The relative importance of acid in Helicobacter pylori (H. pylori) ulcer pathogenesis is in doubt, with possibilities existing that other contributing factors may be involved. Vascular insufficiency may lead to the development of ischemic lesions or ulcers within the gastric mucosa. H. pylori produces a striking inflammatory response following infection and one of the major components of gastrointestinal inflammation is alterations in the vascular structure and function. This suggests that the microcirculation may be a key target of H. pylori-released factors. Recent evidence has accumulated to suggest that H. pylori can affect a number of microcirculatory variables including blood flow, leukocyte activity and also induce changes in the endothelial lining of the vessels themselves. The majority of these findings have been described by employing the technique of fluorescent in vivo microscopy, which allows direct, dynamic and real time observations of the microcirculation to be made. A universal feature of these experimental studies has been the formation of circulating or adherent platelet aggregates. It is now recognized that platelets participate in the inflammatory response by acting as a potent source of inflammatory mediators and modulating the activity of other inflammatory cells. Circulation of platelet emboli may be of cause for concern, especially as a number of studies have demonstrated an association between H. pylori infection and coronary heart disease. The present review highlights the major findings from these studies and proposes an important role for the gastric microcirculation in the pathophysiology of H. pylori-induced injury.