Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis

Bakhtawar K. Mahmoodi; Niclas Eriksson; Gerrit J. A. Vos; Karina Meijer; Agneta Siegbahn; Stefan James; Lars Wallentin; Jurrien M. ten Berg

doi:10.1161/JAHA.120.020025

Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis

Bakhtawar K. Mahmoodi^*, Niclas Eriksson, Gerrit J. A. Vos, Karina Meijer, Agneta Siegbahn, Stefan James, Lars Wallentin, Jurrien M. ten Berg

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

BACKGROUND: The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST-segment-elevation myocardial infarction (STEMI), compared with non-ST-segment-elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden.

METHODS AND RESULTS: Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G-to-A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (>= 70 versus

CONCLUSIONS: In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non-ST-segment-elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI.

Original language	English
Article number	020025
Number of pages	6
Journal	Journal of the American Heart Association
Volume	10
Issue number	11
DOIs	https://doi.org/10.1161/JAHA.120.020025
Publication status	Published - 1 Jun 2021

Keywords

cardiovascular disease
cardiovascular disease risk factors
coagulation/thrombosis
factor V Leiden
genetic polymorphism
METAANALYSIS
INFARCTION
DISEASE

Access to Document

10.1161/JAHA.120.020025

Cite this

@article{db932bbf1ad640e795dd4cdc39cd2dbd,

title = "Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis",

abstract = "BACKGROUND: The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST-segment-elevation myocardial infarction (STEMI), compared with non-ST-segment-elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden.METHODS AND RESULTS: Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G-to-A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (>= 70 versusCONCLUSIONS: In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non-ST-segment-elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI.",

keywords = "cardiovascular disease, cardiovascular disease risk factors, coagulation/thrombosis, factor V Leiden, genetic polymorphism, METAANALYSIS, INFARCTION, DISEASE",

author = "Mahmoodi, {Bakhtawar K.} and Niclas Eriksson and Vos, {Gerrit J. A.} and Karina Meijer and Agneta Siegbahn and Stefan James and Lars Wallentin and {ten Berg}, {Jurrien M.}",

year = "2021",

month = jun,

day = "1",

doi = "10.1161/JAHA.120.020025",

language = "English",

volume = "10",

journal = "Journal of the American Heart Association",

issn = "2047-9980",

publisher = "Wiley",

number = "11",

}

TY - JOUR

T1 - Factor V Leiden Does Not Modify the Phenotype of Acute Coronary Syndrome or the Extent of Myocardial Necrosis

AU - Mahmoodi, Bakhtawar K.

AU - Eriksson, Niclas

AU - Vos, Gerrit J. A.

AU - Meijer, Karina

AU - Siegbahn, Agneta

AU - James, Stefan

AU - Wallentin, Lars

AU - ten Berg, Jurrien M.

PY - 2021/6/1

Y1 - 2021/6/1

N2 - BACKGROUND: The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST-segment-elevation myocardial infarction (STEMI), compared with non-ST-segment-elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden.METHODS AND RESULTS: Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G-to-A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (>= 70 versusCONCLUSIONS: In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non-ST-segment-elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI.

AB - BACKGROUND: The prothrombotic defect factor V Leiden (FVL) may confer higher risk of ST-segment-elevation myocardial infarction (STEMI), compared with non-ST-segment-elevation acute coronary syndrome, and may be associated with more myocardial necrosis caused by higher thrombotic burden.METHODS AND RESULTS: Patients without history of cardiovascular disease were selected from 2 clinical trials conducted in patients with acute coronary syndrome. FVL was defined as G-to-A substitution at nucleotide 1691 in the factor V (factor V R506Q) gene. Odds ratios were calculated for the association of FVL with STEMI adjusted for age and sex in the overall population and in the subgroups including sex, age (>= 70 versusCONCLUSIONS: In a general population with acute coronary syndrome, FVL did not discriminate between a STEMI or non-ST-segment-elevation acute coronary syndrome presentation and was unrelated to peak cardiac necrosis markers in patients with STEMI.

KW - cardiovascular disease

KW - cardiovascular disease risk factors

KW - coagulation/thrombosis

KW - factor V Leiden

KW - genetic polymorphism

KW - METAANALYSIS

KW - INFARCTION

KW - DISEASE

U2 - 10.1161/JAHA.120.020025

DO - 10.1161/JAHA.120.020025

M3 - Article

C2 - 33998271

VL - 10

JO - Journal of the American Heart Association

JF - Journal of the American Heart Association

SN - 2047-9980

IS - 11

M1 - 020025

ER -