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

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

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)701-702
Number of pages2
JournalThrombosis and Haemostasis
Volume75
Issue number5
Publication statusPublished - May 1996

ASJC Scopus subject areas

  • Hematology

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