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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2186-2190
Synergistic Effects of Prothrombotic Polymorphisms and Atherogenic
Factors on the Risk of Myocardial Infarction in Young Males
Aida Inbal,
Dov Freimark,
Baruch Modan,
Angela Chetrit,
Shlomi Matetzky,
Nurit Rosenberg,
Rima Dardik,
Zvia Baron, and
Uri Seligsohn
From the Institute of Thrombosis and Hemostasis, Department of
Hematology, the Institute of Cardiology, and the Institute of Clinical
Epidemiology, Chaim Sheba Medical Center, Tel-Hashomer and Sackler
School of Medicine, Tel-Aviv University and the Israeli Defense
Forces, Israel.
Several recent studies evaluated a possible effect of the
prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C  T, factor V (F V) nt 1691G
A (F V Leiden), and factor II (F II) nt 20210 G A
on the risk of myocardial infarction. In the present study, we analyzed
the effect of these prothrombotic polymorphisms, as well as
apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and
hypercholesterolemia, on the risk of myocardial infarction in young
males. We conducted a case-control study of 112 young males with first
acute myocardial infarction (AMI) before the age of 52 and 187 healthy
controls of similar age. The prevalences of heterozygotes for F V
G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among
cases and controls, respectively). In contrast, the prevalence of MTHFR
677T homozygosity and the allele frequency of Apo E4 were significantly
higher among patients (24.1% v 10.7% and 9.4% v
5.3% among cases and controls, respectively). Concomitant presence of
hypertension, hypercholesterolemia, or diabetes and one or more of the
four examined polymorphisms increased the risk by almost ninefold (odds
ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5)
and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed
simultaneously by a logistic model, the combination of prothrombotic
and Apo E4 polymorphisms with current smoking increased the risk
25-fold (OR = 24.7; 95% CI, 7.17 to 84.9).The presented data suggest
a synergistic effect between atherogenic and thrombogenic risk factors
in the pathogenesis of AMI, as was recently found in a similar cohort
of women.
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