Restoration of von Willebrand factor after transcatheter aortic valve replacement-A possible cause for posttranscatheter aortic valve replacement thrombocytopenia?

OBJECTIVES: The aim of the current study was to analyze the clinical and procedural predictors of thrombocytopenia and the relationship between the decrease in platelet count (DPC) and change in vWF function (ΔvWF) after transcatheter aortic valve replacement (TAVR). BACKGROUND: TAVR often causes temporary thrombocytopenia. At the same time, TAVR leads to a restoration of von Willebrand factor (vWF) function. METHODS: One hundred and forty-one patients with severe aortic stenosis undergoing TAVR were included in the study. Platelet count and vWF function (vWF:Ac/Ag ratio) were assessed at baseline and 6 h after TAVR. Thrombocytopenia was defined as platelet count <150/nL. RESULTS: Median platelet count at baseline was 214/nL (interquartile range [IQR]: 176-261) and decreased significantly to 184/nL (IQR: 145-222) 6 h after TAVR. The number of patients with thrombocytopenia increased from 12.8% at baseline to 29.1% after 6 h. DPC 6 h after TAVR showed a significant correlation with ΔvWF (r = - 0.254, p = 0.002). Patients with DPC > 20% had significantly higher ΔvWF (10.9% vs. 6.5%, p = 0.021). Obese patients showed a significantly lower DPC (11.8% vs. 19.9%, p = 0.001). In multivariate analysis, ΔvWF 6 h after TAVR was the only significant predictor for DPC > 20% (p = 0.017). CONCLUSIONS: The restoration of vWF after TAVR is a significant predictor for DPC after TAVR. An increased platelet consumption due to vWF restoration could play a key role in the development of thrombocytopenia after TAVR.

The impact of bicuspid aortic valve morphology on von Willebrand factor function in patients with severe aortic stenosis and its change after TAVI.

BACKGROUND: Aortic stenosis (AS) can cause acquired von Willebrand syndrome (AVWS) and valve replacement has been shown to lead to von Willebrand factor (vWF) recovery. The aim of the current study was to investigate the prevalence of AVWS in different severe AS phenotypes and its course after transcatheter aortic valve implantation (TAVI). METHODS: 143 patients with severe AS undergoing TAVI were included in the study. vWF function was assessed at baseline, 6 and 24 h after TAVI. AVWS was defined as a reduced vWF:Ac/Ag ratio ≤ 0.7. Phenotypes were classified by tricuspid (TAV) and bicuspid (BAV) valve morphology, mean transvalvular gradient (Pmean), stroke volume index (SVI), ejection fraction (EF) and indexed effective orifice area (iEOA). RESULTS: AVWS was present in 36 (25.2%) patients before TAVI. vWF:Ac/Ag ratio was significantly lower in high gradient compared to low-gradient severe AS [0.78 (IQR 0.67-0.86) vs. 0.83 (IQR 0.74-0.93), p < 0.05] and in patients with BAV compared to TAV [0.70 (IQR 0.63-0.78) vs. 0.81 (IQR 0.71-0.89), p < 0.05]. Normalization of vWF:Ac/Ag ratio was achieved in 61% patients 24 h after TAVI. As in the overall study cohort, vWF:Ac/Ag ratio increased significantly in all severe AS subgroups 6 h after TAVI (each p < 0.05). Regarding binary logistic regression analysis, BAV was the only significant predictor for AVWS. CONCLUSIONS: BAV morphology is a strong predictor for AVWS in severe AS. TAVI restores vWF function in most patients with severe AS independently of AS phenotype and valve morphology.