Antiplatelet and anticoagulation strategies for left ventricular assist devices

Abstract

Left ventricular assist devices (LVAD) have revolutionized the management of advanced heart failure. However, complications rates remain high, among which hemorrhagic and thrombotic complications are the most important. Antiplatelet and anticoagulation strategies form a cornerstone of LVAD management and may directly affect LVAD complications. Concurrently, LVAD complications influence anticoagulation and anticoagulation management. A thorough understanding of device, patient, and management, including anticoagulation and antiplatelet therapies, are important in optimizing LVAD outcomes. This article provides a comprehensive state of the art review of issues related to antiplatelet and anticoagulation management in LVADs. We start with a historical overview, the epidemiology and pathophysiology of bleeding and thrombotic complications in LVADs. We then discuss platelet and anticoagulation biology followed by considerations prior to, during, and after LVAD implantation. This is followed by discussion of anticoagulation and the management of thrombotic and hemorrhagic complications. Specific problems, including management of heparin-induced thrombocytopenia, anticoagulant reversal, novel oral anticoagulants, artificial heart valves, and noncardiac surgeries are covered in detail.

Keywords: Heart failure (HF); anticoagulation; antiplatelet; left ventricular assist devices (LVAD).

Figure 1

Interrelations between patient, LVAD and exogenous factors that lead to specific predisposition to thrombotic or bleeding events. DM, diabetes mellitus; HTN, hypertension; RV, right ventricle; vWF, von Wilebrand Factor; deg: degradation; EC act, endothelial cell activation; Plat act, platelet activation; LVAD, left ventricular assist device.

Figure 2

Platelet and Clotting cascade in LVAD patients. (A) Inactive platelets and its receptors and granules. (B) Hemostatic response to denuded endothelium. Panel depicts platelet activation (adhesion, aggregation, degranulation) and their interaction with the clotting cascade. (C) Depicts the multiple pharmacological targets to interfere with platelet function and clotting cascade. (D) Depicts the LVAD as a source of shear stress and foreign material that leads to platelet activation, vWF degradation. LVAD, left ventricular assist device; AA, arachidonic acid; ADP, adenosine diphosphate; AT3, antithrombin 3; GP, glycoprotein; LVAD, left ventricular assist device; vWF, von Willebrand factor.