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Ulcer bacteria linked to strokes

DALLAS, July 9 Potent strains of ulcer-causing bacteria may play a key role in certain kinds of stroke, researchers report in today's rapid access issue of Circulation: Journal of the American Heart Association.

For the first time, researchers have found that specific strains of Helicobacter pylori (H. pylori) were much more prevalent in the blood of patients who have suffered an atherosclerotic stroke, says lead author Antonio Pietroiusti, M.D., a professor of internal medicine at Tor Vergata University in Rome.

Some studies have linked H. pylori with inflamed artery walls and arterial lesions, including stroke caused by narrowing of the arteries due to atherosclerosis.

H. pylori causes ulcers in the stomach. In large arteries leading to the brain, the researchers report that cytotoxin-producing strains of the bacteria appear to aggravate an already risky environment. The cytotoxin-associated gene-A (CagA) makes strains of H. pylori virulent and especially damaging to arteries. Cytotoxins attack cells, causing tissue inflammation and ultimately lesions. By attacking vulnerable areas of the artery wall, they cause inflammation and swelling, further restricting blood flow and increasing the chance of stroke.

Researchers compared different strains of H. pylori in the bloodstream of 138 patients with large-vessel stroke (group A); 61 patients with cardioembolic stroke (group B); and 151 healthy volunteers. Extensive atherosclerotic changes cause large vessel strokes, says Pietroiusti. Cardioembolic strokes are caused by abrupt blockage of a cerebral artery by a clot that travels to the brain.

Prevalence of H. pylori infection among patients with large-vessel, , and normal controls was about the same. However, the presence of CagA-positive strains was significantly higher in large-vessel stroke patients than the cardioembolic stroke group 42.8 percent versus 19.7 percent. It was also higher than those of the controls 17.9 per
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Contact: Bridgette Mc Neill
bridgette.mcneill@heart.org
214-706-1135
American Heart Association
8-Jul-2002


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