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Effects of warfarin on markers of hypercoagulability in patients with heart failure
S M Jafri1, E F Mammen, J Masura
1Henry Ford Hospital, Heart & Vascular Institute, Detroit, Mich. 48202, USA.
Insights
Warfarin therapy significantly reduced markers of a hypercoagulable state in heart failure patients. This study demonstrates that warfarin can effectively modify the prothrombotic condition associated with heart failure.
Area of Science:
- Cardiology
- Hematology
- Clinical Trials
Background:
- Heart failure is frequently associated with a hypercoagulable state, increasing thrombotic risk.
- Elevated levels of thrombin/antithrombin III (TAT) complexes, prothrombin fragment F1 + 2, and D-dimers indicate hypercoagulability in heart failure patients.
Purpose of the Study:
- To investigate whether warfarin therapy can modify the hypercoagulable state observed in patients with heart failure.
- To compare the effects of warfarin versus placebo on key markers of coagulation.
Main Methods:
- A randomized, double-blind, placebo-controlled trial involving 76 heart failure patients.
- Measurement of plasma TAT complexes, F1 + 2, and D-dimers at baseline and at 1, 2, and 3 months.
- Evaluation of low-intensity (INR 1.3) versus moderate-intensity (INR 2.3) warfarin in a subset of patients.
Main Results:
- Warfarin therapy significantly decreased TAT complexes, F1 + 2, and D-dimers compared to baseline (p < 0.002, p < 0.001, p < 0.001, respectively).
- Placebo group showed persistent elevations in these markers throughout the follow-up period.
- Moderate-intensity warfarin further reduced F1 + 2 levels compared to low-intensity warfarin (p < 0.001).
Conclusions:
- Warfarin therapy effectively modifies the hypercoagulable state in patients with heart failure.
- The findings support the use of warfarin in managing thrombotic risk associated with heart failure.
Abstract:
Heart failure is associated with a hypercoagulable state. A single-center, randomized, double-blind, placebo-controlled trial was performed to test the hypothesis that warfarin will modify a hypercoagulable state in heart failure. This study included 76 patients with heart failure. At baseline, patients had evidence for a hypercoagulable state with elevated plasma levels of thrombin/antithrombin III (TAT) complexes (3.4 +/- 2.0 ng/ml), prothrombin fragment F1 + 2 (1.5 +/- 0.9 nmol/L), and D-dimers (630 +/- 401 ng/ml). Warfarin therapy (international normalized ratio [INR] 2.7 +/- 1.3) significantly decreased plasma levels of TAT complexes (p < 0.002), F1 + 2 (p < 0.001), and D-dimers (p < 0.001) when compared with baseline values at 1, 2, and 3 months of therapy. In contrast, patients receiving placebo had persistent elevation of TAT complexes (p = not significant [NS]), F1 + 2 (p = NS), and D-dimers (p = NS) during follow-up at 1, 2, and 3 months. The two treatment groups followed different trends over time for all three markers (p < 0.001). The effect of low-intensity warfarin (INR 1.3 +/- 0.08) versus moderate-intensity warfarin (INR 2.3 +/- 1.1 ) on markers of hypercoagulability was evaluated in 14 patients. When compared with baseline, low-intensity warfarin administration decreased plasma levels of TAT complexes (p = NS), F1 + 2 (p = 0.05), and D-dimers (p = 0.04). In these patients F1 + 2 was further reduced with moderate-intensity warfarin (p < 0.001). Our findings suggest that a hypercoagulable state in heart failure can be modified by warfarin therapy.