At baseline, there was a decrease in the structural integrity of vWF HMWMs that correlated with increasing heart failure severity as measured by the Interagency Registry for Mechanically Assisted Circulatory Support profile.
Significantly, the A2 disulfide bond is cleaved in ~75% of VWF subunits in healthy human donor plasma but in just ~25% of plasma VWF subunits from heart failure patients who have received extracorporeal membrane oxygenation support.
In the multivariable analysis, higher vWF concentrations (middle tertile hazard ratio [HR] 4.59, 95% confidence interval [CI] 1.55-13.50 [P=0.006]; upper tertile HR 4.10, 95% CI 1.43-11.75 [P=0.009]), age≥75years (HR 5.02, 95% CI 1.53-16.49; P=0.008), heart failure (HR 2.05, 1.01-4.19; P=0.048), C-reactive protein, log<sub>2</sub> per unit increase (HR 1.29, 95% CI 1.04-1.61; P=0.021), no warfarin at discharge (HR 4.96, 95% CI 2.02-12.20; P<0.0001) and no aspirin at discharge (HR 4.41, 95% CI 1.71-11.97; P=0.002) were independently associated with an increased risk of stroke and all-cause death, whereas female sex was a protective factor (HR 0.35, 0.16-0.78; P=0.01).
We have examined the association between the coagulation markers fibrinogen, von Willebrand Factor (VWF), Factors VII, VIII and IX, D-dimer, activated protein C (APC) and activated partial thromboplastin time (aPPT) with NT-proBNP and incident HF.
Compared with those with no daytime sleep, men with daytime sleep >1 hour, defined as excessive daytime sleepiness (EDS), had a higher risk of raised N-terminal pro-brain natriuretic peptide of ≥400 pg/mL, the diagnostic threshold for HF (OR (95% CI)=1.88 (1.15 to 3.1)), higher mean troponin, reduced lung function (forced expiratory volume in 1 s) and elevated von Willebrand factor, a marker of endothelial dysfunction.