Anticoagulation in Patients with Heart Failure

R.   Sacha   Bhatia; Maral      Ouzounian; Jack   V.   Tu; Peter   P.   Liu; Douglas   S.   Lee

Abstract

The decision to anti-coagulate patients with heart failure (HF) is a difficult one, with limited data available to support clinical judgment. Thromboembolic complications, both arterial (stroke) and venous (deep vein thrombosis and pulmonary embolism), remain a significant cause of mortality and morbidity in this population. The pathophysiology of thrombogenesis in HF may be contextualized in the classic triad of stasis, endothelial dysfunction and hypercoagulability. Dilated cardiac chambers, reduced systolic function, and left ventricular aneurysm or thrombus have been suggested as potential contributing factors. HF is associated with activation of inflammatory and neuroendocrine pathways, leading to endothelial dysfunction and a prothrombotic state with dysregulated platelets and activation of the coagulation cascade. The epidemiology of thromboembolic events in HF is poorly defined. Most studies are retrospective and include patients with concurrent atrial fibrillation. The current body of health outcomes research is reviewed to identify the specific etiological factors, prevalence, and impact of thromboembolic events in this patient population. Conflicting analyses exist regarding the risks and benefits of prophylaxis in HF. The data surrounding several classes of therapeutic agents are synthesized. Recent clinical trials on anticoagulation and HF are reviewed, including WATCH, WASH, and WARCEF. The absence of compelling clinical trial data leaves many unanswered questions regarding systemic anticoagulation in patients with HF.

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