Strategies to prevent hemorrhagic transformation after reperfusion therapies for acute ischemic stroke: A literature review.
Hemorrhagic transformation
Reperfusion
Therapeutic time window
Thrombectomy
tPA
Journal
Journal of the neurological sciences
ISSN: 1878-5883
Titre abrégé: J Neurol Sci
Pays: Netherlands
ID NLM: 0375403
Informations de publication
Date de publication:
15 Dec 2020
15 Dec 2020
Historique:
received:
01
09
2020
revised:
09
10
2020
accepted:
29
10
2020
pubmed:
9
11
2020
medline:
15
5
2021
entrez:
8
11
2020
Statut:
ppublish
Résumé
Reperfusion therapies by tissue plasminogen activator (tPA) and mechanical thrombectomy (MT) have ushered in a new era in the treatment of acute ischemic stroke (AIS). However, reperfusion therapy-related HT remains an enigma. To provide a comprehensive review focused on emerging concepts of stroke and therapeutic strategies, including the use of protective agents to prevent HT after reperfusion therapies for AIS. A literature review was performed using PubMed and the ClinicalTrials.gov database. Risk of HT increases with delayed initiation of tPA treatment, higher baseline glucose level, age, stroke severity, episode of transient ischemic attack within 7 days of stroke onset, and hypertension. At a molecular level, HT that develops after thrombolysis is thought to be caused by reactive oxygen species, inflammation, remodeling factor-mediated effects, and tPA toxicity. Modulation of these pathophysiological mechanisms could be a therapeutic strategy to prevent HT after tPA treatment. Clinical mechanisms underlying HT after MT are thought to involve smoking, a low Alberta Stroke Program Early CT Score, use of general anesthesia, unfavorable collaterals, and thromboembolic migration. However, the molecular mechanisms are yet to be fully investigated. Clinical trials with MT and protective agents have also been planned and good outcomes are expected. To fully utilize the easily accessible drug-tPA-and the high recanalization rate of MT, it is important to reduce bleeding complications after recanalization. A future study direction could be to investigate the recovery of neurological function by combining reperfusion therapies with cell therapies and/or use of pleiotropic protective agents.
Sections du résumé
BACKGROUND
BACKGROUND
Reperfusion therapies by tissue plasminogen activator (tPA) and mechanical thrombectomy (MT) have ushered in a new era in the treatment of acute ischemic stroke (AIS). However, reperfusion therapy-related HT remains an enigma.
AIM
OBJECTIVE
To provide a comprehensive review focused on emerging concepts of stroke and therapeutic strategies, including the use of protective agents to prevent HT after reperfusion therapies for AIS.
METHODS
METHODS
A literature review was performed using PubMed and the ClinicalTrials.gov database.
RESULTS
RESULTS
Risk of HT increases with delayed initiation of tPA treatment, higher baseline glucose level, age, stroke severity, episode of transient ischemic attack within 7 days of stroke onset, and hypertension. At a molecular level, HT that develops after thrombolysis is thought to be caused by reactive oxygen species, inflammation, remodeling factor-mediated effects, and tPA toxicity. Modulation of these pathophysiological mechanisms could be a therapeutic strategy to prevent HT after tPA treatment. Clinical mechanisms underlying HT after MT are thought to involve smoking, a low Alberta Stroke Program Early CT Score, use of general anesthesia, unfavorable collaterals, and thromboembolic migration. However, the molecular mechanisms are yet to be fully investigated. Clinical trials with MT and protective agents have also been planned and good outcomes are expected.
CONCLUSION
CONCLUSIONS
To fully utilize the easily accessible drug-tPA-and the high recanalization rate of MT, it is important to reduce bleeding complications after recanalization. A future study direction could be to investigate the recovery of neurological function by combining reperfusion therapies with cell therapies and/or use of pleiotropic protective agents.
Identifiants
pubmed: 33161301
pii: S0022-510X(20)30553-0
doi: 10.1016/j.jns.2020.117217
pii:
doi:
Substances chimiques
Fibrinolytic Agents
0
Pharmaceutical Preparations
0
Tissue Plasminogen Activator
EC 3.4.21.68
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
117217Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.