Anticoagulation in heart failure: current status and future direction
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Anticoagulation in heart failure: current status and future direction Mihai Gheorghiade • Muthiah Vaduganathan • Gregg C. Fonarow • Stephen J. Greene • Barry H. Greenberg • Peter P. Liu • Barry M. Massie Mandeep R. Mehra • Marco Metra • Faiez Zannad • John G. F. Cleland • Dirk J. van Veldhuisen • Ami N. Shah • Javed Butler
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Ó Springer Science+Business Media, LLC 2012
Abstract Despite therapeutic advances, patients with worsening heart failure (HF) requiring hospitalization have unacceptably high post-discharge mortality and re-admission rates soon after discharge. Evidence suggests a hypercoagulable state is present in patients with HF. Although thromboembolism as a direct consequence of HF is not frequently clinically recognized, it may contribute to mortality and morbidity. Additionally, many patients with HF have concomitant disorders conferring additional thrombotic risk, including atrial fibrillation (AF) and coronary artery disease (CAD). Acute coronary syndrome (ACS), a known consequence of coronary thrombosis, is a common precipitating
factor for worsening HF. Coronary thrombosis may also cause sudden death in patients with HF and CAD. Because data are largely derived from observational studies or trials of modest size, guideline recommendations on anticoagulation for HF vary between organizations. The recently presented Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction trial of HF patients in sinus rhythm suggested anticoagulation reduces the risk of stroke, although rates of the combined primary endpoint (death, ischemic stroke, or intracerebral hemorrhage) were similar for acetylsalicylic acid and warfarin. Newer oral anticoagulants dabigatran, apixaban, and rivaroxaban have successfully
M. Gheorghiade (&) S. J. Greene A. N. Shah Center for Cardiovascular Innovation, Northwestern University Feinberg School of Medicine, 645 N. Michigan Avenue, Suite 1006, Chicago, IL 60611, USA e-mail: [email protected]
M. R. Mehra Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
M. Vaduganathan Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA G. C. Fonarow UCLA Division of Cardiology, Ahmanson-UCLA Cardiomyopathy Center, Los Angeles, CA, USA B. H. Greenberg Division of Cardiovascular Medicine, Sulpizio Cardiovascular Center, University of California, San Diego, CA, USA P. P. Liu The Heart and Stroke/Richard Lewar Centre and Peter Munk Cardiac Centre, University Health Network, University of Toronto, Toronto, ON, Canada B. M. Massie Cardiology Division, San Francisco Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, CA, USA
M. Metra Cardiology, Department of Experimental and Applied Medicine, University of Brescia, Brescia, Italy F. Zannad Department of Cardiology, INSERM, Centre d’Investigation Clinique 9501 and Unite´ 961, Centre Hospitalier Universitaire, Nancy University, Nancy, France J. G. F. Cleland Department of Cardiology, Academic Unit, Postgraduate Medical Institute, Un
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