Ann Thorac Surg 1998;65:839-841
© 1998 The Society of Thoracic Surgeons
Case Reports
Right Ventricular Infarction During Left Ventricular Assist System Support
Lawrence R. McBride, MD,
Renato Ruggiero, MD,
Karen A. Powers, RN,
Debra A. Moroney, RN,
Marc T. Swartz, BA
Division of Cardiothoracic Surgery, Department of Surgery, Saint Louis University Health Sciences Center, St. Louis, Missouri, USA
Accepted for publication October 19, 1997.
Dr McBride, Department of Surgery, Saint Louis University Health Sciences Center, 3635 Vista Ave at Grand Blvd, PO Box 15250, St. Louis, MO 63110-0250 (e-mail: mcbridlm@wpogate.slu.edu).
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Abstract
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Left ventricular assist devices are frequently used to bridge patients to cardiac transplantation. As this experience grows, new and unanticipated complications will occur. This report describes a 50-year-old man with ischemic cardiomyopathy being bridged to cardiac transplantation who suffered an acute right ventricular infarction during the interval of support.
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Introduction
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A 50-year-old man with a strong family history of coronary artery disease suffered an anterior myocardial infarction in July 1995. He was initially treated with tissue plasminogen activator and subsequently underwent cardiac catheterization with coronary arteriography. He was found to have severe triple-vessel disease involving the left anterior descending, right coronary, and first obtuse marginal arteries. He underwent coronary artery bypass grafting that same month.
In October 1995, severe angina once again developed, and repeat coronary arteriography showed four of the five bypass grafts occluded. Therefore, in November 1995 he underwent redo coronary artery bypass grafting. Throughout 1996 he had multiple hospitalizations for severe angina, usually to rule out acute myocardial infarction. His ventricular function began to deteriorate, and by late 1996 he had severe refractory congestive heart failure. In December 1996 he had two transient ischemic attacks, which were thought to be embolic (intracardiac) in origin.
On January 24, 1997, he was admitted to St. Louis University with angina and severe congestive heart failure. Dobutamine and nitroglycerin drips were started, and cardiac catheterization showed occluded grafts to the obtuse marginal, posterior descending, and diagonal coronary arteries. His heart failure continued to be unresponsive to 10 µg · kg-1 · min-1 of dobutamine, so an intraaortic balloon pump was placed. His cardiac index remained low at 1.7 L · m-2 · min-1 with a pulmonary capillary wedge pressure of 24 mm Hg. His pulmonary artery pressure was 58/28 mm Hg. He was evaluated and accepted for cardiac transplantation. Due to his deteriorating condition a Novacor (Baxter Healthcare Corp, Oakland, CA) left ventricular assist system (St. Louis University Institutional Review Board protocol 8770) was implanted. His postoperative course was complicated by multiple thromboembolic events even though he was anticoagulated with warfarin and aspirin. After several events we decided to maintain his prothrombin time international normalized ratio at 3.5 to 4.5. (The international normalized ratio had been maintained at 2.5 to 3.0.) He was receiving 325 mg/day of aspirin and 100 mg/day of dipyridamole.
On February 19, 1997, substernal chest pain radiating to the left jaw, left arm, and shoulder developed. This pain was not relieved by sublingual nitroglycerin. In addition, the left ventricular assist system flows dropped from 5.4 to 4.0 L/min. The patient was transferred to the intensive care unit from the step-down floor, a dose of morphine sulfate was given, and a nitroglycerin drip was started. His angina was relieved with the intravenous nitroglycerin; however, he had electrocardiographic changes suggestive of subendocardial lateral ischemia. For this reason, he was taken to the cardiac catheterization laboratory, where selected arteriography showed a mid-right coronary artery thrombus, the result of a ruptured ulcerative plaque (Fig 1). This lesion underwent angioplasty; however, the distal right coronary artery remained partially occluded with fresh thrombus (Fig 2). The option of streptokinase was rejected due to the risk of bleeding because the patient’s international normalized ratio was already 4.49. Creatine kinase-MB values late on the evening of February 20 peaked at 246 ng/mL. He was maintained for several days on a nitroglycerin drip, and then switched to nifedipine, 30 mg twice a day; isosorbide mononitrate, 60 mg once a day; and nitroglycerin paste, 20 cm once a day. He continued to require sublingual nitroglycerin and occasionally a nitroglycerin drip for 12 to 24 hours. He was maintained on a dobutamine regimen of 5 µg · kg-1 · min-1 with left ventricular assist system flows of 5.6 to 6.0 L/min. His blood pressure stabilized at 110 to 120/70 to 80 mm Hg.
