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J Thorac Cardiovasc Surg 2004;128:643-645
© 2004 The American Association for Thoracic Surgery

Brief communication

Use of the AbioCor replacement heart as destination therapy for end-stage heart failure with irreversible pulmonary hypertension

^a Lankenau Hospital, Department of Cardiothoracic Surgery, Wynnewood, Pennsylvania, USA
^b Drexel University, Hahnemann University Hospital, Department of Cardiothoracic Surgery, Philadelphia, Pennsylvania, USA

Received for publication July 24, 2003; accepted for publication March 31, 2004.

^* Address for reprints: Louis E. Samuels, MD, Lankenau Hospital, Department of Cardiothoracic Surgery, MSB Suite 280, 100 Lancaster Avenue, Wynnewood, PA 19096, USA
SamuelsLE@aol.com

The first 20% of the full text of this article appears below.

Because of a potential conflict of interest related to this article on the part of our editors, Dr Robert L. Kormos served as guest editor, assigned reviewers, and made editorial decisions or recommendations leading to its acceptance for publication.

 

Fixed pulmonary hypertension is a contraindication for orthotopic heart transplantation.¹ The AbioCor artificial heart (Abiomed Inc, Danvers, Mass) was designed as a totally internal replacement system for patients with end-stage heart failure who are not eligible for heart transplantation. The purpose of this report is to describe the experience with the AbioCor artificial heart in the setting of a patient with severe biventricular failure and irreversible pulmonary hypertension.

Clinical summary

A 51-year-old, 5-foot 9-inch, 170-pound (body surface area 1.9 m²) man with idiopathic dilated cardiomyopathy presented with progressive shortness of breath and fatigue. His medical history was significant for emphysema and hepatitis B and C viruses. Medications included oral digoxin, hydrazlazine, bumetanide, and fosinopril. Intravenous therapy included dobutamine 10 µg · kg · min and milrinone 0.50 µg · kg · min.

Cardiac evaluation showed normal sinus rhythm with left atrial enlargement, 4-chamber cardiac dilatation, severe global biventricular dysfunction, moderate tricuspid and severe mitral regurgitation, and pulmonary hypertension. Left and right heart catheterization showed normal coronary arteries with elevated pulmonary artery (69/37 mm Hg), central venous (18 mm Hg), and pulmonary capillary wedge (25 mm Hg) pressures. The thermodilution cardiac output was 3.3 L/min with an adjusted cardiac index of 1.7 L · min · m². The pulmonary vascular resistance was 7.8 Wood units. Pharmacologic maneuvers to reduce the pulmonary vascular resistance with nitroglycerin and nitroprusside were unsuccessful. Stress testing showed a peak oxygen consumption (VO₂ max) of 8.3 mL · kg · . . . [Full Text of this Article]