The impact of bicuspid aortic valve morphology on von Willebrand factor function in patients with severe aortic stenosis and its change after TAVI.
Acquired von Willebrand syndrome
Aortic stenosis
Bicuspid aortic valve
Transcatheter aortic valve implantation
von Willebrand factor
Journal
Clinical research in cardiology : official journal of the German Cardiac Society
ISSN: 1861-0692
Titre abrégé: Clin Res Cardiol
Pays: Germany
ID NLM: 101264123
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
10
02
2022
accepted:
30
05
2022
pubmed:
16
7
2022
medline:
25
11
2022
entrez:
15
7
2022
Statut:
ppublish
Résumé
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). 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 (P 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. 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.
Sections du résumé
BACKGROUND
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
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 (P
RESULTS
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
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.
Identifiants
pubmed: 35838799
doi: 10.1007/s00392-022-02047-6
pii: 10.1007/s00392-022-02047-6
pmc: PMC9681694
doi:
Substances chimiques
von Willebrand Factor
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1348-1357Informations de copyright
© 2022. The Author(s).
Références
Int J Cardiol. 2020 Jan 1;298:83-84
pubmed: 31629565
J Thromb Haemost. 2006 Oct;4(10):2103-14
pubmed: 16889557
Circulation. 2005 Feb 22;111(7):920-5
pubmed: 15710758
N Engl J Med. 2003 Jul 24;349(4):343-9
pubmed: 12878741
Biomech Model Mechanobiol. 2012 Sep;11(7):1085-96
pubmed: 22294208
Can J Cardiol. 2015 Jun;31(6):738-43
pubmed: 25935884
J Am Soc Echocardiogr. 2019 Apr;32(4):431-475
pubmed: 30797660
J Thromb Thrombolysis. 2019 Nov;48(4):610-618
pubmed: 31359325
N Engl J Med. 2012 Nov 15;367(20):1954-6
pubmed: 23150964
Blood Adv. 2021 Jan 12;5(1):280-300
pubmed: 33570651
N Engl J Med. 2016 Nov 24;375(21):2067-2080
pubmed: 27959741
Thromb Res. 2017 Mar;151:23-28
pubmed: 28088607
Haemophilia. 2016 Jul;22 Suppl 5:54-9
pubmed: 27405677
Eur J Cardiothorac Surg. 2012 Nov;42(5):S45-60
pubmed: 23026738
J Am Coll Cardiol. 2019 Mar 12;73(9):1078-1088
pubmed: 30846101
Eur Heart J. 2017 Sep 21;38(36):2739-2791
pubmed: 28886619
J Atheroscler Thromb. 2019 Apr 1;26(4):303-314
pubmed: 30867356
J Am Coll Cardiol. 2013 Feb 12;61(6):687-9
pubmed: 23391203
N Engl J Med. 2016 Jul 28;375(4):335-44
pubmed: 27464202
Transfus Apher Sci. 2018 Dec;57(6):721-723
pubmed: 30401518
Clin Appl Thromb Hemost. 2017 Apr;23(3):229-234
pubmed: 27481874
Ann Thorac Surg. 1987 Nov;44(5):514-6
pubmed: 3499881
Eur Heart J Cardiovasc Imaging. 2017 Mar 1;18(3):254-275
pubmed: 28363204
Circ Res. 2015 Mar 27;116(7):1193-201
pubmed: 25670067
JACC Cardiovasc Interv. 2015 Apr 27;8(5):692-700
pubmed: 25946442
J Am Coll Cardiol. 2020 Sep 1;76(9):1018-1030
pubmed: 32854836