Evidence map›Paper›PMID 27491735›Full record

ArticleStroke2016

Aortic Stiffness and the Risk of Incident Mild Cognitive Impairment and Dementia.

Matthew P Pase, Alexa Beiser, Jayandra J Himali, Connie Tsao, Claudia L Satizabal, Ramachandran S Vasan, Sudha Seshadri, Gary F Mitchell

Abstract read
In one paragraph

Article in Stroke, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

97 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  17. Intracranial atherosclerotic disease and neurodegeneration: a narrative review and plausible mechanisms.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2024
    Review
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37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Matthew P PaseFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.). matthewpase@gmail.com.
Alexa BeiserFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Jayandra J HimaliFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Connie TsaoFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Claudia L SatizabalFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Ramachandran S VasanFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Sudha SeshadriFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).
Gary F MitchellFrom the Department of Neurology, Boston University School of Medicine, MA (M.P.P., A.B., J.J.H., C.L.S., S.S.); Framingham Heart Study, MA (M.P.P., A.B., J.J.H., C.L.S., R.S.V., S.S., G.F.M.); Centre for Human Psychopharmacology, Swinburne University of Technology, Hawthorn, Australia (M.P.P.); Department of Biostatistics, Boston University School of Public Health, MA (A.B.); Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Centre, Boston, MA (C.T.); and Cardiovascular Engineering Inc, Norwood, MA (G.F.M.).

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
PRECURSORS OF STROKE INCIDENCE AND PROGNOSISR01NS017950 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Hugo Javier Aparicio, Jose Rafael Romero · 1985 to 2026
$22.9M
EPIDEMIOLOGY OF DEMENTIA IN THE FRAMINGHAM STUDYR01AG008122 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, SESHADRI, SUDHA · 1989 to 2015
$14.4M
Temporal Trends, Novel Imaging and Molecular Characterization of Preclinical and Clinical Alzheimer's Disease in the Framingham CohortsR01AG054076 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DECARLI, CHARLES, SESHADRI, SUDHA · 2016 to 2020
$12.3M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
Framingham: Inflammation, Genes &Cardiovascular DiseaseR01HL076784 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BENJAMIN, EMELIA J. · 2004 to 2008
$3.9M
Ventricular Vascular Coupling: Correlates and PrognosisR01HL080124 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAMACHANDRAN, VASAN S · 2005 to 2009
$3.4M
Preclinical AD: Correlates of Amyloid, Tau PET and fcMRI in Framingham Gen 3 Young AdultsR01AG049607 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SESHADRI, SUDHA · 2015 to 2019
$3.1M
Biomarkers of Ventricular and Vascular RemodelingR01HL077447 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAMACHANDRAN, VASAN S · 2005 to 2009
$2.6M
Aortic Dysfunction, Pulsatile Stress and Target Organ Damage in FraminghamR01HL107385 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MITCHELL, GARY FRANK, RAMACHANDRAN, VASAN S · 2011 to 2014
$2.6M
Vascular Function in the Framingham Third GenerationR01HL070100 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BENJAMIN, EMELIA J. · 2002 to 2005
$2.4M
Aging and Inflammation: Longitudinal Markers and Genetics in the Framingham StudyR01AG028321 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BENJAMIN, EMELIA J. · 2006 to 2010
$1.8M
NHLBI NIH HHS HHSN268201500001CNHLBI NIH HHS HHSN268201500001INHLBI NIH HHS K24 HL004334NHLBI NIH HHS N01 HC025195NHLBI NIH HHS R01 HL060040NHLBI NIH HHS R01 HL070100NHLBI NIH HHS R01 HL071039NHLBI NIH HHS R01 HL076784NHLBI NIH HHS R01 HL077447NHLBI NIH HHS R01 HL080124NHLBI NIH HHS R01 HL107385NIA NIH HHS P30 AG010129NIA NIH HHS R01 AG008122NIA NIH HHS R01 AG028321NIA NIH HHS R01 AG033193NIA NIH HHS R01 AG049607NIA NIH HHS R01 AG054076NINDS NIH HHS R01 NS017950
6 · The paper itself

Abstract

background and purposeAortic stiffening increases the transfers of high pressure and flow pulsatility to small cerebral vessels potentially causing the accumulation of vascular brain injury. Our aim was to investigate the prospective association of aortic stiffness with the risks of incident mild cognitive impairment and dementia.

methodsWe studied 1101 dementia-free Framingham Offspring study participants (mean age, 69±6 years; 54% women). Aortic stiffness was measured as carotid-femoral pulse wave velocity using applanation tonometry and modeled as a linear variable and the top 2 quintiles (>11.4 m/s). Outcomes were the 10-year risk of incident mild cognitive impairment and dementia, including clinically characterized Alzheimer disease. We observed 106, 77, and 59 events of mild cognitive impairment, all-cause dementia, and clinical Alzheimer disease, respectively.

resultsAfter adjustment for age and sex, higher continuous aortic stiffness predicted an increased risk of mild cognitive impairment (hazard ratio, 1.40 [95% confidence interval, 1.13-1.73]), all-cause dementia (hazard ratio, 1.45 [95% confidence interval, 1.13-1.87]), and Alzheimer disease (hazard ratio, 1.41 [95% confidence interval, 1.06-1.87]). In risk factor-adjusted statistical models, aortic stiffness remained a significant predictor of mild cognitive impairment but not incident dementia. In nondiabetic patients, the top 2 quintiles of aortic stiffness were associated with a higher risk of incident all-cause dementia across all statistical models.

conclusionsAortic stiffness was an independent predictor of incident mild cognitive impairment in the whole sample and with incident dementia in nondiabetic patients. Our findings suggest aortic stiffness as a potentially modifiable risk factor for clinical cognitive impairment and dementia.

Indexed as

AgedCognitive DysfunctionDementiaFemaleHumansIncidenceMaleMiddle AgedProspective StudiesPulse Wave AnalysisRiskVascular StiffnessAlzheimer diseasebraindementiarisk factorsvascular stiffness

Identifiers

PMID27491735
PMCPMC4995162

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.