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Adipose tissue density, a novel biomarker predicting mortality risk in older adults.

https://arctichealth.org/en/permalink/ahliterature113601
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Publication Type
Article
Date
Jan-2014
Author
Rachel A Murphy
Thomas C Register
Carol A Shively
J Jeffrey Carr
Yaorong Ge
Marta E Heilbrun
Steven R Cummings
Annemarie Koster
Michael C Nevitt
Suzanne Satterfield
Frances A Tylvasky
Elsa S Strotmeyer
Anne B Newman
Eleanor M Simonsick
Ann Scherzinger
Bret H Goodpaster
Lenore J Launer
Gudny Eiriksdottir
Sigurdur Sigurdsson
Gunnar Sigurdsson
Vilmundur Gudnason
Thomas F Lang
Stephen B Kritchevsky
Tamara B Harris
Author Affiliation
Laboratory of Population Science, National Institute on Aging, 7201 Wisconsin Ave, 3C-309 Bethesda, MD 20814. rachel.murphy@nih.gov.
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Absorptiometry, Photon
Adiponectin - metabolism
Adipose Tissue - metabolism - radiography
Aged
Aged, 80 and over
Aging - physiology
Animals
Biological Markers - metabolism
Body mass index
Female
Follow-Up Studies
Humans
Leptin - metabolism
Macaca fascicularis
Male
Obesity - metabolism - mortality - radiography
Prognosis
Prospective Studies
Risk factors
Survival Rate - trends
Abstract
Knowledge of adipose composition in relation to mortality may help delineate inconsistent relationships between obesity and mortality in old age. We evaluated relationships between abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) density, mortality, biomarkers, and characteristics.
VAT and SAT density were determined from computed tomography scans in persons aged 65 and older, Health ABC (n = 2,735) and AGES-Reykjavik (n = 5,131), and 24 nonhuman primates (NHPs). Associations between adipose density and mortality (4-13 years follow-up) were assessed with Cox proportional hazards models. In NHPs, adipose density was related to serum markers and tissue characteristics.
Higher density adipose tissue was associated with mortality in both studies with adjustment for risk factors including adipose area, total fat, and body mass index. In women, hazard ratio and 95% CI for the densest quintile (Q5) versus least dense (Q1) for VAT density were 1.95 (1.36-2.80; Health ABC) and 1.88 (1.31-2.69; AGES-Reykjavik) and for SAT density, 1.76 (1.35-2.28; Health ABC) and 1.56 (1.15-2.11; AGES-Reykjavik). In men, VAT density was associated with mortality in Health ABC, 1.52 (1.12-2.08), whereas SAT density was associated with mortality in both Health ABC, 1.58 (1.21-2.07), and AGES-Reykjavik, 1.43 (1.07-1.91). Higher density adipose tissue was associated with smaller adipocytes in NHPs. There were no consistent associations with inflammation in any group. Higher density adipose tissue was associated with lower serum leptin in Health ABC and NHPs, lower leptin mRNA expression in NHPs, and higher serum adiponectin in Health ABC and NHPs.
VAT and SAT density provide a unique marker of mortality risk that does not appear to be inflammation related.
PubMed ID
23707956 View in PubMed
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Adipose Tissue, Muscle, and Function: Potential Mediators of Associations Between Body Weight and Mortality in Older Adults With Type 2 Diabetes.

https://arctichealth.org/en/permalink/ahliterature257280
Source
Diabetes Care. 2014 Oct 14;
Publication Type
Article
Date
Oct-14-2014
Author
Rachel A Murphy
Ilse Reinders
Melissa E Garcia
Gudny Eiriksdottir
Lenore J Launer
Rafn Benediktsson
Vilmundur Gudnason
Palmi V Jonsson
Tamara B Harris
Author Affiliation
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, Bethesda, MD rachel.murphy@nih.gov.
Source
Diabetes Care. 2014 Oct 14;
Date
Oct-14-2014
Language
English
Publication Type
Article
Abstract
Studies in type 2 diabetes report both increased mortality for normal weight and no evidence of an obesity paradox. We aimed to examine whether adipose tissue, muscle size, and physical function, which are known to vary by weight, mediate associations between BMI and mortality.
The AGES-Reykjavik cohort comprised participants aged 66-96 years with diabetes defined by fasting glucose, medications, or self-report. BMI was determined from measured height and weight and classified as normal (18.5-24.9 kg/m(2), n = 117), overweight (25.0-29.9 kg/m(2), n = 293, referent group) or obese (=30.0 kg/m(2), n = 227). Thigh muscle area and intermuscular, visceral, and subcutaneous adipose tissues were assessed with computed tomography. Function was assessed from gait speed and knee extensor strength. Hazard ratios (HRs) and 95% CIs were estimated by Cox proportional hazards regression adjusted for demographics and diabetes-related risk factors.
