Helicobacter pylori infection and the risk of myocardial infarction: Role of fibrinogen and its genetic control

The contribution of Helicobacter pylori (HP) infection to the risk of myoca rdial infarction was evaluated. The role of fibrinogen and its genetic cont rol as a possibile mechanism by which KP may influence myocardial infarctio n risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls. HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infect ion was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infe ction and B2 allele of BclI fibrinogen polymorphism in increasing fibrinoge n levels. HP infection showed a stronger effect on the risk of myocardial i nfarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to sub jects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2). We showed that a previous HP infection is a risk factor for myocardial infa rction. An increase in fibrinogen levels is a possible mechanism by which H P may act. Concomitant conditions, like a genetic predisposition in increas ing fibrinogen levels, seem to further increase the effect of HP on myocard ial infarction risk.