doi: 10.1161/CIRCULATIONAHA.107.729988
(Circulation. 2008;117:e8.)
© 2008 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article, "Risk of Thromboembolism in Heart Failure: An Analysis from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT)"
Center for Advanced Heart Failure Lehigh Valley Hospital and Health Network, Allentown, PA
Duke Clinical Research Institute, Durham, NC
Mount Sinai School of Medicine, New York, NY
University of Washington, Seattle, Wash
Seattle Institute for Cardiac Research, Seattle, Wash
for the SCD-HeFT Investigators
We appreciate the comments of Dr. De Boer and colleagues, who ask important questions about the effects of anticoagulant treatment and the characteristics of those patients who experienced thromboembolic events. As we mentioned in the article, it is difficult to accurately assess the effects of warfarin or aspirin in the SCD-HeFT database for several reasons, the most important of which being that such therapy was not randomized.1 On entering the trial, 28% of the patients were taking warfarin and 59% were taking aspirin. These proportions changed substantially during the 45.5 months median follow-up; of those patients taking an antithrombotic agent at entry, 13% discontinued therapy and 14% switched from one type of agent to another over the course of the trial. Furthermore, neither the diagnosis of thromboembolic events nor the intensity of anticoagulant therapy was specified by protocol.
Although we identified some predictors of thromboembolism, the relatively small number of events makes it likely that some predictors would not be detected by multivariable analysis, while the predictive value of others may be overestimated. As in virtually all studies of ischemic events in patients with heart failure, an unknown proportion of the ischemic events we observed may have been due to hypertension, atherosclerosis, or other vascular disease, rather than to cardiogenic embolism.
We agree that a controlled clinical trial of aspirin versus warfarin with well-defined and adjudicated events, close regulation of anticoagulation intensity, and careful tracking and analysis of events in those patients who change therapy or develop an accepted indication for anticoagulation is vital to a better understanding of these issues. Like Dr De Boer and colleagues, we eagerly await the results of the ongoing Warfarin Aspirin Reduced Cardiac Ejection Fraction (WARCEF) trial.2
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Acknowledgments |
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Sources of Funding
This work was supported by grants from the National Institutes of Health–National Institute of Neurological Disorders and Stroke (U01 NS4397510 to Dr Freudenberger) and by grants from the National Heart, Lung, and Blood Institute (UO1 HL55766, UO1 HL55297, and UO1 HL55496 to Drs Bardy, Lee, Mark, Poole, and Anderson).
Disclosures
None.
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References |
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 Top References |
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1. Freudenberger RS, Hellkamp AS, Halperin JL, Poole J, Anderson J, Johnson G, Mark DB, Lee KL, Bardy GH; for the SCD-HeFT Investigators. Risk of thromboembolism in heart failure: an analysis from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). Circulation. 2007; 115: 2637–2641.
2. Pullicino P, Thompson JL, Barton B, Levin B, Graham S, Freudenberger RS; on behalf of the WARCEF Investigators. Warfarin versus aspirin in patients with reduced cardiac ejection fraction (WARCEF): rationale, objectives, and design. J Card Fail. 2006; 12: 39–46.[CrossRef][Medline] [Order article via Infotrieve]
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