[The role of endothelial dysfunction and Chlamydia pneumoniae infection in patients with ischemic stroke].

The research purposed to investigate the Chlamydia Pneumoniae infection in patients with ischemic stroke and to establish the correlation with elevated C. pneumonia antibody titers and endothelial dysfunction. 72 patients with acute ischemic stroke, aged 45 to 75 (45 male and 32 female) have been researched. Patients were grouped according to etiology of stroke (based on International classification TOAST). The blood was taken in 48 hours from stroke onset. ELISA method was applied to detect the antibodies against C. Pneumoniae. The intima-media thickness of the common carotid artery were assessed by B-mode ultrasonography (Acuson128XP/10) with a 7.5-MHz linear-array transducer. Flow-mediated dilatation (FMD) of the brachial artery were measured from high-resolution, 2-dimensional ultrasound images obtained by an ultrasound machine with a 7.5-MHz linear-array transducer. Free NO were examined by Electron Paramagnetic Resonance (EPR) method in blood. Control consisted with 15 healthy volunteers. Multivariate logistic regression showed a significant positive correlation between blood elevated titers of IgA and IgG of stroke patients and the intima-media thickness of the carotid artery (correlation coefficient by Pearson r = 0,31; p<0,05, r = 0,27; p<0,05). On multiple regression analysis, percent FMD showed a significant negative correlation with the intima-media thickness of the common carotid artery (r= -0,57, p<0,05), positive correlation between NO and the intima-media thickness of the carotid artery (r= 0,72, p<0,05). Association between antibody seropositivity for C. pneumoniae and increase of the IMT in the common carotid artery indicates persistent chronic infection in patients with ischemic stroke. Correlation between NO, an increase of the IMT in the common carotid and artery flow-mediated dilation of brachial artery indicates on the participation of NO in development of endothelial dysfunction and its significant role in pathogenesis of ischemic stroke. These findings support the concept that NO-inducible endothelial dysfunction is related to atherogenesis.