Association studies between -1185A/G von Willebrand factor gene polymorphism and coronary artery disease
Related Experiment Video
Updated: Sep 25, 2026

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
D Simon1, C A Paludo, G C Ghisleni
1Departamento de Genética, Instituto de Biociências, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, São Paulo, SP, Brasil. israberg@ufrgs.br
Abstract:
High levels of von Willebrand factor (vWF) have been associated with cardiovascular disease. The A allele of the -1185A/G polymorphism in the 5'-regulatory region of the vWF gene was associated with the highest plasma vWF levels in a normal population. To examine the association between -1185A/G polymorphism and coronary artery disease (CAD), 173 Brazilian Caucasian subjects submitted to coronary angiography were studied. Of these, 57 (33%) had normal coronary arteries (control group) and 116 (67%) had CAD (patient group). Plasma vWF levels were higher in patients (145 U/dl) than in controls (130 U/dl), but the differences were significant only for O blood group subjects. Polymerase chain reaction amplification of the 864-bp vWF promoter region followed by AccII restriction digestion was used to identify the -1185A/G genotypes. The -1185A allele frequency was 43.1% in patients and 44.7% in controls. Allele and genotype frequencies were not significantly different between patients and controls. No association was observed between the -1185A/G genotypes and plasma vWF levels in patients or controls. These results suggest that -1185A/G polymorphism is not an independent risk factor for CAD.
Related Concept Videos
Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...
Single Nucleotide Polymorphisms-SNPs
Coronary Artery Disease I: Introduction
Coronary Artery Disease II: Pathophysiology
Acute Coronary Syndrome III: Diagnostic Studies
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
