Cerebral Small Vessel Disease and Infarct Growth in Acute Ischemic Stroke Treated with Intravenous Thrombolysis.
Ischemic stroke
Lacunar infarct
Small vessel disease
Thrombolysis
White matter changes
rt-PA
Journal
Translational stroke research
ISSN: 1868-601X
Titre abrégé: Transl Stroke Res
Pays: United States
ID NLM: 101517297
Informations de publication
Date de publication:
04 Jul 2024
04 Jul 2024
Historique:
received:
10
03
2024
accepted:
29
06
2024
revised:
03
06
2024
medline:
4
7
2024
pubmed:
4
7
2024
entrez:
4
7
2024
Statut:
aheadofprint
Résumé
We investigated relations between cerebral small vessel disease (cSVD) markers and evolution of the ischemic tissue from ischemic core to final infarct in people with acute ischemic stroke treated with intravenous thrombolysis. Data from the Stroke Imaging Repository (STIR) and Virtual International Stroke Trials Archive (VISTA) were used. Any pre-existing lacunar infarcts and white matter hyperintensities (WMH) were assessed on magnetic resonance (MR) before thrombolytic therapy. Acute ischemic core and final infarct volume were then assessed by two independent radiologists. The relationship among baseline markers of cSVD, acute ischemic core volume, final infarct volume, infarct growth (IG = final infarct - ischemic core), and infarct growth ratio (IGR = final infarct/ischemic core) was then assessed using linear and ordinal regression adjusted for age, sex, onset-to-treatment time, and stroke severity. We included 165 patients, mean (± SD) age 69.5 (± 15.7) years, 74 (45%) males, mean (± SD) ischemic core volume 25.48 (± 42.22) ml, final infarct volume 52.06 (± 72.88) ml, IG 26.58 (± 51.02) ml, IGR 8.23 (± 38.12). Seventy (42%) patients had large vessel occlusion, 20 (12%) acute small subcortical infarct. WMHs were present in 131 (79%) and lacunar infarcts in 61 (37%) patients. Final infarct volumes were 53.8 ml and 45.2 ml (WMHs/no WMHs), p = 0.139, and 24.6 ml and 25.9 ml (lacunar infarcts/no lacunar infarcts), p = 0.842. In linear and ordinal regression analyses, presence of lacunar infarcts was associated with smaller IG (β = - 0.17; p = 0.024; cOR = 0.52; 95%CI = 0.28-0.96, respectively) and WMHs were associated with smaller IGR (β = - 0.30; p = 0.004; cOR = 0.27; 95%CI = 0.11-0.69, respectively). In people with acute ischemic stroke treated with intravenous thrombolysis, cSVD features were associated with smaller growth of the acute ischemic area, suggesting less salvageable tissue at time of reperfusion therapy.
Identifiants
pubmed: 38963535
doi: 10.1007/s12975-024-01277-2
pii: 10.1007/s12975-024-01277-2
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Références
Wardlaw JM, Smith EE, Biessels GJ, et al. STandards for ReportIng Vascular changes on nEuroimaging (STRIVE v1). Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol. 2013;12:822–38.
doi: 10.1016/S1474-4422(13)70124-8
pubmed: 23867200
pmcid: 3714437
Arba F, Mair G, Carpenter T, et al. IST-3 Trial Collaborators. Cerebral white matter hypoperfusion increases with small-vessel disease burden. Data from the third international stroke trial. J Stroke Cerebrovasc Dis. 2017;26:1506–13.
doi: 10.1016/j.jstrokecerebrovasdis.2017.03.002
pubmed: 28314624
IST-3 collaborative group. The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the third international stroke trial [IST-3]): a randomised controlled trial. Lancet. 2012;379:2352–63.
doi: 10.1016/S0140-6736(12)60768-5
Arba F, Testa GD, Limbucci N, et al. Small vessel disease and clinical outcomes after endovascular treatment in acute ischemic stroke. Neurol Sci. 2019;40:1227–35.
doi: 10.1007/s10072-019-03824-4
pubmed: 30874998
Arba F, Inzitari D, Ali M, Warach SJ, Luby M, Lees KR. STIR/VISTA Imaging Collaboration. Small vessel disease and clinical outcomes after IV rt-PA treatment. Acta Neurol Scand. 2017;136:72–7.
doi: 10.1111/ane.12745
pubmed: 28233290
Kongbunkiat K, Wilson D, Kasemsap N, et al. Leukoaraiosis, intracerebral hemorrhage, and functional outcome after acute stroke thrombolysis. Neurology. 2017;88:638–45.
