Nonsurgical bleeding in patients with axial-flow LVADs is driven by acquired von Willebrand disease, GI angiodysplasia, impaired platelet aggregation, and anticoagulation overuse.
This review highlights the mechanisms of nonsurgical bleeding in axial-flow LVAD patients and emphasizes the need for careful risk stratification to balance bleeding and thrombotic risks.
Axial-flow LVADs have become an integral tool in the management of end-stage heart failure. Consequently, nonsurgical bleeding has emerged as a major source of morbidity and mortality in this fragile population. The mechanisms responsible for these adverse events include acquired von Willebrand disease, GI tract angiodysplasia formation, impaired platelet aggregation, and overuse of anticoagulation therapy. Because of ongoing concerns for pump thrombosis and thromboembolic events, the thrombotic/bleeding paradigm has led to a difficult clinical dilemma for those managing patients treated with axial flow LVADs. As the field progresses, advances in the understanding of the pathological mechanisms underlying bleeding/thrombosis risk, careful risk stratification, and potential use of novel anticoagulants will all play a role in the management of the LVAD patient.
Suárez et al. (Tue,) conducted a review in End-stage heart failure with axial-flow LVADs. Axial-flow Left Ventricular Assist Devices (LVADs) was evaluated. Nonsurgical bleeding in patients with axial-flow LVADs is driven by acquired von Willebrand disease, GI angiodysplasia, impaired platelet aggregation, and anticoagulation overuse.
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