Javascript must be enabled to continue!
P4637Elevated von Willebrand factor (VWF) and factor VIII are associated with higher clinical SYNTAX score in patients with stable coronary artery disease
View through CrossRef
Abstract
Background
Von Willebrand factor (VWF plays) central role in thrombogenesis, and circulates in a noncovalent complex with factor VIII (FVIII), acting as a transporter protein and stabilizer. VW factor protects FVIII from proteolytic inactivation and concentrate it at site of endothelial injury. Raised plasma VWF factor is detected in case of endothelial damage and it has been considered as a useful marker of endothelial dysfunction. Increased plasma FVIII has been found in venous thromboembolism and in some clinical conditions associated with chronic inflammation. The connection between FVIII and more incidence of arterial thrombosis is, partly, due to increased platelet adhesion/aggregation, induced by VWF at sites of arterial wall damage. The correlation between VWF factor, FVIII levels and acute coronary syndrome is well documented, but there are no available dates regarding relation between plasma levels of VW factor, FVIII and the severity of coronary artery disease according to SYNTAX I (SS) and Clinical SYNTAX score (CSS).
Purpose
The aim of this study was to determine the association between levels of VW factor and FVIII and the severity of coronary artery disease according to SS and CSS.
Methods
A total of 82 patients with symptoms of stable angina underwent coronary angiography and were divided into three groups according to SS and CSS: Group I (<22 points), Group II (23–32), Group III (>33). We calculated Clinical SYNTAX multiplying the value of SYNTAX score with the modified ACEF score, based on the patients' left ventricular ejection fraction, age and creatinine clearance derived using the Cockcroft–Gault equation.
Results
There were positive association between plasma levels of VW factor and severity of CAD according to SYNTAX I (Group I: 1.16±0.59, Group II: 1.52±0.62, Group III 1.49±0.80, Kruskal Wallis p=0.040) and Clinical SYNTAX score (Group I: 1.15±0.53, Group II: 1.38±0.72, Group III 1.57±0.75, Kruskal Wallis p=0.034). VW factor levels were significantly higher in Group II and Group III compared to Group I (SS: Mann- Whitney p=0.023 and 0.071, respectively), (CSS: p=0.251 and 0.009, respectively). We also found positive association between FVIII levels and severity of CAD according to SYNTAX I (Group I: 2.25±0.75, Group II: 2.21±0.53, Group III 2.97±0.95, Kruskal Wallis p=0.007) and Clinical SYNTAX score (Group I: 2.17±0.71, Group II: 2.26±0.68, Group III 2.89±0.87, Kruskal Wallis p=0.002). This study demonstrates that FVIII levels were significantly higher in Group III compared to Group I and Group II (SS: Mann- Whitney p=0.005 and 0.005, respectively), (CSS: p=0.001 and 0.014, respectively).
The correlation between plasma levels of VW factor
Conclusion
Patients with stable angina pectoris and higher levels of VW and factor VIII had a higher Clinical SYNTAX and SYNTAX I score. Our study revealed that concomitant elevation in both VW and FVIII factors are a significant risk factor and predictor of more severe and extended CAD.
Title: P4637Elevated von Willebrand factor (VWF) and factor VIII are associated with higher clinical SYNTAX score in patients with stable coronary artery disease
Description:
Abstract
Background
Von Willebrand factor (VWF plays) central role in thrombogenesis, and circulates in a noncovalent complex with factor VIII (FVIII), acting as a transporter protein and stabilizer.
VW factor protects FVIII from proteolytic inactivation and concentrate it at site of endothelial injury.
Raised plasma VWF factor is detected in case of endothelial damage and it has been considered as a useful marker of endothelial dysfunction.
Increased plasma FVIII has been found in venous thromboembolism and in some clinical conditions associated with chronic inflammation.
The connection between FVIII and more incidence of arterial thrombosis is, partly, due to increased platelet adhesion/aggregation, induced by VWF at sites of arterial wall damage.
The correlation between VWF factor, FVIII levels and acute coronary syndrome is well documented, but there are no available dates regarding relation between plasma levels of VW factor, FVIII and the severity of coronary artery disease according to SYNTAX I (SS) and Clinical SYNTAX score (CSS).
Purpose
The aim of this study was to determine the association between levels of VW factor and FVIII and the severity of coronary artery disease according to SS and CSS.
Methods
A total of 82 patients with symptoms of stable angina underwent coronary angiography and were divided into three groups according to SS and CSS: Group I (<22 points), Group II (23–32), Group III (>33).
We calculated Clinical SYNTAX multiplying the value of SYNTAX score with the modified ACEF score, based on the patients' left ventricular ejection fraction, age and creatinine clearance derived using the Cockcroft–Gault equation.
