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. 2023 Dec 25;13(6):207-212.
doi: 10.62347/XQBZ7374. eCollection 2023.

Association between Factor-V Leiden and occurrence of acute myocardial infarction using a large NIS database

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Association between Factor-V Leiden and occurrence of acute myocardial infarction using a large NIS database

Luis Zuniga et al. Am J Blood Res. .

Abstract

Factor V Leiden is an inheritable pro-thrombotic genetic condition caused by a point mutation at the 506th codon, resulting in activated protein C resistance. APC resistance has been shown to contribute to the development of venous thrombosis. However, the role of FVL in AMI has yet to be well defined in the current literature. To assess whether a mutation carrier is more apt to develop an AMI, we conducted a retrospective observational analysis of two populations aged 18-40 and 18 through end of life. We used ICD-10 codes to search the NIS, an electronic nationwide patient database, to establish our populations and obtain our data. The ICD-10 codes were specific for activated protein C resistance and acute myocardial infarction. Preliminary data indicated that FVL was related to AMI; however, this finding became insignificant in both populations when stratified for age. We concluded there was no association between Factor V Leiden and acute myocardial infarction across both examined populations. Future investigations into this field of research are warranted as there remains a need for more consensus among the scientific community.

Background: Medical literature regarding the correlation between Factor V Leiden (FVL) and acute myocardial infarctions (AMI) is controversial. We aim to investigate the association between FVL and AMI.

Materials and methods: Using the Nationwide Inpatient Sample database, we evaluated any association between Factor V Leiden and acute myocardial infarction in 2016 using ICD-10 codes.

Results: Univariate analysis (18-40) showed an increase of AMI in patients with FVL 0.6% vs. 0.4%. However, after adjustment for age and comorbid conditions in multivariate analysis, FVL was not significantly associated with acute myocardial infarction (OR 1.44 (95% CI 0.913-2.273, p-value 0.117)). Univariate analysis (all patients over 18 years old) found that 2.9% of patients with FVL experienced AMI vs. 4.4% without the mutation. Multivariate analysis of the entire population ultimately showed no correlation between FVL and AMI.

Conclusion: In a population over 18, Factor V Leiden did not correlate with an increased risk of acute myocardial infarction in our studied population.

Keywords: FVL; Factor V Leiden; MI; activated protein C resistance; deep venous thrombosis; myocardial infarction; primary hypercoagulable state.

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Conflict of interest statement

None.

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