Rapidly Enlarging Abdominal Aortic Aneurysm Requiring Endovascular Repair After LVAD Placement

A 67-year-old man with medical history of ischemic cardiomyopathy with stage D heart failure and infrarenal abdominal aortic aneurysm underwent implantation of a left ventricular assist device (LVAD). Three months after the procedure, he presented with unrelenting back pain and a rapidly increased in size aneurysm. The patient underwent urgent endovascular aneurysm repair with uncomplicated recovery. Growing experience with current-generation LVADs led to the recognition of a novel type of vasculopathy: LVAD-induced aortopathy and a preexisting aortopathy may rapidly progress after LVAD placement. A 67-year-old man with medical history of ischemic cardiomyopathy with stage D heart failure and infrarenal abdominal aortic aneurysm underwent implantation of a left ventricular assist device (LVAD). Three months after the procedure, he presented with unrelenting back pain and a rapidly increased in size aneurysm. The patient underwent urgent endovascular aneurysm repair with uncomplicated recovery. Growing experience with current-generation LVADs led to the recognition of a novel type of vasculopathy: LVAD-induced aortopathy and a preexisting aortopathy may rapidly progress after LVAD placement. We present a case report of a 67-year-old man with history of smoking and ischemic cardiomyopathy who underwent implantation of a HeartMate 3 (Abbott Vascular) left ventricular assist device (LVAD) because of progressive heart failure symptoms. Comorbidities at the time of implantation included chronic kidney disease stage 3 and an infrarenal saccular abdominal aortic aneurysm (AAA; 5.3 × 5.1 cm) that was found incidentally during workup for advanced heart failure therapies. A 67-year-old patient underwent LVAD implantation. The postoperative course was notable for a small bowel obstruction at 9 weeks, requiring hospitalization and a small bowel resection. At 13 weeks, the patient was noted to have an episode of aphasia and right-sided weakness at his rehabilitation center consistent with a cerebrovascular accident, from which he recovered without neurologic sequelae within weeks after a brief hospitalization without intervention. Twenty-five weeks after the LVAD operation, the patient presented to the emergency department with severe back pain in the lumbar spine and sacral region that had gradually worsened during a few days and was acutely exacerbated by a physical therapy session. The physical examination was notable for elevated blood pressure of 160/110 mm Hg and normal neurologic examination findings. LVAD interrogation did not reveal any alarms but exhibited a high pulsatility index of 12 (HeartMate 3 pump speed, 5400 rpm; pump power, 4.1). Outpatient medications included allopurinol, amiodarone, aspirin, atorvastatin, carvedilol, digoxin, fludrocortisone, levetiracetam, losartan, tramadol, and warfarin. The differential diagnosis for the presentation with acute lower back pain included a musculoskeletal cause, given that physical therapy had exacerbated the pain, and symptomatic AAA, given the prior imaging evidence. Computed tomography angiography of the chest, abdomen, and pelvis performed immediately on presentation was notable for an increase in size of the infrarenal AAA measuring 6 × 5.6 cm (Figure 1) compared with 5.3 × 5.1 cm 3 months earlier, with a large mural thrombus and para-aortic stranding, without evidence of extravasation or rupture, and with patent visceral and renal arteries. The hypertension was treated with oral administration of carvedilol and hydralazine as well as with pain control with hydromorphone. The mean arterial pressure was thereby maintained below 70 mm Hg. The patient underwent endovascular repair of the growing AAA with a main body Gore-Tex graft (28.5 mm × 12 cm; Gore Excluder [W. L. Gore]) as well as bilateral iliac artery limbs (left iliac limb: 20-mm-diameter by 10-cm limb as well as a limb extender of 14.5-mm-diameter and 7 cm in length; right iliac limb: 18-mm-diameter by 10 cm). Furthermore, the aneurysm sac was embolized throughout its course with a total of 90 foam embolization plugs (Impede-FX coils [Shape Memory]; Figure 2). The procedure was complicated by unsuccessful vascular closure with the Perclose device (Abbott Vascular), requiring cutdown of the bilateral femoral arteries and bovine patch angioplasty repair. From a surgical perspective, the femoral vessels were noted to be remarkably fragile, and although there was no technical problem with insertion of the Perclose device, an arterial tear necessitated the cutdown repair. The postoperative course was uneventful, and the patient was discharged to a rehabilitation facility on postoperative day 13. After discharge, the patient remains asymptomatic, without LVAD complications and with therapeutic international normalized ratio. Follow-up computed tomography angiography 4 weeks after the aneurysm repair showed a successful repair with no endoleak, and the aneurysm sac had regressed by about 4 mm (Figure 3). Growing experience with current-generation LVADs led to the recognition of a novel type of vasculopathy: continuous-flow (CF) LVAD–induced aortopathy. Replacement of physiologic pulsatile blood flow with continuous flow promotes a remodeling process in the aorta of CF-LVAD patients that starts within 2 to 6 months of support.1Patibandla P.K. Rajasekaran N.S. Shelar S.B. Giridharan G.A. Litovsky S.H. Sethu P. Evaluation of the effect of diminished pulsatility as seen in continuous flow ventricular assist devices on arterial endothelial cell phenotype and function.J Heart Lung Transplant. 