Results
There were positive association between plasma levels of VW factor and severity of CAD according to SYNTAX I (Group I: 1.
16±0.
59, Group II: 1.
52±0.
62, Group III 1.
49±0.
80, Kruskal Wallis p=0.
040) and Clinical SYNTAX score (Group I: 1.
15±0.
53, Group II: 1.
38±0.
72, Group III 1.
57±0.
75, Kruskal Wallis p=0.
034).
VW factor levels were significantly higher in Group II and Group III compared to Group I (SS: Mann- Whitney p=0.
023 and 0.
071, respectively), (CSS: p=0.
251 and 0.
009, respectively).
We also found positive association between FVIII levels and severity of CAD according to SYNTAX I (Group I: 2.
25±0.
75, Group II: 2.
21±0.
53, Group III 2.
97±0.
95, Kruskal Wallis p=0.
007) and Clinical SYNTAX score (Group I: 2.
17±0.
71, Group II: 2.
26±0.
68, Group III 2.
89±0.
87, Kruskal Wallis p=0.
002).
This study demonstrates that FVIII levels were significantly higher in Group III compared to Group I and Group II (SS: Mann- Whitney p=0.
005 and 0.
005, respectively), (CSS: p=0.
001 and 0.
014, respectively).
The correlation between plasma levels of VW factor
Conclusion
Patients with stable angina pectoris and higher levels of VW and factor VIII had a higher Clinical SYNTAX and SYNTAX I score.
Our study revealed that concomitant elevation in both VW and FVIII factors are a significant risk factor and predictor of more severe and extended CAD.
Related Results
Laboratory Diagnosis and Molecular Classification of von Willebrand Disease
Laboratory Diagnosis and Molecular Classification of von Willebrand Disease
A complete set of laboratory investigations, including bleeding time, PFA-100 closure times, factor VIII (FVIII) coagulant activity (FVIII:C), von Willebrand factor (VWF) ristoceti...
Acquired Von Willebrand Syndrome In Mitral Valve Leak
Acquired Von Willebrand Syndrome In Mitral Valve Leak
Abstract
Abstract 4657
Background
Several studies have shown that between 15% to 25% of patients with severe aort...
Early Onset of Coronary Subclavian Steal Syndrome: A Case Report and Literature Review
Early Onset of Coronary Subclavian Steal Syndrome: A Case Report and Literature Review
Abstract
Introduction
Coronary subclavian steal syndrome (CSSS) is a rare phenomenon that often goes undiagnosed and causes severe complications, including death. This report prese...
The Middle and Distal Carboxyl Terminal Domains of ADAMTS13 Are Critical for Docking ADAMTS13 to von Willebrand Factor.
The Middle and Distal Carboxyl Terminal Domains of ADAMTS13 Are Critical for Docking ADAMTS13 to von Willebrand Factor.
Abstract
ADAMTS13 cleaves von Willebrand factor (VWF) at the Tyr1605-Met1606 bond of the central A2 domain. However, the domains of ADAMTS13 required for recognition...
FVIII and VWF PK: Key Aspects in Safety and Efficiency of VWF Concentrates. Review and Reflection
FVIII and VWF PK: Key Aspects in Safety and Efficiency of VWF Concentrates. Review and Reflection
Introduction: Long-term prophylaxis in Von Willebrand Disease (VWD) with a severe or frequent bleeding phenotype generates great interest. Additionally, there is a discrepancy rega...
C2362F mutation gives rise to an ADAMTS13-resistant von Willebrand factor
C2362F mutation gives rise to an ADAMTS13-resistant von Willebrand factor
Summaryvon Willebrand factor (VWF) multimers result from proteolysis by the metalloprotease ADAMTS13. Since C2362F-VWF features abnormally large multimers with their triplet oligom...
Altered Von Willebrand Factor Subunit Proteolysis and Multimer Processing Associated with the Cys1599(2362)Phe Mutation in the B2 Domain.
Altered Von Willebrand Factor Subunit Proteolysis and Multimer Processing Associated with the Cys1599(2362)Phe Mutation in the B2 Domain.
Abstract
Cysteine residues clustered in carboxyl- and amino-terminal domains mediate the assembly of von Willebrand factor (VWF) subunits into dimers and multimers, ...
Emerging Evidence of IgG4-Related Disease in Pericarditis: A Systematic Review
Emerging Evidence of IgG4-Related Disease in Pericarditis: A Systematic Review
Abstract
Introduction
Immunoglobulin G4-related disease (IgG4-RD) is a recently identified immune-mediated condition that is debilitating and often overlooked. While IgG4-RD has be...