The patient remained asymptomatic and free of angina for 5 weeks until a donor heart became available on May 5, 1997. Unfortunately, the patient died in the operating room of a combination of ischemic graft failure and bleeding. Pathologic examination of the explanted native heart showed the coronary arteries and coronary bypass conduits all to be moderately to totally occluded. The right coronary artery and all of the native vessels had marked occlusion of intimal plaque, with the bypass grafts having moderate to total occlusion by fibrointimal proliferation or organized thrombi. This was no evidence of recent infarction or ischemic injury.
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Comment
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As the durations of support in patients bridged to transplantation lengthen and permanent mechanical circulatory support becomes a reality, complications associated with coronary artery disease in ischemic cardiomyopathy patients will present an ever-increasing challenge. To date, there is no evidence to suggest that placement of a left ventricular assist system would halt the natural progression of coronary artery disease. In our bridge to transplantation experience, another patient who was supported for 1 year with a left ventricular assist system had progression of his right coronary artery disease from 65% occlusion to greater than 95% occlusion. Although this patient never suffered an acute myocardial infarction or had angina nearly as severe as the patient presented, he did frequently require sublingual nitroglycerin while ambulating or performing mild exercise. A small group of our postcardiotomy recovery patients also had pathology found at autopsy that suggested acute infarction or extension of an existing infarction during the period of ventricular assist device support. These were acutely ill patients, all of whom were sedated and intubated. Many had cannulation of the left atrium, right atrium, or both, and died within 10 days of ventricular assist device insertion. Although these postcardiotomy patients represent a different patient population, they help to support the concept that patients with severe coronary disease being supported with ventricular assist devices can suffer significant ischemic events.
The right ventricle is probably more susceptible than the left to this type of disease progression because placement of a left ventricular assist system significantly reduces left ventricular myocardial oxygen consumption and wall stress. At the same time a left ventricular assist device can increase right ventricular preload, leading to right ventricular distention, septal deviation, and failure [1]. In most cases a left ventricular assist device increases coronary perfusion by increasing coronary blood flow and perfusion pressure [2]. In some severely ischemic patients such as this, however, right ventricular oxygen demand exceeds supply.
Essentially all we could do in this case was to reduce the incidence and severity of angina. The right coronary artery had been bypassed twice, and the area at risk was thought to be infarcted. However, examination of the explanted heart showed no evidence of recent infarction or ischemia. This man’s angina and symptoms had been controlled for several weeks. The heart, which was removed during a period of stability, would not be expected to show any acute pathologic changes. We never considered discharging this patient because of his thromboembolic events, anticoagulation regimen, angina, and continuous dobutamine infusion.
Until additional information is available it is impossible to determine if this type of complication will significantly affect morbidity in the permanent ventricular assist device population. Whether permanent left ventricular assist device candidates with significant right coronary artery lesions should be excluded, revascularized before or at the time of implantation, or given prophylactic biventricular assist devices has yet to be determined. There are obviously many ischemic cardiomyopathy patients with right coronary lesions who have been successfully supported with left ventricular assist devices. The incidence and severity of this disease progression are not known, but undoubtedly are related to the duration of support. However, patients being supported with ventricular assist devices in whom anginal-type pain develops should be evaluated for coronary occlusion as a result of natural disease progression or thromboembolus.
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References
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- Farrar DJ, Chow E, Compton PG, et al. Effects of acute right ventricular ischemia on ventricular interactions during prosthetic left ventricular support. J Thorac Cardiovasc Surg 1991;102:588-595.[Abstract]
- Ratcliffe MB, Bavaria JE, Wenger RK, Bogen DK, Edmunds LH Left ventricular mechanics of ejecting, postischemic hearts during left ventricular circulatory assistance. J Thorac Cardiovasc Surg 1991;101:245-255.[Abstract]
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Abstract
Introduction