2016; 35: 930-932https://doi.org/10.1016/j.healun.2016.03.008Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar Specifically, functional, structural, and molecular data indicate presence of endothelial dysfunction, suppression of extracellular matrix-degrading enzymes such as matrix metalloproteinases, reduction in vascular elastin/collagen ratio, and decrease in aortic wall tensile strength.2Ambardekar A.V. Stratton M.S. Dobrinskikh E. et al.Matrix-degrading enzyme expression and aortic fibrosis during continuous-flow left ventricular mechanical support.J Am Coll Cardiol. 2021; 78: 1782-1795https://doi.org/10.1016/j.jacc.2021.08.047Crossref PubMed Scopus (9) Google Scholar Notably, elastin degradation is a well-established pathophysiologic mechanism in the formation of aortic aneurysm.3MacSweeney S.T. Powell J.T. Greenhalgh R.M. Pathogenesis of abdominal aortic aneurysm.Br J Surg. 1994; 81: 935-941https://doi.org/10.1002/bjs.1800810704Crossref PubMed Scopus (180) Google Scholar,4Isenburg J.C. Simionescu D.T. Starcher B.C. Vyavahare N.R. Elastin stabilization for treatment of abdominal aortic aneurysms.Circulation. 2007; 115: 1729-1737https://doi.org/10.1161/CIRCULATIONAHA.106.672873Crossref PubMed Scopus (117) Google Scholar Thus, CF-LVAD therapy may accelerate progression of aneurysmal growth by aggravating elastin degradation in the already vulnerable vasculature. Few case reports have described the management of AAA in LVAD recipients, including open or endovascular repair before,5Paul S. Owens C.D. Singh H. Belkin M. Couper G.S. Shekar P. Intraperitoneal HeartMate left ventricular assist device placement after endovascular repair of an abdominal aortic aneurysm.J Heart Lung Transplant. 2006; 25: 253-255https://doi.org/10.1016/j.healun.2005.08.021Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar concurrently with,6Kindo M. Carranza D. Eisenmann B. Mazzucotelli J.P. Biventricular assist device implantation as bridge to heart transplantation concomitant with open repair of infrarenal aortic aneurysm.Interact Cardiovasc Thorac Surg. 2008; 7: 738-739https://doi.org/10.1510/icvts.2007.172114Crossref PubMed Scopus (3) Google Scholar or shortly after operation during the implant admission.7Wong M.K. Ho C.K. Fan K.Y. Au T.W. Left ventricular assist device insertion and open abdominal aortic aneurysm repair in same admission for an end-stage heart failure patient.Interact Cardiovasc Thorac Surg. 2022; 34: 1180-1182https://doi.org/10.1093/icvts/ivab362Crossref PubMed Scopus (0) Google Scholar,8Starr J.E. Elsayed-Awad H. Sai-Sudhakar C.B. Endovascular abdominal aortic aneurysm repair in patients with ventricular assist devices.Ann Vasc Surg. 2014; 28: 1792.e19-1792.e22https://doi.org/10.1016/j.avsg.2014.03.013Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar In these cases, the AAA was recognized during the LVAD evaluation, and aortic interventions were preplanned because the aneurysmal size exceeded established thresholds for repair. In contrast, in this case, the size of the aneurysm was initially below such thresholds and therefore was not intervened on during the index implant admission; however, it then rapidly grew while the patient was on CF-LVAD support. In cases with borderline aortic diameters, concomitant aortic intervention with LVAD implantation should be considered. From a surgical perspective, the patient’s vasculature was noted to be remarkably fragile, possibly reflecting the pathophysiologic consequences of chronically reduced arterial pulsatility. This observation suggests that surgical cutdowns may represent a safer strategy for arterial closure in CF-LVAD patients compared with percutaneous devices. AAA management in CF-LVAD recipients is complex, given the potential for accelerated growth and unknown risk of rupture, possibly making standard surveillance guidelines and thresholds for treatment less reliable. This case advocates for routine assessment of all prospective LVAD candidates for the presence of AAA and, if identified, a multidisciplinary discussion with vascular and cardiothoracic surgeons to consider the possibility of concomitant aneurysm repair during the index implant admission vs frequent follow-up monitoring. Prospective studies are warranted to provide evidence-based recommendations for the care of LVAD candidates with AAA. The authors have no funding sources to disclose.