Despite numerous investigations, to my knowledge, we have not yet solved the mystery of the effect of antithrombotic therapy on clinical outcomes in patients with heart failure (HF) in the absence of atrial fibrillation. The COMMANDER HF (A Study to Assess the Effectiveness and Safety of Rivaroxaban in Reducing the Risk of Death, Myocardial Infarction, or Stroke in Participants with Heart Failure and Coronary Artery Disease Following an Episode of Decompensated Heart Failure) trial1 failed to show a difference in the primary end point of all-cause mortality, myocardial infarction (MI), or stroke between 2.5 mg of rivaroxaban twice daily and placebo with background antiplatelet therapy in patients with recent worsening of chronic HF, reduced left ventricular ejection fraction, coronary artery disease, and sinus rhythm. In this issue of JAMA Cardiology, Greenberg et al2 published an additional analysis that showed improvement with rivaroxaban in a composite of events associated with thromboembolism—MI, ischemic stroke, and symptomatic pulmonary embolism or deep venous thrombosis with or without sudden cardiac death (SCD) or unwitnessed death. The findings are not unexpected, since the rates of the parent trial’s primary end point components of MI and stroke were numerically reduced by rivaroxaban. The authors appropriately conclude that these findings are hypothesis-generating but that they support continued examination of the role of antithrombotic treatment in patients with HF.
Konstam MA. Antithrombotic Therapy in Heart Failure—The Clot Thickens. JAMA Cardiol. 2019;4(6):524–525. doi:10.1001/jamacardio.2019.1108
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