Correlation between stenosis of internal carotid artery and atherosclerosis of cerebral arteries
EANS Academy. Petr O. 09/27/19; 276096; EP01144
Ondra Petr
Ondra Petr

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Background and objective: Arterial hypertension is the main risk factor for atherosclerosis. Low-grade stenoses of pelvic- and limb-arteries showed protective effect on downstream vascular regions most likely due to reduction in blood pressure. Yet, possible impact of cervical ICA-stenoses on cerebral tissue remains unknown.
Methods: Five-hundred-sixty-eight consecutive patients with CTA/MRA of the neck and MRI of the brain were retrospectively analyzed. The level of ICA-stenosis was measured semi-automatically according to the NASCET- and ECST-criteria. Brain atrophy/sulcal dilatation were graduated using the GCA-scale. A visual rating scale for cerebellar atrophy was evaluated according to the criteria of the sulcal GCA-scale. Leukoencephalopathy was assessed using the FAZEKAS-scale for deep white matter (DWM) and periventricular white matter (PVWM). Clinical data, relevant vascular risk factors as well as correlations between stenosis grades and MRI-findings were statistically analyzed.
Results: Low-grade (10-49%) stenoses showed a linear increase in MRI-findings in all used scores whereas no correlation was present in moderate stenoses (50-79%). Similarly, the FAZEKAS-scale for DWM and PVWM showed an equivalently linear increase in low-grade stenoses (P < 0.0001). Also, low-grade (< 50%) carotid stenoses were directly proportional to the GCA-scale in the corresponding hemispheres (P < 0.0001) and even to the cerebellar score (P < 0.0001).
Conclusion: Both low-grade/moderate carotid stenoses had no protective effect on cerebral tissue. Interestingly, the extent of low-grade stenoses was directly related to both supra-/infrantentorial atrophy and leukoencephalopathy. Given the equivalent manifestations of visible atherosclerotic alterations in both anterior/posterior circulations, the proportion of carotid stenosis most likely reflects the degree of cerebral atherosclerosis albeit not implying the causal effects.
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