Aortic insufficiency (AI) affects 25–52% of patients in their first year of left ventricular assist device (LVAD) support.1–3 Progression of AI could be multifactorial but is predominantly due to the higher constant pressure above the aortic valve (AV) due to LVAD.4,5 The progression might result in the fusion of commissures due to alterations in the shear force exerted on the AV after continuous-flow LVAD implantation, resulting in regurgitation.4,5 This contributes to the deterioration of the already failing heart.6 Hence, AI correction is recommended to overcome poor end-organ perfusion and achieve hemodynamic stabilization.7
Management of AI after LVAD implantation has been challenging. Angiotensin-converting-enzyme inhibitor or diuretics are preferred pharmaceutical methods to treat trace and mild AI for volume management. Intermittent opening of the AV can be achieved with the adjustment of LVAD pump speed and transvalvular pressure gradient, which could potentially reduce the severity of AI progression.8–10 While a surgical approach for correction of more than mild AI to avoid worsening LVAD function and potential heart failure is recommended, there is not a consensus.11,12 Several treatment strategies have been previously implemented to treat AI including the use of AV closure,13 repair14 or replacement with a bioprosthetic at the time of LVAD implantation or later.15 It must be stated that AV closure might lead to life-threatening complications in the case of mechanical failure of the LVAD.
Left ventricular assist device patients are frequently poor candidates for reoperative AV surgery. The use of transcatheter aortic valve replacement (TAVR) is indicated for senile, severely calcified, and degenerative AVs. It is contraindicated for pure aortic regurgitation without valve calcification as it might hamper the anchorage of the transcatheter valve. Limited data support the safety and benefits of TAVR in noncalcified valves.3 However, to address the anchoring complications, oversized valves have replaced noncalcified AVs.16 Transcatheter aortic valve replacement may be an alternative technique; thus, an off-label approach of TAVR implantation for AI in LVAD patients is discussed herein.
Between May 2012 and October 2016, a total of 213 patients were implanted with one of the three LVADs (HeartWare [Medtronics, Farmingham, MA], HeartMate II [Abbott Laboratories, Chicago, IL], and HeartMate 3 [Abbott Laboratories]). Among these 213 patients, 148 of them received the HeartMate II. From this group of 148 patients, three patients with postimplant AI underwent TAVR with the Edwards SAPIEN 3 valve (Edwards Lifesciences, Irvine, CA) (Figure 1). Their cases and outcomes are described below.
Patient A was a 74 year old male with a history of interstitial pulmonary fibrosis and was on home oxygen therapy. He received a HeartMate II LVAD as destination therapy in 2015. Echocardiography demonstrated no evidence of AI before LVAD implantation. Ninety-three days after receiving the LVAD, the patient had a thrombus formation resulting in a pump exchange. Left ventricular assist device flow was 6.2 L/min with 8,600 revolutions per minute (rpm) after pump exchange. The patient was hospitalized for gastrointestinal (GI) bleeding 6 months after receiving the LVAD. The first symptoms of AI appeared 147 days postpump exchange/240 days post-LVAD. Echocardiography documented severe AI with moderate mitral regurgitation (MR) and trace tricuspid regurgitation (TR). At this same time, patient A was experiencing dyspnea, worsening renal function, and presyncopal episodes. Patient A’s symptoms recategorized his New York Heart Association (NYHA) class from III to IV. Two prior sternotomies along with right ventricular dysfunction made him a high risk for surgical aortic valve replacement (SAVR). Preinterventional computed tomography (CT) revealed aortic annulus of 24.2 mm in diameter. Thus, 368 days post-LVAD, the AV was replaced with an Edwards SAPIEN 3 valve via TAVR.
TAVR after LVAD procedure details
In each case, the Edwards SAPIEN 3 valve chosen was oversized. In patient A’s case, a 26 mm valve was used. A transfemoral approach was taken and a standard TAVR procedure was completed. Of note, as these were LVAD patients, the LVAD flow was decreased to the lowest possible rate to reduce the risk of the valve being pushed into the ventricle.
Patient A regained hemodynamic stability immediately after the procedure. The efficiency of the LVAD improved as the flow rate decreased from 7.4 L/min before the TAVR to 5.9 L/min after the procedure. We observed an increased pulsatility index indicating the attenuation of AI (Table 1). Postinterventional echocardiogram showed mild AI, and the MR was classified as mild. The patient’s NYHA classification was reduced to II.
The patient is alive 1,120 days post-TAVR and the AI remains classified as mild.
Patient B was a 38 year old male with a family history of cardiomyopathy, atrial flutter, hypertension, and morbid obesity. He underwent gastric sleeve surgery and received HeartMate II LVAD support as destination therapy in 2013; the body mass index of greater than 35 precluding listing for transplant. Echocardiography demonstrated no evidence of AI during the 6-month follow-up period. The patient had one admission in 2016 for chest pain. One-thousand two-hundred eighty-six days post-LVAD implantation, the patient was presented in the clinic with shortness of breath, dyspnea on exertion and NYHA class IV symptoms. The LVAD flow rate was 6.5 L/min with 10,000 rpm at this time. Echocardiography demonstrated severe AI with mild MR and TR (Figure 2). Preinterventional CT reported an aortic annulus diameter of 24.6 mm with no calcification of leaflets. At 1,288 days post-LVAD implantation, the AV was replaced with a 29 mm Edwards SAPIEN 3 valve via TAVR using a transfemoral approach as previously described.
