Prothrombotic genetic risk factors in patients with very early ST-segment elevation myocardial infarction

Abstract

The contribution of prothrombotic genetic risk factors in the pathogenesis of premature acute myocardial infarction (MI) is controversial. We examined the prevalence of prothrombotic polymorphisms (G1691A of factor V gene [FV Leiden] and G20210A of prothrombin [FII] gene), deficiencies of natural anticoagulants (protein C, protein S and antithrombin III) and antiphospholipid syndrome (APS) in patients with early ST-segment elevation MI (STEMI). We recruited 255 consecutive patients who had survived a STEMI ≤ 35 years of age (224 men). The control group consisted of 400 healthy individuals matched with cases for age and sex. G20210A polymorphism of FII gene was more frequent in young patients than in controls (7.4 vs. 3.5%, p = 0.023). The odds ratio (OR) for STEMI for carriers versus non-carriers was 2.239 (95% CI 1.102-4.250). The adjusted OR for major cardiovascular risk factors was 2.569 (95% CI 1.086-6.074). The risk was increased by 22-fold (95% CI 9.192-66.517) when G20210A polymorphism was present in combination with smoking. There was no difference in the prevalence of FV Leiden between patients and controls (7.8 vs. 6.5%, p = 0.512). There was only one patient (0.4%) with protein C deficiency and one with APS (0.4%). G20210A polymorphism of FII gene may be associated with increased risk of premature STEMI and the risk increases substantially when smoking is present. The contribution of other prothrombotic disorders such as deficiencies of protein C, protein S and antithrombin III and APS was minimal in this cohort.

Acute Myocardial Infarction as an Initial Presentation of Protein C and Protein S Deficiency Followed by Dilated Cardiomyopathy in a Young Male

“…A study conducted among 337 patients of heterozygous protein C deficiency showed the prevalence of arterial thrombosis in only 7.1% of subjects [9]. A recent work involving 255 consecutive patients, who had endured a STEMI in <35 years of age, revealed protein C deficiency in only one of them (0.4%) [10]. A cohort family study revealed arterial events in only 8% of the 144 subjects with protein C and protein S deficiency [11].…”

Cerebral Infarction Followed by Myocardial Infarction in a Young Adult with Protein C and S Deficiency

“…A study comprising of 337 patients with heterozygous PC deficiency showed arterial thrombosis in only 7.1% of the subjects [11]. A recent work involving 255 patients with ST-elevation MI in <35 years of age, revealed a deficiency of PC in only one of them (0.4%) [12]. A cohort study highlighted arterial thrombotic events in only 8% of the 144 patients with deficiencies of both PC and PS [13].…”

Hemostatic Gene Polymorphisms in Acute Coronary Syndrome with Nonobstructive Coronary Atherosclerosis

“…В исследовании, включавшем 400 здоровых добровольцев и 255 больных ОИМпST моложе 35 лет, не выявлено различий по частоте носительства лейденовской мутации; определялось увеличение риска развития ОИМпST при сочетании носительства полиморфизма G20210A и курения. Вклад протромботических расстройств, таких как недостаточность протеинов С, S и антитромбина III, у исследованных больных был незначительным [40]. В проведенном ОСТРЫЙ КОРОНАРНЫЙ СИНДРОМ § нами исследовании снижение активности антитромбина III и протеина С выявлялось у 4 (13 %) больных в течение 1-х суток после индексного события и не определялось через 1 год.…”