engleski

The association of inflammatory mediators and transient ischemic attack

Background: Transient ischemic attack (TIA) develops as consequence of atherosclerosis. Our aim was to evaluate inflammatory mediators and early stages of macroangiopathy and microangiopathy in transient ischemic attack, within 12 hours from the onset of symptoms. Materials and methods: Forty- five patients (22 females, range 48-90 years) with transient ischemic attack and thirty-six controls (15 females, range 55-85 years) were included in study. Serum concentrations of cellular adhesion molecules (ICAM-1), interleukin-6 (IL- 6), C-reactive protein (CRP), glucose, lipid profile and sedimentation rate were determined for all participants. Macroangiopathy was assesed by color doppler measurement of carotid intima media thickness. Degree of cerebral vasoreactivity as early marker of microangiopathy was determined by transcranial doppler ultrasound measurement of breath holding index. Results: Levels of inflammatory mediators ICAM- 1, IL-6 and CRP were significantly increased (371.6 ± 161.8 vs. 301.9 ± 91.6 ng/L, P = 0.026 for ICAM- 1, 6.76 (2.72-18.3) vs. 2.46 (1.5-4.61) pg/mL, P < 0.001 for IL-6 and 8.5 (6.7-14.9) vs. 4.5 (2.8- 5.8) mg/L, P < 0.001 for CRP) in patients with transient ischemic attack. Carotid intima-media thickness was significantly higher (1.22 ± 0.17 vs. 0.86 ± 0.19 mm, P < 0.001) and breath holding index was significantly lower (0.67 ± 0.19 vs. 1.16 ± 0.35%/s, P < 0.001) in patients with TIA compared to controls. Conclusion: Inflammatory mediator levels and carotid intima-media thickness measured within the first 12 hours after onset of TIA symptoms are higher than in controls, which together with breath holding index lower than controls indicates high risk of future stroke

inflammation, atherosclerosis, transient ischemic attack

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