The median follow-up was 6.66 years, and there were 85, 59, and 44 deaths among normal weight, overweight, and obese participants, respectively. There was no mortality risk for obese participants and an increased risk among normal weight compared with overweight participants (HR 1.72 [95% CI 1.12-2.64]). Associations remained with adjustment for adipose tissues and knee extensor strength; however, mortality risk for normal weight was attenuated following adjustment for thigh muscle (HR 1.36 [95% CI 0.87-2.11]) and gait speed (HR 1.44 [95% CI 0.91-2.27]). Linear regression confirmed with bootstrapping indicated that thigh muscle size mediated 46% of the relationship between normal weight and mortality.
Normal weight participants had elevated mortality risk compared with overweight participants. This paradoxical association was mediated in part by muscle size.
PubMed ID
25315206 View in PubMed
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Age-related macular degeneration and mortality in community-dwelling elders: the age, gene/environment susceptibility Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature261803
Source
Ophthalmology. 2015 Feb;122(2):382-90
Publication Type
Article
Date
Feb-2015
Author
Diana E Fisher
Fridbert Jonasson
Gudny Eiriksdottir
Sigurdur Sigurdsson
Ronald Klein
Lenore J Launer
Vilmundur Gudnason
Mary Frances Cotch
Source
Ophthalmology. 2015 Feb;122(2):382-90
Date
Feb-2015
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Cause of Death
Cohort Studies
Disease Susceptibility
Female
Follow-Up Studies
Gene-Environment Interaction
Humans
Iceland - epidemiology
Incidence
Macular Degeneration - mortality
Male
Proportional Hazards Models
Prospective Studies
Risk factors
Abstract
To investigate the association between age-related macular degeneration (AMD) and mortality in older persons.
Population-based prospective cohort study.
Participants 67 to 96 years of age (43.1% male) enrolled between 2002 and 2006 in the Age, Gene/Environment Susceptibility-Reykjavik Study.
Retinal photographs of the macula were acquired digitally and evaluated for the presence of AMD lesions using the Wisconsin Age-Related Maculopathy grading scheme. Mortality was assessed prospectively through 2013 with cause of death available through 2009. The association between AMD and death, resulting from any cause and specifically cardiovascular disease (CVD), was examined using Cox proportional hazards regression with age as the time scale, adjusted for significant risk factors and comorbid conditions. To address a violation in the proportional hazards assumption, analyses were stratified into 2 groups based on the mean age at death (83 years).
Mortality resulting from all causes and CVD.
Among 4910 participants, after a median follow-up of 8.6 years, 1742 died (35.5%), of whom 614 (35.2%) had signs of AMD at baseline. Cardiovascular disease was the cause of death for 357 people who died before the end of 2009, of whom 144 (40%) had AMD (101 with early disease and 43 with late disease). After considering covariates, including comorbid conditions, having early AMD at any age or having late AMD in individuals younger than 83 years (n = 4179) were not associated with all-cause or CVD mortality. In individuals 83 years of age and older (n = 731), late AMD was associated significantly with increased risk of all-cause mortality (hazard ratio [HR], 1.76; 95% confidence interval [CI], 1.20-2.57) and CVD-related mortality (HR, 2.37; 95% CI, 1.41-3.98). In addition to having AMD, older individuals who died were more likely to be male and to have low body mass index, impaired cognition, and microalbuminuria.
Competing risk factors and concomitant conditions are important in determining mortality risk resulting from AMD. Individuals with early AMD are not more likely to die than peers of comparable age. Late AMD becomes a predictor of mortality by the mid-octogenarian years.
Notes
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PubMed ID
25264026 View in PubMed
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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature292670
Source
Kidney Int. 2018 Jun 27; :
Publication Type
Journal Article
Date
Jun-27-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 Jun 27; :
Date
Jun-27-2018
Language
English
Publication Type
Journal Article
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min per 1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature300494
Source
Kidney Int. 2018 09; 94(3):608-615
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Date
09-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 09; 94(3):608-615
Date
09-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Keywords
Aged
Albuminuria - physiopathology - urine
Cerebral Small Vessel Diseases - diagnosis - epidemiology
Creatinine - urine
Disease Progression
Female
Follow-Up Studies
Glomerular Filtration Rate - physiology
Humans
Incidence
Independent living
Kidney - physiopathology
Magnetic Resonance Imaging
Male
Prospective Studies
Renal Insufficiency, Chronic - physiopathology - urine
Risk factors
Serum Albumin
White Matter - diagnostic imaging - pathology
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min/1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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Aortic stiffness and change in glomerular filtration rate and albuminuria in older people.

