04/26/2026
Left ventricular assist devices (LVADs) are becoming more prevalent as a bridge-to-transplantation (BTT) or destination therapy (DT) in patients with refractory heart failure. These patients often develop gastrointestinal (GI) bleeds requiring transfusion and endoscopic interventions. But why? 🤔
By unloading the LV with an LVAD, many patients can no longer generate the conditions required to open their aortic valve as often (if at all). Therefore, their LV cardiac output is through the LVAD in a “continuous flow” mode of circulation. These patients often don’t have palpable pulses and have small pulse pressures. 😱
Patients can develop acquired von Willebrand disease (vWD) due to LVAD motor shear forces that destroy high-molecular-weight vWF multimers. These multimeters normally stabilize the platelet plug of primary hemostasis. Furthermore, a low pulse pressure results in relative hypoperfusion of the GI tract. In response, submucosal vascular proliferation occurs. So now you have extra blood vessels in a patient with defective platelet aggregation and on pharmacologic anticoagulation (heparin, Coumadin). No wonder they bleed! 🩸
GI bleeding from angiodysplasia in the context of aortic stenosis (Heyde’s syndrome) has a similar mechanism. Interestingly, in prior studies, vWF multimeter levels increased once pulsatility was regained in LVADs or after an aortic valve replacement in Heyde’s. 😷
Addressing this recurring issue can be extremely challenging! If one decreases the LVAD pump speed to increase native pulsatility, they risk overt heart failure (the patient has an LVAD for a reason!) If anticoagulation is decreased, the risk of clot formation increases. This remains an interesting area of research. 🤓
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