroxysmal supraventricular tachycardia (SVT). Shortly after onset of ECLS, the baby recovered sinus rhythm and subsequent bouts of SVT were controlled by amiodarone infusion and repeated DC shocks. Weaning was possible on the 5th day after implant, once recovery of the left ventricular function and optimization of the antiarrhythmic medication were achieved. In neonates with severe but potentially reversible cardiac dysfunction caused by drug toxicity, ECLS can maintain cardiac output and vital organ perfusion while allowing time for drug redistribution, metabolism, and clearance.
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