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

Diego Ardissino
1   The Division of Cardiology, I.R.C.C.S., Policlinico San Matteo, Pavia
,
Flora Peyvandi
2   The 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
3   University of Milan and the 2nd Division of Cardiology, Niguarda Hospital, Milan, Italy
,
Elisabetta Colombi
1   The Division of Cardiology, I.R.C.C.S., Policlinico San Matteo, Pavia
,
Pier Mannuccio Mannucci
2   The Angelo Bianchi Bonomi Hemophilia and Thrombosis Centre and the Institute of Internal Medicine, I.R.C.C.S. Maggiore Hospital, Milan, Italy
› Author Affiliations
Further Information

Publication History

Received 08 September 1995

Accepted after resubmission 15 January 1996

Publication Date:
10 July 2018 (online)

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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.