|
|
||||||||
Ann Thorac Surg 1998;66:571-573
© 1998 The Society of Thoracic Surgeons
a Divisions of Cardiovascular and Thoracic Surgery and Cardiology, University of Minnesota, Minneapolis, Minnesota, USA
Accepted for publication March 6, 1998.
Address reprint requests to Dr Park, Division of Cardiovascular and Thoracic Surgery, University of Minnesota, Box 207, 420 Delaware St SE, Minneapolis, MN 55455
e-mail: (parkx021{at}maroon.tc.umn.edu)
| Abstract |
|---|
|
|
|---|
| Introduction |
|---|
|
|
|---|
The patient was a 54-year-old man with ischemic cardiomyopathy who had suffered multiple myocardial infarctions in the past. His medications included digoxin, isosorbide dinitrate, high-dose amiodarone, lisinopril, and metoprolol. Before heart transplant evaluation, he had three separate episodes of VT requiring hospitalization. On dobutamine echocardiography and multiple uptake gated acquisition he was found to have no reversible myocardial ischemia, a left ventricular ejection fraction of 0.10, and a right ventricular ejection fraction of 0.33. Transthoracic echocardiography demonstrated biventricular dilatation. Coronary angiography revealed a left dominant system with severe diffuse disease, and a proximally occluded right coronary artery with minimal distal reconstitution. Right heart catheterization revealed a right atrial pressure of 17 mm Hg, a right ventricular pressure of 70/7 mm Hg, a pulmonary artery pressure of 69/39 mm Hg, a pulmonary capillary wedge pressure of 38 mm Hg, a pulmonary vascular resistance of 280 dynes · s-1 · cm-5, and a cardiac index of 1.34 L · min-1 · m-2. His electrocardiogram demonstrated anterior and inferior Q waves with nonspecific ST- and T-wave abnormalities. These findings alone do not identify the arrhythmogenic potential of his heart; however, electrophysiologic study revealed readily inducible sustained VT of several rapidly changing morphologies, for which he underwent ICD implantation (model 7218C PCD; Medtronic, Minneapolis, MN). The patient was listed as a heart transplant candidate, but his condition continued to worsen.
On six separate occasions episodes of VT developed that were not medically manageable. Lidocaine, bretylium, amiodarone, and ß-blockers were not effective in preventing refractory VT. One episode of VT lasted more than 5 minutes, and was finally converted to sinus rhythm with a combination of 11 ICD shocks, doubling of a lidocaine intravenous infusion from 2 mg/min to 4 mg/min, administration of intravenous bretylium, and three transthoracic direct-current cardioversions of 360 joules. By this time, he was incapacitated by these episodes of VT. He was reluctant to move from his bed, reach for a glass of water, or exert himself in any fashion for fear of triggering sudden death.
It was postulated that the ventricular dilatation in the patients globally ischemic myocardium played an essential role in his development of VT. Based on this, the decision was made to implant an LVAD in an attempt to reduce biventricular filling pressures and thereby control his VT. The patient was taken electively to the operating room, and a HeartMate (Thermo Cardiosystems Inc, Woburn, MA) LVAD was placed intraperitoneally. The ICD was left in place, and the distal right coronary artery was bypassed with a saphenous vein graft in a presumptive effort to minimize right ventricular dysfunction often seen with LVAD implantation. The LVAD provided excellent hemodynamic support, and the patient was taken off cardiopulmonary bypass support without difficulty.
Postoperatively, he remained hemodynamically stable, with pump outputs of 4.2 to 5.4 L/min. Pulmonary artery pressure decreased to 37/19 mm Hg, and pulmonary capillary wedge pressure decreased to 13 mm Hg. After the operation, there were no further episodes of VT despite no antiarrhythmic medication administration. Two transient episodes of self-limited atrial fibrillation were the only arrhythmias the patient experienced. The Heartmate support proceeded uneventfully, and 79 days after LVAD implantation the patient successfully underwent orthotopic cardiac transplantation.
| Comment |
|---|
|
|
|---|
Coronary revascularization, when feasible, reduces morbidity and mortality in patients with ischemic cardiomyopathy [3]. However, our patient was a poor candidate for conventional surgical revascularization because of the lack of reversible ischemia, poor distal target vessels, and a suboptimal left ventricular ejection fraction. Right coronary artery bypass grafting was performed presumptively in an effort to minimize right ventricular dysfunction after the HeartMate implantation, because right ventricular function is vital to successful LVAD support. In a published experience of 21 patients who underwent implantation of an LVAD, there was a 19% incidence of malignant ventricular arrhythmias before implantation and a 43% incidence during LVAD support [4]. The patients in this series that experienced arrhythmias during device support did not require biventricular support, although some investigators have observed that right ventricular fibrillation early after LVAD implantation may require biventricular support to maintain hemodynamic stability [5].
Our patient had biventricular dilatation with elevated intracardiac pressures before HeartMate implantation. Increased intracardiac pressures and myocardial wall tension can induce ventricular irritability and subsequent ventricular arrhythmias [6]. Implantation of an LVAD effectively unloads the left ventricle, and the pressure in the right ventricle often is reduced as well [7]. These hemodynamic changes were observed in our patient, and may have been the primary factor in preventing recurrent VT. However, a possible contribution of the right coronary artery bypass grafting cannot be summarily dismissed.
Placement of LVADs is not uncommon for postcardiotomy pump failure, intractable ventricular arrhythmias with associated pump failure, or postmyocardial infarction with primary cardiac failure [813]. Our patient had placement of an LVAD for debilitating, recurrent VT without persistent pump failure.
In summary, we have described successful management of a heart transplant candidate with refractory VT. Implantation of an LVAD along with right coronary artery bypass grafting as a bridge to transplantation was effective in controlling episodes of life-threatening VT, and should be considered for patients with debilitating ventricular arrhythmias.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
J. T. Shirazi, J. C. Lopshire, I. Gradus-Pizlo, M. A. Hadi, T. C. Wozniak, and A. S. Malik Ventricular arrhythmias in patients with implanted ventricular assist devices: a contemporary review Europace, January 1, 2013; 15(1): 11 - 17. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. G. Drakos, J. V. Terrovitis, J. N. Nanas, E. I. Charitos, A. S. Ntalianis, K. G. Malliaras, N. Diakos, D. Koudoumas, S. Theodoropoulos, M. H. Yacoub, et al. Reverse Electrophysiologic Remodeling After Cardiac Mechanical Unloading for End-Stage Nonischemic Cardiomyopathy Ann. Thorac. Surg., March 1, 2011; 91(3): 764 - 769. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. E. Samuels, E. C. Holmes, M. P. Thomas, J. C. Entwistle III, R. J. Morris, J. Narula, and A. S. Wechsler Management of acute cardiac failure with mechanical assist: experience with the ABIOMED BVS 5000 Ann. Thorac. Surg., March 1, 2001; 71(2007): S67 - S72. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. J. Thomas and A. T. Harvey BRIDGE TO RECOVERY WITH THE ABIOMED BVS-5000 DEVICE IN A PATIENT WITH INTRACTABLE VENTRICULAR TACHYCARDIA J. Thorac. Cardiovasc. Surg., April 1, 1999; 117(4): 831 - 832. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |