Factor V Q506 (Resistance to Activated Protein C) and Prognosis after Acute Coronary Syndrome

Johan Holm; Andreas Hillarp; Bengt Zöller; Leif Erhardt; Erik Berntorp; Björn Dahlbäck

doi:10.1055/s-0037-1614587

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1999; 81(06): 857-860
DOI: 10.1055/s-0037-1614587

Letters to the Editor

Schattauer GmbH

Factor V Q⁵⁰⁶ (Resistance to Activated Protein C) and Prognosis after Acute Coronary Syndrome

Johan Holm

¹From the Department of Cardiology and Coagulation Disorders, University Hospital, Malmö, Sweden

,

Andreas Hillarp

²Department of Clinical Chemistry and Coagulation Disorders, University Hospital, Malmö, Sweden

,

Bengt Zöller

²Department of Clinical Chemistry and Coagulation Disorders, University Hospital, Malmö, Sweden

,

Leif Erhardt

¹From the Department of Cardiology and Coagulation Disorders, University Hospital, Malmö, Sweden

,

Erik Berntorp

²Department of Clinical Chemistry and Coagulation Disorders, University Hospital, Malmö, Sweden

,

Björn Dahlbäck

²Department of Clinical Chemistry and Coagulation Disorders, University Hospital, Malmö, Sweden

› Author Affiliations

Abstract

Summary

Factor V:Q⁵⁰⁶ causing resistance to activated protein C (APC-resistance), is a risk factor for venous thrombosis. Some studies have indicated an association with arterial disease, especially in women. We investigated the prevalence of the FV:Q⁵⁰⁶ allele prospectively in 295 patients with acute coronary syndrome. Mortality and myocardial infarction rate were evaluated after 30 days and after 2 years. The FV:Q⁵⁰⁶ allele was found in 38 patients. In a Cox proportional hazards model, smokers carrying FV:Q⁵⁰⁶ had a higher risk of infarction or death within 30 days, compared to non-smokers with a normal genotype (relative risk 2.9 [95% CI 1.2-7.0]). The difference remained significant after 2 years (relative risk 2.8 [95% CI 1.2-6.5]). The effect of the FV:Q⁵⁰⁶ allele on clinical outcome in acute coronary syndrome has not previously been described. Our results demonstrate a gene-environment interaction between smoking and the FV:Q⁵⁰⁶ allele, with an increased risk of early complications after an acute ischemic event.

Full Text

References

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