https://arctichealth.org/en/permalink/ahliterature272828
Source
Nephrol Dial Transplant. 2016 Mar 28;
Publication Type
Article
Date
Mar-28-2016
Author
Naya Huang
Meredith C Foster
Gary F Mitchell
Margret B Andresdottir
Gudny Eiriksdottir
Hrefna Gudmundsdottir
Tamara B Harris
Lenore J Launer
Runolfur Palsson
Vilmundur Gudnason
Andrew S Levey
Lesley A Inker
Source
Nephrol Dial Transplant. 2016 Mar 28;
Date
Mar-28-2016
Language
English
Publication Type
Article
Abstract
Aortic stiffness increases with age and increases pulsatile stress in the microcirculation. Abnormalities in kidney microvascular structure and function may contribute to development or progression of chronic kidney disease in older people.
We performed a longitudinal analysis of 629 community-dwelling elderly Icelandic adults from the Age, Gene/Environment Susceptibility-Reykjavik Study with two visits over a mean follow-up of 5.3 years. We evaluated the associations of carotid-femoral pulse wave velocity (CFPWV), carotid pulse pressure (CPP) and augmentation index (AI), with the change in estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) assessed as annual change and dichotomized as large changes. Models were adjusted for age, sex, height, heart rate, traditional cardiovascular disease risk factors and baseline kidney measures.
When eGFR was analyzed as a continuous variable, higher baseline CFPWV and CPP, but not AI, were significantly associated with a larger annual decline in eGFR in models adjusted for age, sex, height, heart rate and baseline eGFR, but not after additional adjustment for the mean arterial pressure. When eGFR was analyzed as a categorical variable, higher CFPWV was significantly associated with a decrease in eGFR of =3 mL/min/1.73 m(2)/year [odds ratio (OR) 1.53, 95% confidence interval (CI) 1.11-2.13] and higher AI was associated with 30% eGFR decline during follow-up (OR 1.44 and 95% CI 1.03-2.00) in fully adjusted models. None of the tonometry measures was associated with change in UACR.
Abnormalities in vascular health may play a role in large declines in eGFR beyond the traditional cardiovascular disease risks in this older Icelandic cohort.
PubMed ID
27190377 View in PubMed
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Apolipoprotein E genotype and statins affect CRP levels through independent and different mechanisms: AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature53039
Source
Atherosclerosis. 2006 May;186(1):222-4
Publication Type
Article
Date
May-2006
Author
Gudny Eiriksdottir
Thor Aspelund
Kristjana Bjarnadottir
Elin Olafsdottir
Lenore J Launer
Tamara B Harris
Vilmundur Gudnason
Author Affiliation
Icelandic Heart Association, Holtasmara 1, 201 Kopavogur, Iceland.
Source
Atherosclerosis. 2006 May;186(1):222-4
Date
May-2006
Language
English
Publication Type
Article
Abstract
OBJECTIVE: C-reactive protein (CRP), an inflammatory marker, was linked to coronary heart disease (CHD) in the Reykjavik study cohort. Recent genetic studies have shown that the apolipoprotein E (APOE) varepsilon4 allele is associated with lower CRP levels. Statin treatment has also been shown to lower CRP levels. In the Age Gene/Environment Susceptibility (AGES)-Reykjavik Study, we examined the association of APOE genotypes with CRP accounting for the effect of statin treatment, previous CHD and a mid-life measurement of erythrocyte sedimentation rate (ESR), an inflammatory marker associated with risk in this cohort. METHODS AND RESULTS: The first 2296 participants (mean age 76+/-6 years, 42% men) in the AGES-Reykjavik Study were genotyped for APOE CRP concentration was measured with a high sensitivity method. A general linear model was used to evaluate the association of APOE genotype to CRP levels. The frequencies of the APOE alleles are varepsilon2=0.06, varepsilon3=0.78 and varepsilon4=0.16. CRP levels ranged from 0.2 to 56.6mg/L, median 1.9mg/L. Participants carrying one or two varepsilon4 alleles have significantly lower CRP levels than non-carriers and this effect was observed in a dose-dependent manner. This trend is the same in users and non-users of statin treatment. CONCLUSIONS: This study suggests that the contribution of the varepsilon4 allele towards lowering CRP levels is independent and may be by a different mechanism than how statins affect inflammation.