After the TAVR procedure, echocardiography showed no residual AI and no significant paravalvular leak. Mitral regurgitation was classified as mild postprocedure, indicating an excellent outcome (Figure 3). The patient also regained hemodynamic stability immediately after the procedure (Table 1). The efficiency of the LVAD also improved as the flow rate decreased from 6.5 L/min to 4.6 L/min after the procedure indicating the elimination of AI.
The patient died 616 days after the procedure at home. Cause of death is unknown as an autopsy was not completed. Before the patient’s death, records indicate that the AI did not return and no significant complications due to the TAVR procedure were reported.
Patient C was a 67 year old female with nonischemic cardiomyopathy and stage D heart failure. She was implanted with the HeartMate II LVAD as a bridge to transplant therapy after evaluation in 2015. The LVAD flow rate was 4.0 L/min with 9,200 rpm immediately after implantation. Echocardiography demonstrated no AI before LVAD implant. She had GI bleeding and hip fracture after LVAD implantation. After 180 days post-LVAD implantation, the echocardiography revealed the development of mild AI and MR with trace TR. The patient was admitted 337 days post-LVAD with transaminitis, abdominal pain, generalized weakness, and nausea. Gradual onset of worsening dyspnea and cardiogenic shock were reported. At presentation, the patient had moderate AI with severe MR and TR on LVAD support. At 342 days post-LVAD implantation, patient experienced worsening dyspnea on exertion, increasing generalized fatigue, poor appetite, and intermittent abdominal pain. The patient also experienced cardiogenic shock, leaving her at a high surgical risk for SAVR. Preinterventional CT revealed aortic annulus of 23.3 mm in diameter with no reported calcification. As a candidate for TAVR, she underwent percutaneous implantation of a 26 mm Edwards SAPIEN 3 valve via a transfemoral approach.
Postinterventional echocardiography showed successful implantation of TAVR with no residual AI, and she was hemodynamically stable (Table 1). Mitral regurgitation was classified as mild. The patient returned to NYHA class I and has had no adverse symptoms since TAVR.
The patient was successfully transplanted (229 days post-TAVR procedure) and is currently alive (884 days post-TAVR procedure).
Aortic insufficiency development in LVAD patients might be due to the changes in aortic blood flow dynamics following LVAD implantation.6 High diastolic luminal pressures and shear stress on the AV are other possible causes of the AI post-LVAD. Aortic atrophy was observed after 90 days following Jarvik 2000 (Jarvik Heart Inc., New York, NY) LVAD support in patients along with a decrease in medical aortic thickness, elastin content, and medical smooth muscle cell number. Together, these conditions might synergistically promote valve malcoaptation and postimplant AI development.17 Progressive AI might reduce the rate of AV opening, which affects its function and results in commissural fusion along with remodeling of the aortic leaflets.6,18,19
Even though AI is a well-known complication after LVAD implantation, the best way to manage AI has yet to be determined. Surgical aortic valve replacement is an established modality, though not without complications. Percutaneous and surgical implantation of the CoreValve (Medtronic, Minneapolis, MN) were previously reported.20–22 Complications such as periprosthetic regurgitation resulting in valve-in-valve implantation of a second CoreValve and fusion of cusps and formation of pseudomembrane were observed.21,22
The TAVR approach to correct AI has been previously reported. A case used the transaortic approach of an Edwards SAPIEN 3 valve in patients supported with Heartware Ventricular Assist Device (HVAD) (HeartWare International Inc, Miami Lakes, FL).16 Recently, another approach was used to significantly oversize the prostheses by using the largest CoreValve (31 mm) and Edwards SAPIEN 3 (29 mm) at the same time to maximize radial forces.20
To minimize the cost of the procedure and to attenuate progressive AI in patients with LVAD, we chose to use the Edwards SAPIEN 3 alone. Implantation of Edwards SAPIEN 3 was anchored within the annulus, and the procedure was achieved without any complications or compromised hemodynamic functions. All three patients had an immediate improvement in symptoms as they moved from NYHA IV to NYHA II and I. The efficiency of the LVAD function was also improved as evident from the reduced flow rates after the procedure. There was also a significant improvement in their mobility, and all were able to be discharged to home.
Without question, use of TAVR in LVAD patients retains certain risks. Thrombus, valve closure and embolization, as well as degeneration and recurrent cusp fusing are known adverse events for any LVAD-supported patient with native or bioprosthetic valves; however, those complications were not observed in these three cases. Follow-up on these cases was as long as 3 years. While conclusions must be tempered because of the small number of cases, the length of follow-up shows support for this approach. Transcatheter aortic valve replacement via a transfemoral approach is a viable alternative to treat AI in LVAD patients, who are prone to high surgical risk. Further, individualized assessments should be made in a multidisciplinary fashion as surgical AVR remains the gold standard for AI in LVAD patients.
Immediate and midlength outcomes are good; however, long-term studies on a larger cohort are needed to evaluate the long-term benefit of TAVR for LVAD-associated AI. It must also be noted that the procedure discussed here is a “bridge” therapy, and the long-term solution remains to be a heart transplant in eligible patients.
The authors would like to acknowledge the contribution of Dr. Rajko Radovancevic for his assistance with this project. Additional thanks to Isabella Candelaria and Jacinda Gonzalez-Lopez for data collection assistance and to Dr. R. Michelle Sauer Gehring for editorial support.
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