R. Junker et al., PLASMINOGEN-ACTIVATOR INHIBITOR-1 4G 5G-POLYMORPHISM AND FACTOR-V Q506 MUTATION ARE NOT ASSOCIATED WITH MYOCARDIAL-INFARCTION IN YOUNG MEN/, Blood coagulation & fibrinolysis, 9(7), 1998, pp. 597-602
Several recent studies have reported contradicting results concerning
the relevance of the plasminogen activator inhibitor-1 (PAI-1) 4G/5G-p
olymorphism for myocardial infarction. In addition, the common factor
V Q506 (FV:Q506) mutation is frequently discussed as a risk factor for
arterial thrombosis, but evidence is rare. In order to further highli
ght the role of both polymorphisms in myocardial infarction, we invest
igated 241 young male myocardial infarction patients (less than or equ
al to 45 years-of-age) aged 38.6 +/- 4.4 years (mean +/- SD) for the p
resence of both genotypes. The control group consisted of 179 healthy
men aged 47.1 +/- 6.4 years (mean +/- SD) of the same ethnic backgroun
d as the patients. Neither the distribution of the PAI-I 4G/5G-polymor
phism nor the prevalence of the FV:4506 mutation was significantly dif
ferent between young patients and controls (4G/4G-genotype: chi(2) = 2
.08, NS; odds ratio 1.36, 95% confidence interval 0.89-2.06; FV: 4506
mutation: chi(2) = 0.33, NS; odds ratio 1.33, 95% confidence interval
0.64-2.78). Moreover, the PAI-I 4G/5G-distribution did not differ sign
ificantly between patients and controls in subgroups by tertiles of tr
iglyceride levels. In conclusion, in the present study neither homozyg
osity for the 4G allele of the PAI-I 4G/5G-polymorphism nor the FV:450
6 mutation led to an increased risk of myocardial infarction in young
men. (C) 1998 Lippincott Williams & Wilkins.