Factor V (Arg506⟶ Gln) Mutation in Young Survivors of Myocardial Infarction

Diego Ardissino; Flora Peyvandi; Piera Angelica Merlini; Elisabetta Colombi; Pier Mannuccio Mannucci

doi:10.1055/s-0038-1650350

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1996; 75(05): 701-702
DOI: 10.1055/s-0038-1650350

Original Article

Schattauer GmbH Stuttgart

Factor V (Arg⁵⁰⁶⟶ Gln) Mutation in Young Survivors of Myocardial Infarction

Authors

Diego Ardissino

¹The Division of Cardiology, I.R.C.C.S., Policlinico San Matteo, Pavia
Flora Peyvandi

²The Angelo Bianchi Bonomi Hemophilia and Thrombosis Centre and the Institute of Internal Medicine, I.R.C.C.S. Maggiore Hospital, Milan, Italy
Piera Angelica Merlini

³University of Milan and the 2nd Division of Cardiology, Niguarda Hospital, Milan, Italy
Elisabetta Colombi

¹The Division of Cardiology, I.R.C.C.S., Policlinico San Matteo, Pavia
Pier Mannuccio Mannucci

²The Angelo Bianchi Bonomi Hemophilia and Thrombosis Centre and the Institute of Internal Medicine, I.R.C.C.S. Maggiore Hospital, Milan, Italy

Abstract

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Summary

Many young patients with venous thromboembolic disease are partially resistant to the anticoagulant action of activated protein C as a result of factor V (Arg⁵⁰⁶ ⟶ Gln) mutation. The frequency of this mutation in young patients with arterial thrombotic diseases, such as myocardial infarction, is less well established. We studied 100 young patients with myocardial infarction and 100 age- and sex-matched controls. One patient (1%; 95% CL 0.05-6.2) and two controls (2%; 95% CL 0.3-7.7) were heterozygotes for the mutation; there was no homozygote in either group. Hence, premature myocardial infarction is not associated with heterozygosity for factor V (Arg⁵⁰⁶ ⟶ Gln) mutation.

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References

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