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Does cerebral hemodynamic compromise contribute to cerebral cortical microinfarcts: A proof of concept study in patients with internal carotid artery occlusion
Author(s) -
van den Brink Hilde,
Ferro Doeschka A,
de Bresser Jeroen,
Bron Esther E,
Onkenhout Laurien P,
Kappelle Jaap,
Biessels Geert Jan
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.040256
Subject(s) - medicine , occlusion , internal carotid artery , cerebral blood flow , cardiology , hemodynamics , dementia , cerebral arteries , disease
Background Cerebral cortical microinfarcts (CMI) are small ischemic lesions that are associated with cognitive impairment and are often detected in patients with dementia, also in patients with a clinical diagnosis of Alzheimer’s disease (AD). CMI probably have multiple etiologies. Cerebral hypoperfusion has also been proposed as a causal factor. We studied CMI in patients with internal carotid artery (ICA) occlusion, as a model for cerebral hemodynamic compromise, addressing CMI presence and spatial distribution, also in relation to the condition of the remaining arterial supply. Methods We included 95 patients with a complete ICA occlusion (age 66.2±8.3, 22% female) and a reference group of 125 participants (age 65.5±7.4, 47% female) from the Heart‐Brain Study. Participants underwent an extensive evaluation including clinical and neuropsychological assessment, and 3T brain MR, on which CMI were rated according to standardized criteria. Results CMI were more common in patients with an ICA occlusion (54%, median 2, range 1‐33) than in the reference group (6%, median 0; range 1‐7) (OR 14.3; 95% CI 6.2‐33.1; p <.001). Among patients with a unilateral ICA occlusion, CMI were more common ipsilateral to the occlusion than in the contralateral hemisphere (median 2 and 0 respectively; p <.001). In patients with CMI the number of (other) occluded or stenosed cervical arteries was higher ( p =.038), and cerebral blood flow tended to be lower (B ‐6.2 ml/min/100ml; 95% CI ‐12.4‐0.02; p =.05) than in patients without CMI. Conclusion CMI are very common in patients with an ICA occlusion, preferably in the hemisphere of the occluded ICA and CMI burden was related to the severity of cervical arterial compromise. Supporting the etiological role of hemodynamics in the occurrence of CMI. Given the common occurrence of CMI in patients with AD and known effects of AD on cerebral perfusion, further studies on the interplay between AD pathologies, cerebral perfusion and CMIs in relation to clinical outcomes, in particular cognitive decline, are warranted.