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Article: Retinal microvascular signs and 10-year risk of cerebral atrophy: The atherosclerosis risk in communities (ARIC) study

TitleRetinal microvascular signs and 10-year risk of cerebral atrophy: The atherosclerosis risk in communities (ARIC) study
Authors
Keywordscerebral atrophy
retinal microvascular signs
sulcal widening
ventricular enlargement
Issue Date2010
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://stroke.ahajournals.org
Citation
Stroke, 2010, v. 41 n. 8, p. 1826-1828 How to Cite?
AbstractBackground and Purpose-: Cerebral atrophy, detected as ventricular enlargement or sulcal widening on MRI, is recognized as a risk factor for vascular dementia or Alzheimer disease. However, its underlying pathophysiology is not known. We examined whether retinal microvascular assessment could provide predictive information on the risk of ventricular enlargement and sulcal widening on MRI. Methods-: A prospective, population-based study was conducted of 810 middle-aged persons without clinical stroke or MRI infarcts. All participants had a first cranial MRI and retinal photography in 1993 to 1995 and returned for a repeated MRI in 2004 to 2006 (median follow-up of 10.5 years). Retinal photographs were graded for presence of retinopathy and retinal microvascular abnormalities, and MRI images were graded for ventricular size and sulcal size according to standardized protocols. Ventricular enlargement and sulcal widening were defined as an increase in ventricular size or sulcal size of ≥3 of 10 grades between baseline and follow-up. Results-: After adjusting for age, gender, and cardiovascular risk factors, retinopathy and arteriovenous nicking at baseline were associated with 10-year ventricular enlargement (OR and 95% CI: 2.03, 1.20 to 4.42 for retinopathy and 2.19, 1.23 to 3.90 for arteriovenous nicking). Retinal signs were not associated with 10-year sulcal widening. Conclusions-: Retinopathy and arteriovenous nicking are predictive of long-term risk of ventricular enlargement, but not of sulcal widening, independent of cardiovascular risk factors. These data support a microvascular etiology for subcortical but not cortical cerebral atrophy. © 2010 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/183595
ISSN
2023 Impact Factor: 7.8
2023 SCImago Journal Rankings: 2.450
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKawasaki, Ren_US
dc.contributor.authorCheung, Nen_US
dc.contributor.authorMosley, Ten_US
dc.contributor.authorIslam, AFMen_US
dc.contributor.authorSharrett, ARen_US
dc.contributor.authorKlein, Ren_US
dc.contributor.authorCoker, LHen_US
dc.contributor.authorKnopman, DSen_US
dc.contributor.authorShibata, DKen_US
dc.contributor.authorCatellier, Den_US
dc.contributor.authorWong, TYen_US
dc.date.accessioned2013-05-28T06:15:08Z-
dc.date.available2013-05-28T06:15:08Z-
dc.date.issued2010en_US
dc.identifier.citationStroke, 2010, v. 41 n. 8, p. 1826-1828en_US
dc.identifier.issn0039-2499en_US
dc.identifier.urihttp://hdl.handle.net/10722/183595-
dc.description.abstractBackground and Purpose-: Cerebral atrophy, detected as ventricular enlargement or sulcal widening on MRI, is recognized as a risk factor for vascular dementia or Alzheimer disease. However, its underlying pathophysiology is not known. We examined whether retinal microvascular assessment could provide predictive information on the risk of ventricular enlargement and sulcal widening on MRI. Methods-: A prospective, population-based study was conducted of 810 middle-aged persons without clinical stroke or MRI infarcts. All participants had a first cranial MRI and retinal photography in 1993 to 1995 and returned for a repeated MRI in 2004 to 2006 (median follow-up of 10.5 years). Retinal photographs were graded for presence of retinopathy and retinal microvascular abnormalities, and MRI images were graded for ventricular size and sulcal size according to standardized protocols. Ventricular enlargement and sulcal widening were defined as an increase in ventricular size or sulcal size of ≥3 of 10 grades between baseline and follow-up. Results-: After adjusting for age, gender, and cardiovascular risk factors, retinopathy and arteriovenous nicking at baseline were associated with 10-year ventricular enlargement (OR and 95% CI: 2.03, 1.20 to 4.42 for retinopathy and 2.19, 1.23 to 3.90 for arteriovenous nicking). Retinal signs were not associated with 10-year sulcal widening. Conclusions-: Retinopathy and arteriovenous nicking are predictive of long-term risk of ventricular enlargement, but not of sulcal widening, independent of cardiovascular risk factors. These data support a microvascular etiology for subcortical but not cortical cerebral atrophy. © 2010 American Heart Association, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://stroke.ahajournals.orgen_US
dc.relation.ispartofStrokeen_US
dc.subjectcerebral atrophy-
dc.subjectretinal microvascular signs-
dc.subjectsulcal widening-
dc.subjectventricular enlargement-
dc.subject.meshAtherosclerosis - Complications - Pathologyen_US
dc.subject.meshAtrophy - Complications - Pathologyen_US
dc.subject.meshCerebral Cortex - Pathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLogistic Modelsen_US
dc.subject.meshMagnetic Resonance Imagingen_US
dc.subject.meshMaleen_US
dc.subject.meshMicrovessels - Pathologyen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPredictive Value Of Testsen_US
dc.subject.meshProspective Studiesen_US
dc.subject.meshRetinal Diseases - Complications - Pathologyen_US
dc.subject.meshRetinal Vessels - Pathologyen_US
dc.subject.meshRisken_US
dc.subject.meshRisk Assessmenten_US
dc.titleRetinal microvascular signs and 10-year risk of cerebral atrophy: The atherosclerosis risk in communities (ARIC) studyen_US
dc.typeArticleen_US
dc.identifier.emailCheung, N: dannycheung@hotmail.comen_US
dc.identifier.authorityCheung, N=rp01752en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1161/STROKEAHA.110.585042en_US
dc.identifier.pmid20576949en_US
dc.identifier.pmcidPMC2935462-
dc.identifier.scopuseid_2-s2.0-77955174345en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77955174345&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume41en_US
dc.identifier.issue8en_US
dc.identifier.spage1826en_US
dc.identifier.epage1828en_US
dc.identifier.isiWOS:000280330700040-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKawasaki, R=35229910100en_US
dc.identifier.scopusauthoridCheung, N=8054683900en_US
dc.identifier.scopusauthoridMosley, T=6603754517en_US
dc.identifier.scopusauthoridIslam, AFM=16033054600en_US
dc.identifier.scopusauthoridSharrett, AR=7006662570en_US
dc.identifier.scopusauthoridKlein, R=35232138400en_US
dc.identifier.scopusauthoridCoker, LH=7003840574en_US
dc.identifier.scopusauthoridKnopman, DS=7004497868en_US
dc.identifier.scopusauthoridShibata, DK=7102096855en_US
dc.identifier.scopusauthoridCatellier, D=6604075920en_US
dc.identifier.scopusauthoridWong, TY=7403531208en_US
dc.identifier.issnl0039-2499-

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