Complex Case Interventions

Aortic Root and Valve Thrombosis After Implantation of a Left Ventricular Assist Device

Benjamin H. Freed, MD*, Valluvan Jeevanandam, MD§, Neeraj Jolly, MD*
Benjamin H. Freed, MD*, Valluvan Jeevanandam, MD§, Neeraj Jolly, MD*
ABSTRACT: We describe the case of a 60-year-old female who presented with a non-ST elevation myocardial infarction 3 months following placement of a non-pulsatile left ventricular assist device (LVAD). Aortic root angiography not only revealed extensive aortic root thrombosis and left main thrombotic obstruction, but also vividly demonstrated the causative mechanism. To our knowledge, this rarely described mechanism of LVAD thrombosis has not been reported as clearly as this case illustrates.
J INVASIVE CARDIOL 2011;23:E63–E65
Key words: aortic root thrombosis, coronary catheterization, LVAD
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Editor’s Note: This is an unusual complication of long-term LV assist devices and underscores the need for strict follow up and adequacy of anticoagulation after device use. If a medical condition requires temporary discontinuation of anticaogulation, LV assist devices should be managed similar to prosthetic heart valves; use low molecular weight heparin as bridge. Timely diagnosis and aggressive treatment, such as in this case, will save the patient's life. — Samin K. Sharma, MD, Mount Sinai Medical Center, New York, New York

Left ventricular assist device (LVAD) thrombosis is a rare but well-described adverse event following this surgery. It is generally believed that the clot develops on the device itself, because the original texturing inside the pump facilitates thrombus formation.1 Newer designs using smooth titanium surfaces have helped rectify this problem. Aortic root and aortic valve cusp thromboses are rarely described, but have occurred with the newer, continuous-flow LVAD. Increased anticoagulation or decreased pump speed to allow for more flow across the aortic valve may prevent this serious adverse event.1

Case Report. A 60-year-old female with a history of ischemic cardiomyopathy, biventricular implantable cardioverter-defibrillator (ICD) and placement of a continuous-flow HeartWare LVAD (HeartWare Inc., Framingham, Massachusetts) two months prior presented with severe, exertional chest pain similar to her previous myocardial infarction (MI) several years ago. She had been on low-dose warfarin for her LVAD, but had stopped it three days earlier in anticipation of a routine right heart catheterization. It was also noted that the pump speed was increased two weeks earlier. A 12-lead electrocardiogram was performed; it revealed a ventricular paced rhythm with underlying atrial fibrillation. Cardiac enzymes revealed a creatine kinase of 4073 U/L and troponin T of 9.41 ng/dl. The patient was given an aspirin and started on a heparin and nitroglycerin drip. Coronary angiography was performed; it illustrated significant thrombus burden in the aortic root with extension of the clot into the left main coronary artery (Figure 1). Multiple attempts were made to remove the clot with both rheolytic and aspiration thrombectomy. Intracoronary eptifibatide was given and balloon angioplasty of the left main was performed. There was a decrease in the thrombus burden following the procedure, but overall the revascularization of the left main trunk was unsuccessful. The patient was continued on intravenous eptifibatide and heparin. Surveillance transesophageal echocardiography performed 1 day after the coronary angiogram revealed thrombus persisting in the left coronary cusp of the aortic valve and no color flow into the left main, suggesting flow obstruction (Figure 2). The patient was continued on eptifibatide for 24 hours and heparin for 1 week. Computed tomography of the proximal aorta and coronaries revealed persistent thrombus in the left coronary cusp of the aortic valve and left main coronary artery (Figure 3). Subsequent angiography confirmed these results (Figure 4). A decision was made to not pursue any further percutaneous coronary intervention. She was continued on oral anticoagulation and her pump speed was decreased to 3 liters/minute. She underwent successful orthotopic heart transplantation within the next 6 months.

