Helicobacter pylori infection in coronary artery disease.

The role of inflammation in the pathogenesis and progression of coronary artery disease (CAD) has been increasingly discussed, but still remains unclear. Inflammatory changes in the vessel wall play an important role in the pathogenesis of atherosclerosis. Systemic inflammatory reaction can be detected by showing increased plasma levels of different proinflammatory cytokines and acute-phase proteins. Infectious agents have been linked to coronary heart disease on epidemiological and pathogenetic grounds. The prevalent condition and the exact mechanism of initiation of atherosclerotic vascular disease remain unclear. Nevertheless, many similarities exist between the processes of inflammation and atherogenesis, and the evidence is growing for the role of an active inflammation in the atherosclerosis in the coronary circulation and elsewhere. Although the seroepidemiological and eradication studies have suggested a causal relationship between Helicobacter pylori (Hp) infection and coronary heart disease; the issue is still controversial. The detection of Hp specific DNA in atheromatous plaque material from coronary arteries, but more important, the reduction in restenosis of coronary vessels after Hp eradication could be interpreted as an evidence for the involvement of a Hp infection in the progression of CAD induced by a local inflammatory process.