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 journalArticle

57 Citations (Scopus)

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

Fingerprint

Factor V
Survivors
Myocardial Infarction
Mutation
Homozygote
Mutation Rate
Heterozygote
Protein C
Anticoagulants

ASJC Scopus subject areas

  • Hematology

Cite this

Factor V (Arg506 → Gln) Mutation in Young Survivors of Myocardial Infarction. / Ardissino, Diego; Peyvandi, Flora; Merlini, Piera Angelica; Colombi, Elisabetta; Mannucci, Pier Mannuccio.

In: Thrombosis and Haemostasis, Vol. 75, No. 5, 05.1996, p. 701-702.

Research output: Contribution to journalArticle

Ardissino, Diego ; Peyvandi, Flora ; Merlini, Piera Angelica ; Colombi, Elisabetta ; Mannucci, Pier Mannuccio. / Factor V (Arg506 → Gln) Mutation in Young Survivors of Myocardial Infarction. In: Thrombosis and Haemostasis. 1996 ; Vol. 75, No. 5. pp. 701-702.
@article{664449035119415bbcee31289ab68b75,
title = "Factor V (Arg506 → Gln) Mutation in Young Survivors of Myocardial Infarction",
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.",
author = "Diego Ardissino and Flora Peyvandi and Merlini, {Piera Angelica} and Elisabetta Colombi and Mannucci, {Pier Mannuccio}",
year = "1996",
month = "5",
language = "English",
volume = "75",
pages = "701--702",
journal = "Thrombosis and Haemostasis",
issn = "0340-6245",
publisher = "Schattauer GmbH",
number = "5",

}

TY - JOUR

T1 - Factor V (Arg506 → Gln) Mutation in Young Survivors of Myocardial Infarction

AU - Ardissino, Diego

AU - Peyvandi, Flora

AU - Merlini, Piera Angelica

AU - Colombi, Elisabetta

AU - Mannucci, Pier Mannuccio

PY - 1996/5

Y1 - 1996/5

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0029943533&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029943533&partnerID=8YFLogxK

M3 - Article

C2 - 8725707

AN - SCOPUS:0029943533

VL - 75

SP - 701

EP - 702

JO - Thrombosis and Haemostasis

JF - Thrombosis and Haemostasis

SN - 0340-6245

IS - 5

ER -