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 journalArticleAcademicpeer-review


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 languageEnglish
Article number020025
Number of pages6
JournalJournal of the American Heart Association
Issue number11
Publication statusPublished - 1 Jun 2021


  • cardiovascular disease
  • cardiovascular disease risk factors
  • coagulation/thrombosis
  • factor V Leiden
  • genetic polymorphism

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