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Deep subcortical infarct burden in relation to apolipoprotein B/AI ratio in patients with intracranial atherosclerotic stenosis

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dc.contributor.authorPark, J. -H.-
dc.contributor.authorHong, K. -S.-
dc.contributor.authorLee, J.-
dc.contributor.authorKim, Y. -J.-
dc.contributor.authorSong, P.-
dc.date.accessioned2021-09-06T03:12:28Z-
dc.date.available2021-09-06T03:12:28Z-
dc.date.created2021-06-14-
dc.date.issued2013-04-
dc.identifier.issn1351-5101-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/103675-
dc.description.abstractBackground and purpose Pre-existing brain infarct (PBI), frequently seen on magnetic resonance imaging and usually silent, is recognized as a risk factor for future stroke. Increased apolipoprotein B (apoB)/apoAI ratio is known to be a risk predictor of ischaemic stroke and is associated with intracranial atherosclerotic stenosis (ICAS). However, little is known about the association of apoB/apoAI ratio with PBI. Methods A total of 522 statin-/fibrate-naive Korean patients, who experienced acute ischaemic stroke, were categorized into three groups: ICAS (n=254), extracranial (n=51), and no cerebral atherosclerotic stenosis (n=217). We explored the association between apoB/apoAI ratio and PBI lesions according to atherosclerosis type (ICAS, ECAS, and NCAS), PBI location (deep subcortical [ds-PBI] versus hemispheric [h-PBI]), and symptomatic PBI (s-PBI) which was relevant to a prior clinical stroke event. Results Pre-existing brain infarct(+) patients showed a higher apoB/apoAI ratio than PBI() patients (0.81 +/- 0.28 vs. 0.72 +/- 0.23, P<0.001). In ICAS group, patients with higher apoB/apoAI ratio quartiles had more PBIs, ds-PBIs, and s-PBIs (P=0.020, P=0.025, and P=0.001, respectively). With multivariable analyses, the highest apoB/apoAI ratio quartile was associated with PBI (OR, 2.56; 95% CI, 1.394.73), ds-PBI (2.48; 1.334.62), and advanced (3) ds-PBIs (2.68; 1.275.63) in ICAS group, but not with h-PBI. s-PBI had a doseresponse relationship with apoB/apoAI ratio quartiles (6.18; 1.3129.13 for the second; 5.34; 1.0626.83 for the third; and 12.17; 2.5059.19 for the fourth quartile), when referenced to the first quartile. Conclusion ApoB/apoAI ratio is associated with asymptomatic deep subcortical ischaemic burden as well as with symptomatic lesion in patients with ICAS.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherWILEY-BLACKWELL-
dc.subjectMIDDLE CEREBRAL-ARTERY-
dc.subjectSILENT BRAIN INFARCTS-
dc.subjectISCHEMIC-STROKE-
dc.subjectA-I-
dc.subjectMETABOLIC SYNDROME-
dc.subjectVASCULAR EVENTS-
dc.subjectRISK-
dc.subjectDISEASE-
dc.subjectPROGRESSION-
dc.subjectMANAGEMENT-
dc.titleDeep subcortical infarct burden in relation to apolipoprotein B/AI ratio in patients with intracranial atherosclerotic stenosis-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, J.-
dc.identifier.doi10.1111/ene.12021-
dc.identifier.scopusid2-s2.0-84875036750-
dc.identifier.wosid000316258800018-
dc.identifier.bibliographicCitationEUROPEAN JOURNAL OF NEUROLOGY, v.20, no.4, pp.671 - 680-
dc.relation.isPartOfEUROPEAN JOURNAL OF NEUROLOGY-
dc.citation.titleEUROPEAN JOURNAL OF NEUROLOGY-
dc.citation.volume20-
dc.citation.number4-
dc.citation.startPage671-
dc.citation.endPage680-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusMIDDLE CEREBRAL-ARTERY-
dc.subject.keywordPlusSILENT BRAIN INFARCTS-
dc.subject.keywordPlusISCHEMIC-STROKE-
dc.subject.keywordPlusA-I-
dc.subject.keywordPlusMETABOLIC SYNDROME-
dc.subject.keywordPlusVASCULAR EVENTS-
dc.subject.keywordPlusRISK-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusMANAGEMENT-
dc.subject.keywordAuthorapolipoprotein AI-
dc.subject.keywordAuthorapolipoprotein B-
dc.subject.keywordAuthoratherosclerosis-
dc.subject.keywordAuthorbrain infarction-
dc.subject.keywordAuthorintracranial-
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