Percutaneous continuous-flow (CF) micro axial blood pumps, like the Impella 5.0, are commonly used for short-term (ST) mechanical circulatory support in patients with acute decompensated heart failure.1 The Impella device often serves as a bridge to implantation of a long-term (LT) CF left ventricular assist device (CF-LVAD), such as the centrifugal-flow HeartWare (HVAD). All patients supported with axial CF-LVADs develop acquired von Willebrand syndrome (AVWS) as a result of mechanical shear stress. Increased shear stress leads to excessive proteolysis of von Willebrand factor (vWF) and loss of high molecular-weight (HMW) multimers, thus contributing to platelet dysfunction and increased gastrointestinal bleeding.2–4 Bleeding events associated with AVWS have been reported in patients supported with LT CF-LVADs5–7; however, the relation between early perioperative bleeding complications and AVWS remains poorly characterized in ST CF-LVADs. We sought to describe the relation between the development of AVWS and excessive intraoperative bleeding in a patient who was sequentially bridged with an ST micro axial device to a LT centrifugal CF-LVAD. This case highlights the importance of monitoring these hemostatic changes when bridging to LT CF-LVADs.
A 45 years old male with a history of coronary artery disease and multi-vessel coronary artery bypass grafting with preserved left ventricular (LV) ejection fraction (EF) presented to an outside hospital with an acute non-ST segment elevation myocardial infarction. The patient underwent emergent percutaneous revascularization with stent placement; however, he developed new-onset severe LV dysfunction (EF 10%) and required intra-aortic balloon pump placement. Ongoing cardiogenic shock, despite an intra-aortic balloon pump and inotropic support, required surgical implantation of an Impella 5.0 via the left subclavian artery.
The patient underwent urgent evaluation for cardiac transplantation and consideration of an LT CF-LVAD as bridge to transplantation. Hemodynamics showed a central venous pressure of 9 mm Hg and a cardiac index of 2.5 with a heart rate of 98 beats per minute and mean arterial blood pressure of 83 mm Hg. An echocardiogram demonstrated severe LV dysfunction with normal right ventricular size and function, normal valve function, and adequate position of the Impella device. Interrogation of the Impella revealed a speed of 30,000 revolutions per minute (rpm) with an estimated flow of 4.4 L/min. Laboratory values measured during intravenous heparin and aspirin therapy (81 mg daily) are outlined in Table 1. Despite hemodynamic stability and reversal of end-organ dysfunction during Impella support, the patient developed progressive hemolysis and anemia requiring multiple blood transfusions.
Although the patient was considered a suitable candidate for cardiac transplantation, he was found to have type O blood, and therefore, on hospital day (HD) 6, the Impella device was removed and the HVAD centrifugal CF-LVAD was surgically implanted. Despite an expedited intervention and a short cardiopulmonary bypass time (88 min), the patient developed severe perioperative coagulopathy requiring 11 units of packed red blood cells, 10 units of fresh-frozen plasma, 6 units of platelets, and 2,000 μg of factor VII. No other perioperative complications were observed, and by HD 9, hemolysis and coagulopathy improved without further need for blood transfusions. Per standard Vanderbilt anticoagulation protocol after CF-LVAD implantation, the patient was treated with aspirin (325 mg) and coumadin (goal INR 2–3). Clopidogrel (75 mg/day) was also initiated after surgery, given the recent placement of a drug-eluting stent. The patient was discharged home 16 days after HVAD implantation without additional bleeding events.
This case characterized the effects of a micro axial and a centrifugal CF-LVAD on vWF function in a single patient who sequentially received an Impella 5.0 and an HVAD device. Despite an uncomplicated surgical course, the patient experienced major perioperative bleeding. Before LT CF-LVAD implantation and during Impella support, an antiplatelet assay indicated that the patient’s aspirin regimen was nontherapeutic. This suggests that perioperative bleeding could be attributed, in part, to AVWS-mediated platelet dysfunction. Interestingly, 60 days after LT CF-LVAD implantation, hemolysis and anemia had completely resolved (Table 1); however, a residual but less impressive loss of vWF HMW multimers was observed (Figure 1). We propose that increased blood sheer stress from micro axial design and high pump speed in the Impella 5.0 contributed to the development of early AVWS and excessive perioperative bleeding when bridged to an LT CF-LVAD only 6 days after ST CF-LVAD implantation.
Nonsurgical bleeding in patients supported with CF-LVADs is multifactorial and partially related to AVWS-mediated platelet dysfunction.2,3,7,8 Previous studies have reported an association of AVWS with increased risk of gastrointestinal bleeding in LT CF-LVADs.5 This case describes the early development of AVWS-mediated platelet dysfunction resulting in increased surgical bleeding and transfusion requirements. The significant loss of vWF HMW multimers only 6 days after ST CF-LVAD implantation supports our hypothesis that AVWS was a possible etiology of these bleeding events. The early development of AVWS likely contributes to an increased risk of perioperative bleeding complications in patients who transition from ST CF-LVAD support to LT CF-LVADs. This case illustrates a qualitative recovery of vWF HMW multimers between ST axial and LT centrifugal CF-LVADs, thus demonstrating the variable and device-specific differences between hematologic profiles for each device type. For this reason, routine assessment of vWF profiles may assist clinicians in estimating operative bleeding risk and appropriate timing of surgery when transitioning from ST to LT devices. Furthermore, clinicians should carefully consider the choice between ST or LT device implantation in patients who are transplant candidates, given the increased risk of bleeding, transfusion requirements, and risk of donor-specific antibody development. Improving our understanding of hemostatic disturbances and associated surgical bleeding risk is critical for the management of these challenging patients.
The authors thank the Vanderbilt Advanced Heart Failure Registry for data acquisition and David Gailani for von Willebrand panel interpretation.
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