Recurrent outflow graft compression of HeartMate3: When the left ventricular assist device sticks to the rib

A 77-year-old male patient with a history of dilated nonischemic cardiomyopathy was implanted with a HM3 LVAD in September 2018 as destination therapy via median sternotomy; the left atrial appendage was ligated, and aortic valve was repaired with a Park stitch. Postimplant course was uneventful. The LVAD speed was 5400 rpm, flow 4 to 5 L per minute (LPM) at discharge. Two years later, the patient presented with complaints of lightheadedness, new-onset exertional dyspnea, and multiple low-flow alarms. Computed tomography angiography (CTA) revealed a moderate-to-severe luminal stenosis of the outflow graft at its origin, with a 13-mm hypodensity within the bend relief in close proximity to the seventh rib (Figure 1, A and B). Biodebris removal was performed using subxiphoid incision. The bend relief and an additional ring-reinforced polytetrafluoroethylene graft were incised longitudinally, fully evacuating the biodebris. Nine months later, occasional low-flow alarms recurred. A repeat CTA revealed an 8-mm hypodensity with moderate luminal narrowing at the previous interspace of the outflow graft (Figure 1, C). Sixteen months later, low-flow alarms occurred daily and were associated with presyncopal events. Notably, these low-flow alarms were positional, being exacerbated by leaning forward. A CTA showed circumferential and crescentic hypodensity proximally within the bend relief, causing now severe narrowing (Figure 1, D-F). The repeat surgery was done through a skin incision at the sixth intercostal space, exposing the seventh rib (Figure 2, A). Over the entire course, the patient was maintained on therapeutic warfarin (international normalized ratio goal 2.0-2.5) and aspirin 81 mg orally daily. Partial removal of the seventh rib was done, with immediate improvement in flow to 4.2 LPM from 3 LPM (Figure 2, B and C). Bend relief was cut to evacuate biodebris, with further improvement in flow to 4.7 LPM (Figure 2, D-F). The polytetrafluoroethylene graft around the bend relief was partially removed. The patient was discharged on postoperative day 4 with complete resolution of symptoms. A repeat CTA was done 4 months after the surgery that showed a residual 4-mm peripheral hypodensity in the proximal aspect of the outflow cannula without clinical manifestations (Figure 3). The patient was seen in follow-up 9 months after surgery, with no further alarms or symptoms.

External outflow graft compression following HM3 implant is a well-recognized complication that is associated with longer time on LVAD support and wide clinical presentation from asymptomatic to potentially lethal. The etiology of this complication relates to seepage of blood components through the endograft material into the aneurysmal sac and leads to gradual aneurysm enlargement. This is a well-recognized phenomenon in endovascular surgery and is attributed to the inherent porosity of the endograft. Similarly, with LVADs, the outflow graft is constructed of a knitted polyethylene terephthalate material that has its own inherent porosity, permitting seepage of blood components that are then trapped in between the impermeable graft, thereby forming an extravascular thrombus. Gradual enlargement of this thrombus eventually leads to outflow graft impingement. Several potential treatment options are available that include urgent heart transplant listing in transplant eligible patients, endovascular repair in high-risk target population, and ultimately surgical decompression. This is the first report illustrating the recurrent nature of the problem following initial surgical decompression and the need for rib removal to potentially prevent future events.

The case presentation was approved by the institutional review board (reference; AAAU2877, August 1, 22), and informed consent was waived.