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Ann Thorac Surg 2007;83:1863-1864
© 2007 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Lankenau Hospital, Wynnewood, Pennsylvania
b Department of Medicine, Division of Cardiology, Section of Interventional Cardiology, Lankenau Hospital, Wynnewood, Pennsylvania
c Department of Medicine, Division of Cardiology, Section of Electrophysiology, Lankenau Hospital, Wynnewood, Pennsylvania
d Department of Cardiothoracic Surgery, Bryn Mawr Hospital, Bryn Mawr, Pennsylvania
Accepted for publication November 20, 2006.
* Address correspondence to Dr Samuels, The Lankenau Medical Center, Medical Science Bldg, Suite 280, 100 Lancaster Ave, Wynnewood, PA 19096 (Email: samuelsle{at}aol.com).
| Dr Samuels discloses that he has a financial relationship with Abiomed Inc.
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The AB5000 Ventricular Assist Device (VAD) (Abiomed Inc, Danvers, MA) is a paracorporeal system introduced as an upgrade to the BVS5000 unit (Abiomed) [1]. The Food and Drug Administration approved indication for use of the AB5000 VAD in any type of acute cardiogenic shock that is potentially reversible. Among the most common reasons for its use has been cardiogenic shock after acute myocardial infarction or after coronary artery bypass grafting. The goal is myocardial recovery with eventual VAD explantation. However, among the reasons for recovery failure is persistent myocardial dysfunction or intractable arrhythmia associated with VAD dependence, or both. The purpose of this report is to describe the role of percutaneous coronary intervention and arrhythmia ablative therapy as adjuncts to VAD support resulting in successful myocardial recovery.
A 66-year-old man presented to the emergency department with progressive shortness of breath. A pulmonary evaluation showed diffuse pulmonary infiltrates on chest roentgenogram and a positive influenza A titer on serology. After admission, the patient had substernal chest pain develop and was found to have suffered a myocardial infarction. Cardiac catheterization showed severe coronary artery disease with left main involvement. Several days later he underwent coronary artery bypass grafting. The initial postoperative period was unremarkable with no perioperative arrhythmia. After transfer to the step down unit, the patient suffered an acute ventricular tachycardia with fibrillation arrest requiring cardiopulmonary resuscitation and multiple defibrillations. Hemodynamic instability persisted with intractable ventricular arrhythmia requiring his return to the operating room, establishment of cardiopulmonary bypass, and preparation for VAD placement. An Abiomed BVS5000 LVAD was placed with inflow from the left atrium and outflow to the ascending aorta.
The patient was transferred to Lankenau Hospital for further management. Coronary angiography was performed showing patent bypass grafts and the same subtotal ostial left main stenosis observed in the initial study. Because there was concern about the possibility of residual ischemia from a large (unbypassed) ramus intermedius branch, a 3.0 x 12 mm Liberte bare metal stent (Boston Scientific Inc, Natick, MA) was placed in the left main. The next day, the BVS5000 was switched to the AB5000 ventricle because of thrombus formation in the BVS5000 blood pump. While on VAD support, his ventricular dysrhythmias continued despite amiodarone and lidocaine infusions. Electrophysiology consultation was obtained. Based on multiple rhythm strips, the impression was that the episodes of polymorphic ventricular tachycardia were initiated exactly the same way by a single ventricular premature depolarization, most likely related to the Purkinje system at the interventricular septum. Because lidocaine would have no effect on this condition and amiodarone was ineffective in suppressing the ventricular tachycardia, the patients treatment was changed to procainamide and was considered a candidate for radiofrequency ablation. The patient was taken to the electrophysiology laboratory where mapping and ablation took place. The procedure consisted of pacing in the right ventricle at 300 msec, which induced the left-sided ventricular premature depolarization resulting in a reproducible ventricular tachycardia. Using a Chilli catheter (Boston Scientific Inc, Natick, MA), four radiofrequency lesions were placed in the left ventricular aspect of the posteromedial mitral valve annulus. Attempts at reinducing the ventricular tachycardia from the right ventricle and the left ventricle failed to cause the ventricular tachycardia previously observed. Post-procedure, the patient was maintained on procainamide with no further episodes of arrhythmia in normal sinus rhythm. After a week of a stable cardiac rhythm, the VAD was explanted, approximately 3 weeks since the original implant.
The patient remained in the hospital for several weeks, requiring a percutaneous tracheostomy and gastrostomy. Approximately 3 weeks after removing the VAD, the patient was transferred to a rehabilitation center having been successfully weaned from the ventilator and eating orally. Prior to his discharge, a dual-chamber Entrust Implantable Cardiac Defibrillator (Medtronic Inc, Minneapolis, MN) was implanted. For the next several months the procainamide was discontinued and metoprolol was up titrated to maintain a heart rate between 50 and 60 bpm. At 6-months follow-up the patient remains alive and well in New York Heart Association functional class II.
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