Zuniga Luis, Davis Mitchell, Movahed Mohammad Reza, Hashemzadeh Mehrtash, Hashemzadeh Mehrnoosh
University of Nebraska Medical Center Omaha, NE, USA.
Department of Dermatology, University of California San Francisco, CA, USA.
Am J Blood Res. 2023 Dec 25;13(6):207-212. doi: 10.62347/XQBZ7374. eCollection 2023.
Factor V Leiden is an inheritable pro-thrombotic genetic condition caused by a point mutation at the 506 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.
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.
Using the Nationwide Inpatient Sample database, we evaluated any association between Factor V Leiden and acute myocardial infarction in 2016 using ICD-10 codes.
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, -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.
In a population over 18, Factor V Leiden did not correlate with an increased risk of acute myocardial infarction in our studied population.
因子V莱顿突变是一种可遗传的促血栓形成遗传疾病,由506密码子处的点突变引起,导致活化蛋白C抵抗。已证明活化蛋白C抵抗会导致静脉血栓形成。然而,因子V莱顿突变在急性心肌梗死中的作用在当前文献中尚未得到明确界定。为了评估突变携带者是否更易发生急性心肌梗死,我们对两个年龄段的人群进行了回顾性观察分析,一个年龄段为18 - 40岁,另一个年龄段为18岁至生命结束。我们使用国际疾病分类第十版(ICD - 10)编码在全国电子患者数据库国家住院样本(NIS)中进行搜索,以确定我们的研究人群并获取数据。ICD - 10编码专门用于活化蛋白C抵抗和急性心肌梗死。初步数据表明因子V莱顿突变与急性心肌梗死有关;然而,在按年龄分层后,这一发现在两个人群中均无统计学意义。我们得出结论,在两个研究人群中,因子V莱顿突变与急性心肌梗死之间均无关联。鉴于科学界仍需要更多共识,因此有必要对该研究领域进行进一步调查。
关于因子V莱顿突变(FVL)与急性心肌梗死(AMI)之间相关性的医学文献存在争议。我们旨在研究FVL与AMI之间的关联。
利用全国住院样本数据库,我们在2016年使用ICD - 10编码评估因子V莱顿突变与急性心肌梗死之间的任何关联。
单因素分析(18 - 40岁人群)显示,因子V莱顿突变患者的急性心肌梗死发生率有所增加,分别为0.6%和0.4%。然而,在多因素分析中对年龄和合并症进行调整后,因子V莱顿突变与急性心肌梗死无显著关联(比值比1.44(95%可信区间0.913 - 2.273,P值0.117))。单因素分析(所有18岁以上患者)发现,因子V莱顿突变患者发生急性心肌梗死的比例为2.9%,未发生突变的患者比例为4.4%。对整个人群的多因素分析最终表明因子V莱顿突变与急性心肌梗死之间无相关性。
在18岁以上人群中,因子V莱顿突变与我们研究人群中急性心肌梗死风险增加无关。