Helicobacter Pylori Infection and the Risk of Myocardial Infarction: Role of Fibrinogen and Its Genetic Control

Abstract

SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction 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 infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects 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 infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.

Genes Encoding Fibrinogen and Cardiovascular Risk

“…46 Zito et al 16 showed that the BclI polymorphisms of ␤-fibrinogen gene modulated the effect of HP on both fibrinogen levels and the risk of myocardial infarction. HP, a life-long bacterial infection, was found to be associated with chronically increased plasma levels of fibrinogen.…”

“…The rare B2B2 genotype has been consistently associated with levels of fibrinogen 15% to 20% higher than that of the B1B1 genotype. [12][13][14][15][16] However, because of its location on the gene, it would be difficult to consider a biological function for this polymorphism, which has been mainly considered as a marker for another locus on the fibrinogen gene.…”

“…However, the risk was present only when patients with a family history of ischemic vascular disease were selected. 15,16 Only few studies have found an association between Ϫ455 G/A polymorphism and the risk of ischemic vascular disease (Table). 25,26,32,35,36 In particular, out of 14 studies in which the relation between Ϫ455 G/A polymorphism and the risk was evaluated, only 5 reported the presence of an association.…”

Psoriasis vulgaris and digestive system disorders: is there a linkage?

“…Animal studies demonstrated that the bacteria disrupted interstitial and intravascular cell to cell interactions, leading to marked microvascular dysfunction [32]. Furthermore, it is probably associated with increased levels of fibrinogen [33], and platelet activation and aggregation [34], other processes implicated in the microvascular dysfunction and inflammatory-cell recruitment.…”

Population variability in some genes involving the haemostatic system: data on the general population of Corsica (France), Sardinia and Sicily (Italy)

“…Some of these polymorphic sites have been reported as being associated with the risk for cardiovascular disease (de Maat et al, 1995;de Maat et al, 1997;van der Bom et al, 1997;Weiss et al, 1996;Zito et al, 1999;Di Castelnuovo et al, 2000).…”