PubMed ID
16445917 View in PubMed
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Association Between Interstitial Lung Abnormalities and All-Cause Mortality.

https://arctichealth.org/en/permalink/ahliterature270345
Source
JAMA. 2016 Feb 16;315(7):672-81
Publication Type
Article
Date
Feb-16-2016
Author
Rachel K Putman
Hiroto Hatabu
Tetsuro Araki
Gunnar Gudmundsson
Wei Gao
Mizuki Nishino
Yuka Okajima
Josée Dupuis
Jeanne C Latourelle
Michael H Cho
Souheil El-Chemaly
Harvey O Coxson
Bartolome R Celli
Isis E Fernandez
Oscar E Zazueta
James C Ross
Rola Harmouche
Raúl San José Estépar
Alejandro A Diaz
Sigurdur Sigurdsson
Elías F Gudmundsson
Gudny Eiríksdottír
Thor Aspelund
Matthew J Budoff
Gregory L Kinney
John E Hokanson
Michelle C Williams
John T Murchison
William MacNee
Udo Hoffmann
Christopher J O'Donnell
Lenore J Launer
Tamara B Harrris
Vilmundur Gudnason
Edwin K Silverman
George T O'Connor
George R Washko
Ivan O Rosas
Gary M Hunninghake
Source
JAMA. 2016 Feb 16;315(7):672-81
Date
Feb-16-2016
Language
English
Publication Type
Article
Keywords
Cause of Death
Cohort Studies
Coronary Artery Disease - epidemiology - mortality
Female
Humans
Male
Neoplasms - mortality
Prevalence
Proportional Hazards Models
Prospective Studies
Pulmonary Disease, Chronic Obstructive - epidemiology - mortality - radiography
Pulmonary Emphysema - epidemiology - mortality
Smoking - epidemiology
Abstract
Interstitial lung abnormalities have been associated with lower 6-minute walk distance, diffusion capacity for carbon monoxide, and total lung capacity. However, to our knowledge, an association with mortality has not been previously investigated.
To investigate whether interstitial lung abnormalities are associated with increased mortality.
Prospective cohort studies of 2633 participants from the FHS (Framingham Heart Study; computed tomographic [CT] scans obtained September 2008-March 2011), 5320 from the AGES-Reykjavik Study (Age Gene/Environment Susceptibility; recruited January 2002-February 2006), 2068 from the COPDGene Study (Chronic Obstructive Pulmonary Disease; recruited November 2007-April 2010), and 1670 from ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints; between December 2005-December 2006).
Interstitial lung abnormality status as determined by chest CT evaluation.
All-cause mortality over an approximate 3- to 9-year median follow-up time. Cause-of-death information was also examined in the AGES-Reykjavik cohort.
Interstitial lung abnormalities were present in 177 (7%) of the 2633 participants from FHS, 378 (7%) of 5320 from AGES-Reykjavik, 156 (8%) of 2068 from COPDGene, and in 157 (9%) of 1670 from ECLIPSE. Over median follow-up times of approximately 3 to 9 years, there were more deaths (and a greater absolute rate of mortality) among participants with interstitial lung abnormalities when compared with those who did not have interstitial lung abnormalities in the following cohorts: 7% vs 1% in FHS (6% difference [95% CI, 2% to 10%]), 56% vs 33% in AGES-Reykjavik (23% difference [95% CI, 18% to 28%]), and 11% vs 5% in ECLIPSE (6% difference [95% CI, 1% to 11%]). After adjustment for covariates, interstitial lung abnormalities were associated with a higher risk of death in the FHS (hazard ratio [HR], 2.7 [95% CI, 1.1 to 6.5]; P?=?.03), AGES-Reykjavik (HR, 1.3 [95% CI, 1.2 to 1.4]; P?
Notes
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PubMed ID
26881370 View in PubMed
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Association Between Unrecognized Myocardial Infarction and Cerebral Infarction on Magnetic Resonance Imaging.

https://arctichealth.org/en/permalink/ahliterature300114
Source
JAMA Neurol. 2019 May 20; :
Publication Type
Journal Article
Date
May-20-2019
Author
Alexander E Merkler
Sigurdur Sigurdsson
Gudny Eiriksdottir
Monika M Safford
Caroline L Phillips
Costantino Iadecola
Vilmundur Gudnason
Jonathan W Weinsaft
Hooman Kamel
Andrew E Arai
Lenore J Launer
Author Affiliation
Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York.
