Histological evaluation of acute ischemic stroke thrombi may indicate the occurrence of vessel wall injury during mechanical thrombectomy.
stroke
thrombectomy
vessel wall
Journal
Journal of neurointerventional surgery
ISSN: 1759-8486
Titre abrégé: J Neurointerv Surg
Pays: England
ID NLM: 101517079
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
12
01
2021
revised:
26
03
2021
accepted:
06
04
2021
pubmed:
13
5
2021
medline:
23
3
2022
entrez:
12
5
2021
Statut:
ppublish
Résumé
Several animal studies have demonstrated that mechanical thrombectomy (MT) for acute ischemic stroke (AIS) may cause vessel wall injury (VWI). However, the histological changes in human cerebral arteries following MT are difficult to determine. To investigate the occurrence of VWI during MT by histological and immunohistochemical evaluation of AIS clots. As part of the multicenter STRIP registry, 277 clots from 237 patients were analyzed using Martius Scarlett Blue stain and immunohistochemistry for CD34 (endothelial cells) and smooth muscle actin (smooth muscle cells). MT devices used were aspiration catheters (100 cases), stentriever (101 cases), and both (36 cases). VWI was found in 33/277 clots (12%). There was no significant correlation between VWI and MT device. The degree of damage varied from grade I (mild intimal damage, 24 clots), to grade II (relevant intimal and subintimal damage, 3 clots), and III (severe injury, 6 clots). VWI clots contained significantly more erythrocytes (p=0.006*) and less platelets/other (p=0.005*) than non-VWI clots suggesting soft thrombus material.Thrombolysis correlated with a lower rate of VWI (p=0.04*). VWI cases showed a significantly higher number of passes (2 [1-4] vs 1 [1-3], p=0.028*) and poorer recanalization outcome (p=0.01*) than cases without VWI. Histological markers of VWI were present in 12% of AIS thrombi, suggesting that VWI might be related to MT. VWI was associated with soft thrombus consistency, higher number of passes and poorer revascularization outcome. There was no significant correlation between VWI and MT device.
Sections du résumé
BACKGROUND
BACKGROUND
Several animal studies have demonstrated that mechanical thrombectomy (MT) for acute ischemic stroke (AIS) may cause vessel wall injury (VWI). However, the histological changes in human cerebral arteries following MT are difficult to determine.
OBJECTIVE
OBJECTIVE
To investigate the occurrence of VWI during MT by histological and immunohistochemical evaluation of AIS clots.
METHODS
METHODS
As part of the multicenter STRIP registry, 277 clots from 237 patients were analyzed using Martius Scarlett Blue stain and immunohistochemistry for CD34 (endothelial cells) and smooth muscle actin (smooth muscle cells).
RESULTS
RESULTS
MT devices used were aspiration catheters (100 cases), stentriever (101 cases), and both (36 cases). VWI was found in 33/277 clots (12%). There was no significant correlation between VWI and MT device. The degree of damage varied from grade I (mild intimal damage, 24 clots), to grade II (relevant intimal and subintimal damage, 3 clots), and III (severe injury, 6 clots). VWI clots contained significantly more erythrocytes (p=0.006*) and less platelets/other (p=0.005*) than non-VWI clots suggesting soft thrombus material.Thrombolysis correlated with a lower rate of VWI (p=0.04*). VWI cases showed a significantly higher number of passes (2 [1-4] vs 1 [1-3], p=0.028*) and poorer recanalization outcome (p=0.01*) than cases without VWI.
CONCLUSIONS
CONCLUSIONS
Histological markers of VWI were present in 12% of AIS thrombi, suggesting that VWI might be related to MT. VWI was associated with soft thrombus consistency, higher number of passes and poorer revascularization outcome. There was no significant correlation between VWI and MT device.
Identifiants
pubmed: 33975922
pii: neurintsurg-2021-017310
doi: 10.1136/neurintsurg-2021-017310
pmc: PMC8581068
mid: NIHMS1716008
doi:
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
356-361Subventions
Organisme : NINDS NIH HHS
ID : R01 NS076491
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS105853
Pays : United States
Organisme : NINDS NIH HHS
ID : R43 NS110114
Pays : United States
Organisme : NINDS NIH HHS
ID : R44 NS107111
Pays : United States
Informations de copyright
© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: RK reports NIH funding (R01 NS076491, R43 NS110114, and R44 NS107111), is a research consultant for Cerenovus, Insera Therapeutics LLC, Marblehead Medical LLC, Microvention Inc, MIVI Neuroscience Inc, Neurogami Medical Inc, and Triticum Inc, and has stock in Neurosigma Inc (money paid to institution). AJY receives research support from Medtronic, Cerenovus, Penumbra, and Stryker, and is a consultant for Penumbra, Cerenovus, Zoll Circulation, and Vesalio. He is on the Scientific Advisory Board of XCath and Nico-lab, and has equity interest in Insera Therapeutics LLC. JEDA declares competing interests in the form of employment (modest compensation) from Medtronic and Penumbra. AMD received honoraria from Medtronic for continuing medical education events.RGN declares competing interests in the form of Stryker (DAWN Trial (DWI or CTP Assessment With Clinical Mismatch in the Triage of Wake-Up and Late Presenting Strokes Undergoing Neurointervention With TREVO) principal investigator, no compensation; TREVO Registry Steering Committee, no compensation; TREVO-2 Trial principal investigator, modest compensation; consultant, modest compensation), Medtronic (SWIFT Trial (The Solitaire With the Intention for Thrombectomy) Steering Committee, modest compensation; SWIFT-Prime Trial Steering Committee, no compensation; STAR Trial (Solitaire FR Thrombectomy for Acute Revascularisation) Angiographic Core Lab, significant compensation), Penumbra (no compensation), Cerenovus/Neuravi (ENDOLOW Trial principal investigator, EXCELLENT Registry principal investigator, ARISE-2 Trial (Analysis of Revascularization in Ischemic Stroke With EmboTrap) Steering Committee, no compensation; Physician Advisory Board, modest compensation), Phenox (Physician AdvisoryBoard, modest compensation), Anaconda (Physician Advisory Board, modest compensation), Genentech (Physician Advisory Board, modest compensation), Biogen (Physician Advisory Board, modest compensation), Prolong Pharmaceuticals (Physician Advisory Board, modest compensation), IschemaView (speaker, modest compensation), Brainomix (Research Software Use, no compensation), Sensome (Research Device Use, no compensation), Viz-AI (Physician Advisory Board, stock options), Philips (Research Software Use, no compensation; speaker, modest compensation), and Corindus Vascular Robotics (Physician Advisory Board, stock options).DFK is president of Marblehead Medical and has patent pending in balloon catheter technologies, and receives research support from Cerenovus, Insera Therapeutics LLC, Medtronic, MicroVention, MIVI Neuroscience Inc, NeuroSave, Neurogami Medical Inc, Sequent Medical and Insera, and has stock in Neurosigma Inc (money paid to institution). He is on the Scientific Advisory Board of Triticum and previously served on a SAB for Boston Scientific.WB is CMO of Marblehead Medical and has a patent pending in balloon catheter technologies, and he is a consultant for Cerenovus and Microvention. He reports NIH funding (R01 NS105853). The other authors report no conflicts.
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