Zito F, Di Castelnuovo A, D'Orazio A, Negrini R, De Lucia D, Donati M B, Iacoviello L
Istituto di Ricerche Farmacologiche Mario Negri, Department of Vascular Medicine and Pharmacology, S. Maria Imbaro, Italy.
Thromb Haemost. 1999 Jul;82(1):14-8.
The contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possible 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 polymorphism 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.
评估了幽门螺杆菌（HP）感染对心肌梗死风险的影响。在此背景下，探讨了纤维蛋白原的作用及其基因控制作为HP可能影响心肌梗死风险的一种潜在机制。对101例心肌梗死患者和101例对照进行了一项病例对照研究。独立于混杂变量，HP感染与心肌梗死风险增加相关（比值比4.1，95%置信区间：1.8 - 9.4）。在病例组和对照组中，HP感染均与较高水平的纤维蛋白原显著相关。此外，HP感染和BclI纤维蛋白原多态性的B2等位基因在增加纤维蛋白原水平方面存在相加效应。与携带B1B1基因型的受试者（比值比3.3，95%置信区间：1.2 - 9.2）相比，HP感染对B2等位基因携带者的心肌梗死风险影响更强（比值比7.6，95%置信区间：1.8 - 31.6）。我们表明，既往HP感染是心肌梗死的一个危险因素。纤维蛋白原水平升高是HP可能发挥作用的一种潜在机制。诸如增加纤维蛋白原水平的遗传易感性等伴随情况，似乎会进一步增加HP对心肌梗死风险的影响。
