von Willebrand factor Ristocetin co-factor activity to von Willebrand factor antigen level ratio for diagnosis of acquired von Willebrand syndrome caused by aortic stenosis.

VWF Ristocetin co-factor activity VWF:RCo/VWF:Ag acquired von Willebrand syndrome aortic stenosis von Willebrand factor

Journal

Research and practice in thrombosis and haemostasis
ISSN: 2475-0379
Titre abrégé: Res Pract Thromb Haemost
Pays: United States
ID NLM: 101703775

Informations de publication

Date de publication:
Jan 2024
Historique:
received: 20 02 2023
revised: 15 11 2023
accepted: 16 11 2023
medline: 25 1 2024
pubmed: 25 1 2024
entrez: 25 1 2024
Statut: epublish

Résumé

Severe aortic stenosis (AS) causes acquired von Willebrand syndrome by the excessive shear stress-dependent cleavage of high molecular weight multimers of von Willebrand factor (VWF). While the current standard diagnostic method is so-called VWF multimer analysis that is western blotting under nonreducing conditions, it remains unclear whether a ratio of VWF Ristocetin co-factor activity (VWF:RCo) to VWF antigen levels (VWF:Ag) of <0.7, which can be measured with an automated coagulation analyzer in clinical laboratories and is used for the diagnosis of hereditary von Willebrand disease. To evaluated whether the VWF:RCo/VWF:Ag is useful for the diagnosis of AS-induced acquired von Willebrand syndrome. VWF:RCo and VWF:Ag were evaluated with the VWF large multimer index as a reference, which represents the percentage of a patient's VWF high molecular weight multimer ratio to that of standard plasma in the VWF multimer analysis. We analyzed 382 patients with AS having transaortic valve maximal pressure gradients of >30 mmHg, 27 patients with peripheral artery disease, and 46 control patients free of cardiovascular disease with osteoarthritis, diabetes, and so on. We assumed a large multimer index of <80% as loss of VWF large multimers since 59.0% of patients with severe AS had the indices of <80%, while no control patients or patients with peripheral artery disease, except for 2 patients, exhibited the indices of <80%. The VWF:RCo/VWF:Ag ratios, measured using an automated blood coagulation analyzer, were correlated with the indices (r VWF:RCo/VWF:Ag ratios of <0.7 may indicate loss of VWF large multimers with high specificity, but low sensitivity. VWF:RCo/VWF:Ag ratios in patients with AS having a ratio of <0.7 may be useful for monitoring the loss of VWF large multimers during their clinical courses.

Sections du résumé

Background UNASSIGNED
Severe aortic stenosis (AS) causes acquired von Willebrand syndrome by the excessive shear stress-dependent cleavage of high molecular weight multimers of von Willebrand factor (VWF). While the current standard diagnostic method is so-called VWF multimer analysis that is western blotting under nonreducing conditions, it remains unclear whether a ratio of VWF Ristocetin co-factor activity (VWF:RCo) to VWF antigen levels (VWF:Ag) of <0.7, which can be measured with an automated coagulation analyzer in clinical laboratories and is used for the diagnosis of hereditary von Willebrand disease.
Objectives UNASSIGNED
To evaluated whether the VWF:RCo/VWF:Ag is useful for the diagnosis of AS-induced acquired von Willebrand syndrome.
Methods UNASSIGNED
VWF:RCo and VWF:Ag were evaluated with the VWF large multimer index as a reference, which represents the percentage of a patient's VWF high molecular weight multimer ratio to that of standard plasma in the VWF multimer analysis.
Results UNASSIGNED
We analyzed 382 patients with AS having transaortic valve maximal pressure gradients of >30 mmHg, 27 patients with peripheral artery disease, and 46 control patients free of cardiovascular disease with osteoarthritis, diabetes, and so on. We assumed a large multimer index of <80% as loss of VWF large multimers since 59.0% of patients with severe AS had the indices of <80%, while no control patients or patients with peripheral artery disease, except for 2 patients, exhibited the indices of <80%. The VWF:RCo/VWF:Ag ratios, measured using an automated blood coagulation analyzer, were correlated with the indices (r
Conclusion UNASSIGNED
VWF:RCo/VWF:Ag ratios of <0.7 may indicate loss of VWF large multimers with high specificity, but low sensitivity. VWF:RCo/VWF:Ag ratios in patients with AS having a ratio of <0.7 may be useful for monitoring the loss of VWF large multimers during their clinical courses.

