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Chronic Infection May Contribute to Stroke Risk
E-Newsletter No. 33
It is well known that chronic inflammation is a significant contributor to atherosclerotic disease. Serologic positively for Chlamydia pneumoniae and Helicobacter pylori have been associated with atherosclerosis independent of other risk factors. These organisms have been linked to disease in the coronary arteries, carotid system, and peripheral vasculature. Although H pylori often presents as peptic ulcer disease and chlamydia rarely produces pneumonia, these chronic infections are usually entirely asymptomatic and thus are rarely treated.
In the current report, Pietroiusti and colleagues present data linking a particular virulent H pylori strain (bearing the cytotoxin-associated gene A [CagA]) with stroke due to atherosclerosis. Dividing stroke patients into etiologic subtypes, 138 patients with large vessel stroke were compared to 61 patients with cardioembolic infarcts and 151 healthy controls. H pylori infection in general was highly prevalent in all groups, occurring in approximately 70% of patients. The prevalence of CagA-positive strains, however, was much higher in patients with larger vessel strikes (43%) than among patients with cardioembolism (20%) or controls (18%) ?P <0.001 for either comparison. C-reactive protein levels, indicating an inflammatory state, were also significantly higher in the presence of CagA.
By dividing infarcts into specific subtypes, rather than treating them at a lump sum. Pietroiusti et al were able to make significant insights into stroke pathophysiology. These data indicate that inflammation appears to play a role in strokes mediated by atherosclerosis, but not strokes related to cardiac thrombi. Similarly, stroke is not associated with all H pylori infections (an exceedingly common phenomenon), but rather with a specific more virulent (and less common) strain.
In a related article, Franceschi and colleagues (Circulation. 2002: 106:430-434) further elucidate this interesting link. In an ex vivo, immunochemical model, they demonstrate that Anti-CagA antibodies specifically bind to epitopes on atherosclerotic blood vessels. H pylori may, therefore, promote atherosclerosis through a much more discrete process than merely nonspecific inflammation. Antibodies made against CagA may cross react with antigens expressed by cells involved in atherogenesis such as vascular smooth muscle, fibroblasts, or endothelial cells.
While mass treatments with antibiotics to prevent stroke and myocardial infarction are not yet justified, there is compelling evidence that particular chronic infections may significantly contribute to vascular disease.
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