Quantification and mapping of cerebral hemodynamics before and after carotid endarterectomy, using four-dimensional flow magnetic resonance imaging.


Journal

Journal of vascular surgery
ISSN: 1097-6809
Titre abrégé: J Vasc Surg
Pays: United States
ID NLM: 8407742

Informations de publication

Date de publication:
09 2021
Historique:
received: 13 10 2020
accepted: 26 01 2021
pubmed: 4 4 2021
medline: 28 9 2021
entrez: 3 4 2021
Statut: ppublish

Résumé

Carotid stenosis can profoundly affect cerebral hemodynamics, which cannot simply be inferred from the degree of stenosis. We quantified and mapped the distribution of the blood flow rate (BFR) in the cerebral arteries before and after carotid endarterectomy using four-dimensional (4D) phase-contrast (PC) magnetic resonance imaging (MRI). Nineteen patients (age, 71 ± 6 years; 2 women) with symptomatic carotid stenosis (≥50%) undergoing carotid endarterectomy (CEA) were investigated using 4D PC-MRI before and after surgery. The BFR was measured in 17 cerebral arteries and the ophthalmic arteries. Collateral recruitment through the anterior and posterior communicating arteries, ophthalmic arteries, and leptomeningeal arteries was quantified. BFR laterality was significantly different between the paired contralateral and ipsilateral arteries. Subgroups were defined according to the presence of collateral recruitment. The total cerebral blood flow had increased by 15% (P < .01) after CEA. Before CEA, laterality was seen in the internal carotid artery, anterior cerebral artery, and middle cerebral artery (MCA). On the ipsilateral side, an increased BFR was found after CEA in the internal carotid artery (246 ± 62 mL/min vs 135 ± 80 mL/min; P < .001), anterior cerebral artery (87 ± mL/min vs 38 ± 58 mL/min; P < .01), and MCA (149 ± 43 mL/min vs 119 ± 34 mL/min; P < .01), resulting in a postoperative BFR distribution without signs of laterality. In the nine patients with preoperatively recruited collaterals, BFR laterality was found in the MCA before, but not after, CEA (P < .01). This laterality was not found in the 10 patients without collateral recruitment (P = .2). The degree of stenosis did not differ between the groups with and without collateral recruitment (P = .85). Using 4D PC-MRI, we have presented a comprehensive and noninvasive method to evaluate the cerebral hemodynamics due to carotid stenosis before and after CEA. MCA laterality, seen in the patients with collateral recruitment before CEA, pointed toward a hemodynamic disturbance in MCA territory for those patients. This methodologic advancement provides an insight into the pathophysiology of cerebral hemodynamics in patients with carotid stenosis.

Sections du résumé

BACKGROUND
Carotid stenosis can profoundly affect cerebral hemodynamics, which cannot simply be inferred from the degree of stenosis. We quantified and mapped the distribution of the blood flow rate (BFR) in the cerebral arteries before and after carotid endarterectomy using four-dimensional (4D) phase-contrast (PC) magnetic resonance imaging (MRI).
METHODS
Nineteen patients (age, 71 ± 6 years; 2 women) with symptomatic carotid stenosis (≥50%) undergoing carotid endarterectomy (CEA) were investigated using 4D PC-MRI before and after surgery. The BFR was measured in 17 cerebral arteries and the ophthalmic arteries. Collateral recruitment through the anterior and posterior communicating arteries, ophthalmic arteries, and leptomeningeal arteries was quantified. BFR laterality was significantly different between the paired contralateral and ipsilateral arteries. Subgroups were defined according to the presence of collateral recruitment.
RESULTS
The total cerebral blood flow had increased by 15% (P < .01) after CEA. Before CEA, laterality was seen in the internal carotid artery, anterior cerebral artery, and middle cerebral artery (MCA). On the ipsilateral side, an increased BFR was found after CEA in the internal carotid artery (246 ± 62 mL/min vs 135 ± 80 mL/min; P < .001), anterior cerebral artery (87 ± mL/min vs 38 ± 58 mL/min; P < .01), and MCA (149 ± 43 mL/min vs 119 ± 34 mL/min; P < .01), resulting in a postoperative BFR distribution without signs of laterality. In the nine patients with preoperatively recruited collaterals, BFR laterality was found in the MCA before, but not after, CEA (P < .01). This laterality was not found in the 10 patients without collateral recruitment (P = .2). The degree of stenosis did not differ between the groups with and without collateral recruitment (P = .85).
CONCLUSIONS
Using 4D PC-MRI, we have presented a comprehensive and noninvasive method to evaluate the cerebral hemodynamics due to carotid stenosis before and after CEA. MCA laterality, seen in the patients with collateral recruitment before CEA, pointed toward a hemodynamic disturbance in MCA territory for those patients. This methodologic advancement provides an insight into the pathophysiology of cerebral hemodynamics in patients with carotid stenosis.

Identifiants

pubmed: 33812036
pii: S0741-5214(21)00470-5
doi: 10.1016/j.jvs.2021.01.074
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

910-920.e1

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Laleh Zarrinkoob (L)

Division of Neuroscience, Department of Clinical Sciences, Umeå University, Umeå, Sweden; Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden. Electronic address: laleh.zarrinkoob@umu.se.

Anders Wåhlin (A)

Department of Radiation Sciences, Umeå University, Umeå, Sweden; Centre for Biomedical Engineering and Physics, Umeå University, Umeå, Sweden; Umeå Center for Functional Brain Imaging, Umeå University, Umeå, Sweden.

Khalid Ambarki (K)

Department of Radiation Sciences, Umeå University, Umeå, Sweden; Centre for Biomedical Engineering and Physics, Umeå University, Umeå, Sweden.

Anders Eklund (A)

Department of Radiation Sciences, Umeå University, Umeå, Sweden; Centre for Biomedical Engineering and Physics, Umeå University, Umeå, Sweden.

Jan Malm (J)

Division of Neuroscience, Department of Clinical Sciences, Umeå University, Umeå, Sweden.

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