BACKGROUND AND PURPOSE: Several lines of evidence point toward a relationship 
between infection and atherosclerotic vascular disease. Thus, infection and 
inflammation often precede ischemic neurological events. Transient alterations 
in coagulation and direct arterial invasion by certain microorganisms have been 
reported. Helicobacter pylori infection is the major cause of peptic ulcer 
disease and appears to be a risk factor for ischemic cerebrovascular disease. 
However, in contrast to other chronic infectious agents, H pylori has not been 
consistently isolated from atherosclerotic lesions.
METHODS: We investigated the presence of H pylori in 38 atherosclerotic plaques 
obtained at carotid endarterectomy by using morphological and 
immunohistochemical techniques and a highly sensitive polymerase chain reaction 
method. We performed immunohistochemical detection of intercellular adhesion 
molecule-1, a marker related to inflammatory cell response. We also examined 7 
carotid arteries obtained at autopsy from subjects without carotid 
atherosclerosis.
RESULTS: H pylori DNA was found in 20 of 38 atherosclerotic plaques. Ten of the 
H pylori DNA-positive plaques also showed morphological and immunohistochemical 
evidence of H pylori infection. None of 7 normal carotid arteries was positive 
for H pylori. Intercellular adhesion molecule-1 was expressed in 75% of H 
pylori-positive plaques and in 22% of H pylori-negative plaques. The presence of 
the microorganism was associated with male sex but was independent of age, 
vascular risk factor profile, and prior neurological symptoms.
CONCLUSIONS: H pylori is present in a substantial number of carotid 
atherosclerotic lesions and is associated with features of inflammatory cell 
response. This study provides additional evidence of the relationship between H 
pylori infection and atherosclerotic disease.