Platelet P-selectin expression is associated with helicobacter pylori seropositivity in patients with peripheral arterial disease

Abstract

The prevalence of Helicobacter pylori seropositivity is higher in patients with cardiovascular and peripheral arterial disease (PAD), and H. pylori DNA has been identified within atherosclerotic plaque. Although a causal link has not been proven, proposed mechanisms have included direct or immunogenic injury to the vessel wall and indirect effects on platelet adhesion and activation. Intermittent claudication is associated with increased cardiovascular mortality and enhanced plate- let activation [1]. We measured H. pylori serology, platelet activation by flow cytometry, and von Will- ebrand Factor antigen by ELISA, in 125 patients with intermittent claudication, who were admitted for diag- nostic angiography. We found that 62 patients (49.6%) had a positive IgG antibody titre against H. pylori. Platelet P-selectin expression was significantly higher in H. pylori-positive patients (median; range 0.815; 0.17/ 4.77%) compared to seronegative patients (0.65; 0.12/ 4.53; P B/0.05). Platelet fibrinogen binding was not significantly different (2.135; 0.48/8.37 vs 1.85; 0.35/ 8.16%). There were no significant differences in plasma von Willebrand factor levels (196.4; 78.5/365.8 vs 179.4; 83.8/405.4 U/ml). Demographic, socioeconomic fac- tors, and disease severity were similar in both groups. We conclude that H pylori-positive patients with inter- mittent claudication have enhanced platelet activation. This suggests a potential mechanism whereby previous infection could represent a cardiovascular risk factor.