The association of inflammatory markers with cerebral vasoreactivity and carotid atherosclerosis in transient ischaemic attack

Abstract

ObjectivesInflammatory mediators have an important role in the pathogenesis of stroke. Increased activity of inflammatory mediators initiates the development of atherosclerosis independently of other risk factors, thus compromising brain microcirculation and causing transient ischaemic attack (TIA). The aim of our study was to evaluate the relationship between serum level of cellular adhesion molecules (ICAM-1), interleukin-6 (IL-6) and C-reactive protein (CRP) with carotid intima–media thickness (IMT) and breath-holding index (BHI) in subjects with transient ischaemic attack. We also aimed to assess the difference of those markers between TIA patients and disease-free control individuals. Design and methodsThe study included 45 TIA patients and 36 disease-free controls matched for age, gender and vascular risk profile. The degree of carotid atherosclerosis was assessed by colour Doppler with measurements of carotid IMT. Transcranial Doppler (TCD) ultrasound was performed in order to assess BHI. IMT, TCD, BHI and serum concentrations of ICAM-1, IL-6, and CRP were measured for all study subjects. ResultsInflammatory markers IL-6, ICAM-1 and CRP were significantly higher in TIA patients than in disease-free controls (P<0.001, P=0.026, P<0.001, respectively). TIA patients had significantly lower values of BHI and higher IMT relative to disease-free control individuals (P<0.001). ConclusionsTIA is associated with higher ICAM-1, IL-6 and CRP, pointing to the marked inflammatory response to cerebral ischaemia. Inflammatory markers are associated with higher IMT and lower BHI, indicating the insufficient cerebral perfusion due to the underlying atherosclerotic disease. Our findings highlight the key significance of inflammation in the early response to ischaemia during the transitory ischaemic episode.