Department of Cardiology St. Antonius Hospital Nieuwegein the Netherlands.
Division of Hemostasis and Thrombosis Department of Hematology UMC GroningenUniversity of Groningen the Netherlands.
J Am Heart Assoc. 2021 Jun;10(11):e020025. doi: 10.1161/JAHA.120.020025. Epub 2021 May 17.
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 <70 years), and traditional cardiovascular risk factors. The peak biomarker levels (ie, creatine kinase-myocardial band and high-sensitivity troponin I or T) after STEMI were contrasted between FVL carriers and noncarriers. Because of differences in troponin assays, peak high-sensitivity troponin levels were converted to a ratio scale. The prevalence of FVL mutation was comparable in patients with STEMI (6.0%) and non-ST-segment-elevation acute coronary syndrome (5.8%). The corresponding sex- and age-adjusted odds ratio was 1.06 (95% CI, 0.86-1.30; =0.59) for the association of FVL with STEMI. Subgroup analysis did not show any differences. In patients with STEMI, neither the median peak creatine kinase-myocardial band nor the peak high-sensitivity troponin ratio showed any differences between wild-type and FVL carriers ( for difference: creatine kinase-myocardial band=0.33; high sensitivity troponin ratio=0.54). 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. Registration URL: https://www.clinicaltrials.gov; Unique identifiers: NCT00391872 and NCT01761786.
与非 ST 段抬高型急性冠脉综合征相比，促血栓形成缺陷因子 V 莱顿（FVL）可能会增加 ST 段抬高型心肌梗死（STEMI）的风险，并且可能与更高的血栓负荷导致的更多心肌坏死有关。
从两项急性冠脉综合征患者的临床试验中选择了无心血管疾病史的患者。FVL 定义为因子 V（因子 V R506Q）基因中核苷酸 1691 处的 G 到 A 取代。在总体人群和包括性别、年龄（≥70 岁与＜70 岁）和传统心血管危险因素的亚组中，根据年龄和性别调整 FVL 与 STEMI 的关联，计算 FVL 的比值比。比较 STEMI 后 FVL 携带者和非携带者的峰值生物标志物水平（即肌酸激酶-MB 和高敏肌钙蛋白 I 或 T）。由于肌钙蛋白检测方法的差异，将高敏肌钙蛋白的峰值水平转换为比例尺度。STEMI 患者的 FVL 突变患病率与非 ST 段抬高型急性冠脉综合征患者（5.8%）相似。FVL 与 STEMI 相关的性别和年龄调整比值比为 1.06（95%CI，0.86-1.30；=0.59）。亚组分析未显示任何差异。在 STEMI 患者中，野生型和 FVL 携带者之间的中位峰值肌酸激酶-MB 和高敏肌钙蛋白比值均无差异（差异中位数：肌酸激酶-MB=0.33；高敏肌钙蛋白比值=0.54）。
在急性冠脉综合征的一般人群中，FVL 不能区分 STEMI 或非 ST 段抬高型急性冠脉综合征的表现，与 STEMI 患者的峰值心脏坏死标志物无关。
https://www.clinicaltrials.gov；唯一标识符：NCT00391872 和 NCT01761786。
