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Inflammation can play a key role in some manifestations of atherosclerosis including coronary artery disease and cerebrovascular ischemia. According to several researchers, the importance of inflammation in myocardial infarction and stroke is beginning to be recognized. C. pneumoniae has been suspected as a potential trigger of atherosclerotic plaque inflammation. A recent study presented at the 60th Annual Meeting of the Society for Vascular Surgery suggests that Chlamydia pneumoniae (C. Pneumoniae) and plaque inflammation have been associated with cerebrovascular symptomatology in carotid disease patients.

Several inflammatory mediators are involved in atherosclerotic lesion inflammation. One class of inflammatory mediators is cytokines, and one of the best known is TNF-α. “When specific cells of the lesion come in contact with non-self antigens as in the case of an infectious agent, they are activated and produce large amounts of cytokines including TNF-α,” said lead author Elias A. Kaperonis, MD, from the 2nd Dept of Propedeutic Surgery at Laiko Hospital, Athens University Medical School in Greece.

“When cytokines, including TNF-α, are produced like this, they induce the expression of matrix metalloproteinases (MMP)” said Dr. Kaperonis, who explained that MMPs are proteases, substances that take apart proteins. “When MMPs attack the cap of the plaque, it may lead to rupture, thrombosis or both, which causes myocardial infarctions and strokes,” added Dr. Kaperonis.

“We wanted to detect C. Pneumoniae on plaque and measure TNF-α plaque values in 78 patients who underwent carotid endartectomy in this study (46 were symptomatic and 32 asymptomatic)” said Dr. Kaperonis. He noted that there was no significant statistical differences in traditional cardiovascular risks in patients, however hypertension was more common in symptomatic patients. Four out of five patients in this same group stained positive for C. Pneumoniae; only one-quarter of the asymptomatic patients strained positive for it. Chronic inflammation and infection seem to have an important role in the complications of carotid atherosclerotic lesions, as the mean TNF-α symptomatic lesion level was many times higher than the corresponding asymptomatic lesion value.

Hypertensive, hypercholesterolemic men were more likely to have C. Pneumoniae infected carotid plaques and those plaques had higher TNF-α concentrations. “TNF-α is produced by almost all cells of the atherosclerotic plaque when infected by C. Pneumoniae and we found that C. Pneumoniae was detected much more often and TNF-α levels were much higher in atheromas of patients with cerebrovascular events,” said Dr. Kaperonis. 

He suggested that the results of his study could be corroborated by others. “This could prove to be very important because serum markers could help identify plaques in risk of rupture and intervene either pharmacologically or surgically to prevent cerebral infarctions,” said Dr. Kaperonis. “In addition, the value and effectiveness of specific therapeutic agents against C. Pneumoniae and TNF-α for the prevention of strokes could be further investigated.