In this review we focus on available evidence and controversies regarding the relationship between the classic inherited VTE risk factors (factor V Leiden, prothrombin 20210A, deficiencies of antithrombin, protein C, and protein S) and the risk of myocardial infarction (MI).
We report the case of a young patient with a coagulation disorder secondary to a mutation of factor V Leiden, who presented with upper digestive bleeding as the first manifestation of Budd Chiari syndrome and who also was associated with myocardial infarction in his past medical history.
Myocardial infarction (MI) can be due to inherited thrombophilia caused by resistance to activated protein C resulting from factor V Leiden (FVL) mutation.
Myocardial infarction in a young patient with a previous history of repeated thrombophlebitis: combination of factor V Leiden and prothrombin G20210A gene polymorphisms with coronary artery disease.
We studied 609 patients with venous thromboembolism (287 with factor V Leiden, and 322 with prothrombin 20210A), 174 patients with myocardial infarction (78 with factor V Leiden, and 96 with prothrombin 20210A), and 198 controls (96 with factor V Leiden, and 102 with prothrombin 20210A).
The prevalence of factor V Leiden in patients with myocardial infarction was 8.7% (44/507), a significant increase in the prevalence of this mutation compared with the control group (3.7%, P =.0025).
Patients with no flow-limiting stenosis after MI had increased frequencies of 2 inherited thrombophilias (Factor V Leiden and beta-fibrinogen 448 A allele), and there was a trend toward an increased frequency of prothrombin variant G20210A compared with patients with > or =1 stenosis.
Studies associating the prothrombin 20210G>A (FII 20210A), factor V Leiden (FVL), and factor XIII Leu34 (FXIII-A Leu34) alleles with myocardial infarction (MI) have yielded conflicting results.
We investigated the relationship between polymorphisms in the Factor V (Leiden), prothrombin (20210 GgA) and thrombomodulin (Ala455Val) genes in patients with a myocardial infarction (MI) <45 years of age (n=195) and in unaffected siblings (n=107) and unrelated healthy race-matched individuals drawn from the same community (n=300).
Odds ratios and relative risks of MI in FVL carriers (heterozygotes + homozygotes) versus noncarriers were 1.24 (95% confidence interval [CI], 0.91-1.69) and 0.83 (0.58-1.20) in case-control and prospective studies, respectively.
The factor V Leiden and prothrombin G20201A mutations did not significantly correlate with myocardial infarction (OR 1.26, 95% CI 0.94 to 1.67, P=0.12 and OR 0.89, 95% CI 0.59 to 1.35, P=0.6, respectively).
Factor V Leiden was found in 13 patients (12.1%) who had a myocardial infarction without significant coronary artery stenosis, 11 patients (4.5%) who had a myocardial infarction with significant coronary artery stenosis (p = 0.01) and in 20 controls (5%) (p = 0.01).
The frequencies of factor V Leiden and prothrombin variant G20210A were determined in 41 patients age <50 years who had "normal" or "near normal" coronary arteries (no stenosis >50%) at angiography three to four weeks after MI (the study group) and compared with those in 114 patients who had at least one angiographic stenosis >50% after MI (the control group).
Coagulation factors II, V, VII, and X, prothrombin gene 20210G-->A transition, and factor V Leiden in coronary artery disease: high factor V clotting activity is an independent risk factor for myocardial infarction.
Interaction of coagulation defects and cardiovascular risk factors: increased risk of myocardial infarction associated with factor V Leiden or prothrombin 20210A.
When a coagulation defect was present (ie, the 20210 AG prothrombin genotype or the factor V Leiden mutation), the risk of myocardial infarction for carriers versus noncarriers was 1.4 (95% CI, 0.9 to 2.2).
The odds ratios for each event with heterozygous factor V Leiden were: MI, 0.46 (95% CI 0.17 to 1.25); angina, 1.0 (95% CI 0.45 to 2.23); stroke, 0.77 (95% CI 0.35 to 1.70): TIA, 1.33 (95% CI 0.5 to 3.55); any outcome, 0.83 (95% CI 0.48 to 1.44).
The study sought to determine whether coagulation factor V Leiden (FV Leiden) plays a role in the pathogenesis of coronary artery disease and/or myocardial infarction.
To assess whether factor V Leiden increases the risk of myocardial infarction (MI), we conducted a population-based case-control study among women 18 to 44 years of age in western Washington state.