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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Role of factor V Leiden mutation in patients with angiographically demonstrated coronary artery disease

S T Dunn1, C R Roberts, E Schechter

  • 1Department of Pathology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

Thrombosis Research
|August 29, 1998
PubMed

Insights

Coagulation factor V Leiden (FV Leiden) mutation is linked to venous clots but not independently associated with coronary artery disease or myocardial infarction in this study. Further research is needed to clarify its role in arterial thrombosis.

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Thrombosis

Background:

  • The association of factor V Leiden (FV Leiden) mutation with venous thromboembolism is established.
  • Its role in arterial thrombotic events, including coronary artery disease (CAD) and myocardial infarction (MI), remains controversial.
  • Previous studies suggest a possible link in younger individuals, but evidence in atherosclerosis is limited.

Purpose of the Study:

  • To investigate the potential role of the FV Leiden mutation in the pathogenesis of coronary artery disease and myocardial infarction.
  • To analyze the association between FV Leiden genotype and the presence of atherosclerosis and history of myocardial infarction in a cohort of patients undergoing coronary angiography.

Main Methods:

  • Genotyping for FV Leiden mutation was performed in 850 predominantly white patients undergoing coronary angiography.
  • Coronary artery disease risk factors and history of myocardial infarction were analyzed in relation to FV Leiden genotype.
  • Logistic regression analysis was used to assess FV Leiden as a predictor of atherosclerosis, adjusting for traditional risk factors.

Main Results:

  • The FV Leiden mutation was present in 6.4% of patients, with allele frequencies consistent with the white population.
  • FV Leiden was not a significant predictor of clinically defined atherosclerosis (≥50% stenosis) after adjusting for other risk factors (p=0.23).
  • No significant difference in FV Leiden frequency was observed between patients with and without a history of myocardial infarction (p=0.51).

Conclusions:

  • The heterozygous state of the FV Leiden mutation is not independently associated with coronary artery disease or myocardial infarction in this patient cohort.
  • The findings do not support FV Leiden as a significant independent risk factor for atherosclerosis or myocardial infarction in this population.
  • The study contributes to the ongoing debate regarding the role of FV Leiden in arterial thrombosis.

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