Source
JAMA Neurol. 2019 May 20; :
Date
May-20-2019
Language
English
Publication Type
Journal Article
Abstract
It is uncertain whether unrecognized myocardial infarction (MI) is a risk factor for cerebral infarction.
To determine whether unrecognized MI detected by cardiac magnetic resonance imaging (MRI) is associated with cerebral infarction.
This is a cross-sectional study of ICELAND MI, a cohort substudy of the Age, Gene/Environment Susceptibility-Reykjavik Study conducted in Iceland. Enrollment occurred from January 2004 to January 2007 from a community-dwelling cohort of older Icelandic individuals. Participants aged 67 to 93 years who underwent both brain MRI and late gadolinium enhancement cardiac MRI were included. Data analysis was performed from September 2018 to March 2019.
Unrecognized MI identified by cardiac MRI.
Unrecognized MI was defined as cardiac MRI evidence of MI without a history of clinically evident MI. Recognized MI was defined as cardiac MRI evidence of MI with a history of clinically evident MI. Cerebral infarctions on brain MRI were included regardless of associated symptoms. Multiple logistic regression was used to evaluate the association between MI status (no MI, unrecognized MI, or recognized MI) and cerebral infarction after adjustment for demographic factors and vascular risk factors. In addition, we evaluated the association between unrecognized MI and embolic infarcts of undetermined source.
Five enrolled participants had nondiagnostic brain MRI studies and were excluded. Among 925 participants, 480 (51.9%) were women; the mean (SD) age was 75.9 (5.3) years. There were 221 participants (23.9%) with cardiac MRI evidence of MI, of whom 68 had recognized MI and 153 unrecognized MI. There were 308 participants (33.3%) with brain MRI evidence of cerebral infarction; 93 (10.0%) had embolic infarcts of undetermined source. After adjustment for demographic factors and vascular risk factors, the likelihood (odds ratio) of having cerebral infarction was 2.0 (95% CI, 1.2-3.4; P?=?.01) for recognized MI and 1.5 (95% CI, 1.02-2.2; P?=?.04) for unrecognized MI. After adjustment for demographics and vascular risk factors, unrecognized MI was also associated with embolic infarcts of undetermined source (odds ratio, 2.0 [95% CI, 1.1-3.5]; P?=?.02).
In a population-based sample, we found an association between unrecognized MI and cerebral infarction. These findings suggest that unrecognized MI may be a novel risk factor for cardiac embolism and cerebral infarction.
PubMed ID
31107514 View in PubMed
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Association of change in brain structure to objectively measured physical activity and sedentary behavior in older adults: Age, Gene/Environment Susceptibility-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature266168
Source
Behav Brain Res. 2015 Sep 10;296:118-124
Publication Type
Article
Date
Sep-10-2015
Author
Nanna Yr Arnardottir
Annemarie Koster
Dane R Van Domelen
Robert J Brychta
Paolo Caserotti
Gudny Eiriksdottir
Johanna E Sverrisdottir
Sigurdur Sigurdsson
Erlingur Johannsson
Kong Y Chen
Vilmundur Gudnason
Tamara B Harris
Lenore J Launer
Thorarinn Sveinsson
Source
Behav Brain Res. 2015 Sep 10;296:118-124
Date
Sep-10-2015
Language
English
Publication Type
Article
Abstract
Many studies have examined the hypothesis that greater participation in physical activity (PA) is associated with less brain atrophy. Here we examine, in a sub-sample (n=352, mean age 79.1 years) of the Age, Gene/Environment Susceptibility-Reykjavik Study cohort, the association of the baseline and 5-year change in magnetic resonance imaging (MRI)-derived volumes of gray matter (GM) and white matter (WM) to active and sedentary behavior (SB) measured at the end of the 5-year period by a hip-worn accelerometer for seven consecutive days. More GM (ß=0.11; p=0.044) and WM (ß=0.11; p=0.030) at baseline was associated with more total physical activity (TPA). Also, when adjusting for baseline values, the 5-year change in GM (ß=0.14; p=0.0037) and WM (ß=0.11; p=0.030) was associated with TPA. The 5-year change in WM was associated with SB (ß=-0.11; p=0.0007). These data suggest that objectively measured PA and SB late in life are associated with current and prior cross-sectional measures of brain atrophy, and that change over time is associated with PA and SB in expected directions.
PubMed ID
26363425 View in PubMed
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