Digoxin did not reduce overall mortality, but it reduced the rate of hospitalization both overall and for worsening heart failure. These findings define more precisely the role of digoxin in the management of chronic heart failure.

Summary. Background: Mitral valve regurgitation is associated with an acquired hemostatic defect. Objective: We sought to assess the prevalence and severity of acquired von Willebrand syndrome in patients with native valve mitral regurgitation (MR). Patients/Methods: Fifty-three patients were prospectively observed with bleeding questionnaires and laboratory tests when undergoing an echocardiographic assessment of MR. In patients referred for mitral valve surgery, testing was repeated postoperatively. , respectively (all P < 0.001). Nine patients reported clinically significant bleeding, and seven had intestinal angiodysplasia and transfusion-dependent gastrointestinal bleeding (Heyde syndrome), with the median number of transfusions required being 20 . In patients who underwent mitral valve repair (n = 13) or replacement (n = 7), all measures of VWF function reported above improved significantly. Conclusion: The high-shear environment of moderate to severe MR is sufficient to produce prevalent perturbations in VWF activity.Acquired von Willebrand syndrome may occur in this setting, and appears to be reversible with mitral valve surgery.

We correlated von Willebrand factor activity indices and brain natriuretic peptide (BNP) with measures of aortic stenosis (AS) severity, bleeding, symptoms, and freedom from death or aortic valve replacement. Patients with AS (n=66 [16 mild, 20 moderate, 30 severe]) and aortic valve replacement (n=21) were assessed with VWF antigen (VWF:Ag), VWF latex agglutination immunoturbidic activity (VWF:Ltx), platelet function analyzer collagen plus adenosine diphosphate (PFA-CADP), VWF multimer ratio (VWF:mult ratio), and BNP level after echocardiography. In AS patients, mean gradient correlated with BNP (Spearman r=0.29, P=.02), VWF:Ltx/VWF:Ag (r=–0.41, P<.001), PFA-CADP (r=0.49, P<.001), and VWF:mult ratio (r=–0.76, P<.001). The area under the curve (95% CI) for detection of severe AS was 0.62 (0.48-0.77) by elevated BNP, 0.81 (0.69-0.92) by PFA-CADP closure time, 0.69 (0.55-0.82) by VWF:Ltx/VWF:Ag ratio, and 0.86 (0.76-0.95) by VWF:mult ratio. For VWF:mult ratio, a threshold of 0.15 yielded sensitivity and specificity for severe AS of 77% and positive predictive value of 74%. Bleeding (in 14%) was associated with prolonged PFA-CADP and reduced VWF:Ltx/VWF:Ag. Symptoms were associated with elevated BNP and low Duke Activity Status Index score. In 66 AS patients, freedom from death (n=4) or aortic valve replacement (n=22) was associated with PFA-CADP (P=.003), VWF high molecular weight multimers (HMWM) (P=.009), and VWF:Ltx/VWF:Ag (P<.001), but not BNP (P=.32). In severe AS vs aortic valve replacement, PFA-CADP and VWF:mult ratio differed (P<.001), but BNP and VWF:Ltx/VWF:Ag did not. In conclusion, VWF activity indices are associated with AS severity and bleeding, and predictive of cardiovascular outcome.

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