doi: 10.1212/WNL.0000000000003605
pubmed: 28130468
pmcid: 5317383
Rocha M, Jovin TG. Fast versus slow progressors of infarct growth in large vessel occlusion stroke: clinical and research implications. Stroke. 2017;48:2621–7.
doi: 10.1161/STROKEAHA.117.017673
pubmed: 28794271
Henninger N, Lin E, Haussen DC, et al. Leukoaraiosis and sex predict the hyperacute ischemic core volume. Stroke. 2013;44:61–7.
doi: 10.1161/STROKEAHA.112.679084
pubmed: 23233384
Ay H, Arsava EM, Rosand J, et al. Severity of leukoaraiosis and susceptibility to infarct growth in acute stroke. Stroke. 2008;39:1409–13.
doi: 10.1161/STROKEAHA.107.501932
pubmed: 18340093
van Swieten JC, Hijdra A, Koudstaal PJ, van Gijn J. Grading white matter lesions on CT and MRI: a simple scale. J Neurol Neurosurg Psychiatry. 1990;53:1080–3.
doi: 10.1136/jnnp.53.12.1080
pubmed: 2292703
pmcid: 488320
IST-3 collaborators. Association between brain imaging signs, early and late outcomes, and response to intravenous alteplase after acute ischaemic stroke in the third International Stroke Trial (IST-3): secondary analysis of a randomised controlled trial. Lancet Neurol. 2015;14:485–96.
doi: 10.1016/S1474-4422(15)00012-5
Curtze S, Haapaniemi E, Melkas S, et al. White matter lesions double the risk of post-thrombolytic intracerebral hemorrhage. Stroke. 2015;46:2149–55.
doi: 10.1161/STROKEAHA.115.009318
pubmed: 26111888
Boulouis G, Bricout N, Benhassen W, et al. White matter hyperintensity burden in patients with ischemic stroke treated with thrombectomy. Neurology. 2019;93:e1498–506.
doi: 10.1212/WNL.0000000000008317
pubmed: 31519778
pmcid: 6815208
Wheeler HM, Mlynash M, Inoue M, et al. DEFUSE 2 Investigators. The growth rate of early DWI lesions is highly variable and associated with penumbral salvage and clinical outcomes following endovascular reperfusion. Int J Stroke. 2015;10:723–9.
doi: 10.1111/ijs.12436
pubmed: 25580662
pmcid: 4478123
Hakimelahi R, Vachha BA, Copen WA, et al. Time and diffusion lesion size in major anterior circulation ischemic strokes. Stroke. 2014;45:2936–41.
doi: 10.1161/STROKEAHA.114.005644
pubmed: 25190444
McCabe C, Gallagher L, Gsell W, Graham D, Dominiczak AF, Macrae IM. Differences in the evolution of the ischemic penumbra in stroke-prone spontaneously hypertensive and Wistar-Kyoto rats. Stroke. 2009;40:3864–8.
doi: 10.1161/STROKEAHA.109.559021
pubmed: 19797186
pmcid: 3145096
Kim BJ, Lee SH. Prognostic impact of cerebral small vessel disease on stroke outcome. J Stroke. 2015;17:101–10.
doi: 10.5853/jos.2015.17.2.101
pubmed: 26060797
pmcid: 4460329
Bani-Sadr A, Pavie D, Mechtouff L, et al. Brush sign and collateral supply as potential markers of large infarct growth after successful thrombectomy. Eur Radiol. 2023;33:4502–9.
doi: 10.1007/s00330-022-09387-x
pubmed: 36633674
Lee JS, Bang OY. Collateral status and outcomes after thrombectomy. Transl Stroke Res. 2023;14:22–37.
doi: 10.1007/s12975-022-01046-z
pubmed: 35687300
Lin MP, Brott TG, Liebeskind DS, Meschia JF, Sam K, Gottesman RF. Collateral recruitment is impaired by cerebral small vessel disease. Stroke. 2020;51:1404–10.
doi: 10.1161/STROKEAHA.119.027661
pubmed: 32248770
Seners P, Turc G, Maïer B, Mas JL, Oppenheim C, Baron JC. Incidence and predictors of early recanalization after intravenous thrombolysis: a systematic review and meta-analysis. Stroke. 2016;47:2409–12.
doi: 10.1161/STROKEAHA.116.014181
pubmed: 27462117
Kong Q, Wang Z, Zhao J, Zhang Yi, Zhou X, Lingshan Wu, Zhiyuan Yu, Huang H, Luo X. Cerebral small vessel disease and outcomes in patients with acute ischemic stroke receiving endovascular treatment: a systematic review and meta-analysis. Stroke Vasc Interv Neurol. 2023;3: e000866. https://doi.org/10.1161/SVIN.123.000866 .
doi: 10.1161/SVIN.123.000866