Discussion. The last 10 years have witnessed significant advances in the management of patients with systolic heart failure. The focus on new therapies for this disease was necessary due, in part, to the low 1-year survival rate of patients with heart failure on continuous intravenous inotropes and the long waiting time for a heart transplant. LVAD have garnered much attention and enthusiasm since the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial was published in 2001.2 In this study, the 2-year survival rate in patients with an LVAD was statistically higher than those patients who received medical therapy alone. Despite the improved outcomes, these first-generation LVADs were cumbersome to place and led to significant comorbidities. Since then, the design of these mechanical assist devices has rapidly evolved. Many of the newer LVADs provide continuous instead of pulsatile flow. This allows them to be smaller and eliminates the need for external venting. They have also been shown to be more durable and less likely to cause infection. In a recent randomized trial comparing continuous- and pulsatile-flow LVAD in patients with advanced heart failure, the newer generation continuous-flow pumps significantly improved the probability of survival free of stroke, reoperation for device repair, or replacement at 2 years.3 In addition, the 2-year survival rate in patients with a continuous-flow device was more than double that of patients with a pulsatile-flow device. Although the newer generation continuous pumps are seemingly a vast improvement, there are concerns over the increased incidence of thrombosis of the aortic valve and aortic root with this iteration of LVAD. In one report, 5/28 patients with the continuous-flow HeartMate II LVAD (Thoratec, Pleasanton, California) were discovered to have aortic root thrombosis.4 The majority were asymptomatic. The authors noted that this phenomenon was not previously seen with pulsatile-flow devices. Several studies have tried to explain the increased potential for thrombosis in continuous-flow devices. In one, the authors created an in vitro mock circulatory loop that compared dye washout time as a marker of flow stagnation between pulsatile and non-pulsatile devices.5 They found that the dye washout time was significantly longer in non-pulsatile devices, especially when the outflow was anastamosed to the descending aorta rather than the ascending aorta. Another study using computer-generated flow models to represent continuous-flow devices showed that, indeed, location of the outflow anastamosis plays a significant role in stagnation of blood, particularly in the aortic root.6 Our patient had an outflow anastamosis to her ascending aorta and angiography demonstrated a clear demarcation of respective streams of blood flow from the heart and the pump. The resultant stagnation of blood flow from the heart likely precipitated the thrombotic complication in the sinus of Valsalva. We present a case involving aortic root and left main coronary thrombosis in a patient with a continuous-flow left ventricular mechanical assist device. Resultant myocardial infarction is unique and describes yet another thrombotic complication attendant upon such continuous flow pumps.

References

  1. John R. Current axial flow devices — The HeartMate II and Jarvik 2000 left ventricular assist devices. Semin Thorac Cardiovasc Surg 2008;20:264–272.
  2. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med 2001;345:1435–1443.
  3. Slaughter MS, Rogers JG, Milano CA, et al. HeartMate II Investigators. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med 2009;361:2241–2251.
  4. Khodanerdian RA, Mason NO, Horton SC, et al. Aortic valve/root thrombosis with continuous flow left ventricular assist devices. J Heart Lung Transplant 2008;27:S132–S133.
  5. DiGiorgi PL, Smith DL, Naka Y, Oz MC. In vitro characterization of aortic retrograde and antegrade flow from pulsatile and non-pulsatile ventricular devices. J Heart Lung Transplant 2004;23:186–192.
  6. Kar B, Delgado RM, Frazier OH. The effect of LVAD aortic outflow-graft placement on hemodynamics and flow. Tex Heart Inst J 2005;32:294–298.
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From the *Section of Cardiology, Department of Internal Medicine and the §Section of Cardiothoracic Surgery, Department of Surgery, University of Chicago Medical Center, Chicago, Illinois. Disclosure: Dr. Jeevanandam discloses that he is a consultant for Thoratec Corporation. The other authors have no relevant disclosures. Manuscript submitted July 7, 2010 and accepted August 9, 2010. Address for correspondence: Neeraj Jolly, MD, University of Chicago MC 5084, 5841 South Maryland Avenue, Chicago IL, 60637. Email: njolly@medicine.bsd.uchicago.edu