Identifiants

pubmed: 38268521
doi: 10.1016/j.rpth.2023.102284
pii: S2475-0379(23)05712-6
pmc: PMC10805667
doi:

Types de publication

Journal Article

Langues

eng

Pagination

102284

Informations de copyright

© 2023 The Author(s).

Auteurs

Noriyuki Okubo (N)

Department of Clinical Laboratory Medicine, Tohoku University Hospital, Sendai, Japan.

Shingo Sugawara (S)

Department of Clinical Laboratory Medicine, Tohoku University Hospital, Sendai, Japan.

Tohru Fujiwara (T)

Department of Clinical Laboratory Medicine, Tohoku University Hospital, Sendai, Japan.
Department of Hematology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Ko Sakatsume (K)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.
Division of Cardiovascular Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.

Tsuyoshi Doman (T)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Mihoko Yamashita (M)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Kota Goto (K)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Masaki Tateishi (M)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Misako Suzuki (M)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Ryutaro Shirakawa (R)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yuka Eura (Y)

Department of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Japan.

Koichi Kokame (K)

Department of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Japan.

Masaki Hayakawa (M)

Department of Blood Transfusion Medicine, Nara Medical University, Kashihara, Japan.

Masanori Matsumoto (M)

Department of Blood Transfusion Medicine, Nara Medical University, Kashihara, Japan.

Yasunori Kawate (Y)

Medical Affairs 2, Medical & Scientific Affairs, Sysmex Corporation, Kobe, Japan.

Mizuki Miura (M)

Department of Cardiology, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Hiroshi Takiguchi (H)

Department of Cardiology, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Yoshimitsu Soga (Y)

Department of Cardiology, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Shinichi Shirai (S)

Department of Cardiology, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Kenji Ando (K)

Department of Cardiology, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Yoshio Arai (Y)

Department of Cardiovascular Surgery, Kokura Memorial Hospital, Kokura-kitaku, Kitakyushu, Japan.

Takaharu Nakayoshi (T)

Division of Cardiovascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.

Yoshihiro Fukumoto (Y)

Division of Cardiovascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.

Hiroyuki Takahama (H)

Cardiovascular Department, National Cerebral and Cardiovascular Center, Suita, Japan.
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Satoshi Yasuda (S)

Cardiovascular Department, National Cerebral and Cardiovascular Center, Suita, Japan.
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Toshihiro Tamura (T)

Department of Cardiology, Tenri Hospital, Tenri, Japan.

Shin Watanabe (S)

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Takeshi Kimura (T)

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Nobuhiro Yaoita (N)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Hiroaki Shimokawa (H)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yoshikatsu Saiki (Y)

Division of Cardiovascular Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.

Koichi Kaikita (K)

Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Center for Metabolic Regulation of Healthy Aging, Kumamoto University, Kumamoto, Japan.

Kenichi Tsujita (K)

Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Center for Metabolic Regulation of Healthy Aging, Kumamoto University, Kumamoto, Japan.

Shinji Yoshii (S)

Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Hiroshi Nakase (H)

Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Shin-Ichi Fujimaki (SI)

Department of Clinical Laboratory Medicine, Tohoku University Hospital, Sendai, Japan.

Hisanori Horiuchi (H)

Department of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University Graduate School of Medicine, Sendai, Japan.

Classifications MeSH