Skip header and navigation

Refine By

18 records – page 1 of 2.

Association of Low-Density Lipoprotein Cholesterol-Related Genetic Variants With Aortic Valve Calcium and Incident Aortic Stenosis.

https://arctichealth.org/en/permalink/ahliterature257726
Source
JAMA. 2014 Oct 26;
Publication Type
Article
Date
Oct-26-2014
Author
J Gustav Smith
Kevin Luk
Christina-Alexandra Schulz
James C Engert
Ron Do
George Hindy
Gull Rukh
Line Dufresne
Peter Almgren
David S Owens
Tamara B Harris
Gina M Peloso
Kathleen F Kerr
Quenna Wong
Albert V Smith
Matthew J Budoff
Jerome I Rotter
L Adrienne Cupples
Stephen Rich
Sekar Kathiresan
Marju Orho-Melander
Vilmundur Gudnason
Christopher J O'Donnell
Wendy S Post
George Thanassoulis
Author Affiliation
Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden2Department of Heart Failure and Valvular Disease, Skåne University Hospital, Lund, Sweden3Department of Clinical Sciences, Lund University, Malmö, Sweden4Program in Medical and Pop.
Source
JAMA. 2014 Oct 26;
Date
Oct-26-2014
Language
English
Publication Type
Article
Abstract
Plasma low-density lipoprotein cholesterol (LDL-C) has been associated with aortic stenosis in observational studies; however, randomized trials with cholesterol-lowering therapies in individuals with established valve disease have failed to demonstrate reduced disease progression.
To evaluate whether genetic data are consistent with an association between LDL-C, high-density lipoprotein cholesterol (HDL-C), or triglycerides (TG) and aortic valve disease.
Using a Mendelian randomization study design, we evaluated whether weighted genetic risk scores (GRSs), a measure of the genetic predisposition to elevations in plasma lipids, constructed using single-nucleotide polymorphisms identified in genome-wide association studies for plasma lipids, were associated with aortic valve disease. We included community-based cohorts participating in the CHARGE consortium (n?=?6942), including the Framingham Heart Study (cohort inception to last follow-up: 1971-2013; n?=?1295), Multi-Ethnic Study of Atherosclerosis (2000-2012; n?=?2527), Age Gene/Environment Study-Reykjavik (2000-2012; n?=?3120), and the Malmö Diet and Cancer Study (MDCS, 1991-2010; n?=?28?461).
Aortic valve calcium quantified by computed tomography in CHARGE and incident aortic stenosis in the MDCS.
The prevalence of aortic valve calcium across the 3 CHARGE cohorts was 32% (n?=?2245). In the MDCS, over a median follow-up time of 16.1 years, aortic stenosis developed in 17 per 1000 participants (n?=?473) and aortic valve replacement for aortic stenosis occurred in 7 per 1000 (n?=?205). Plasma LDL-C, but not HDL-C or TG, was significantly associated with incident aortic stenosis (hazard ratio [HR] per mmol/L, 1.28; 95% CI, 1.04-1.57; P?=?.02; aortic stenosis incidence: 1.3% and 2.4% in lowest and highest LDL-C quartiles, respectively). The LDL-C GRS, but not HDL-C or TG GRS, was significantly associated with presence of aortic valve calcium in CHARGE (odds ratio [OR] per GRS increment, 1.38; 95% CI, 1.09-1.74; P?=?.007) and with incident aortic stenosis in MDCS (HR per GRS increment, 2.78; 95% CI, 1.22-6.37; P?=?.02; aortic stenosis incidence: 1.9% and 2.6% in lowest and highest GRS quartiles, respectively). In sensitivity analyses excluding variants weakly associated with HDL-C or TG, the LDL-C GRS remained associated with aortic valve calcium (P?=?.03) and aortic stenosis (P?=?.009). In instrumental variable analysis, LDL-C was associated with an increase in the risk of incident aortic stenosis (HR per mmol/L, 1.51; 95% CI, 1.07-2.14; P?=?.02).
Genetic predisposition to elevated LDL-C was associated with presence of aortic valve calcium and incidence of aortic stenosis, providing evidence supportive of a causal association between LDL-C and aortic valve disease. Whether earlier intervention to reduce LDL-C could prevent aortic valve disease merits further investigation.
PubMed ID
25344734 View in PubMed
Less detail

Association of Triglyceride-Related Genetic Variants With Mitral Annular Calcification.

https://arctichealth.org/en/permalink/ahliterature283391
Source
J Am Coll Cardiol. 2017 Jun 20;69(24):2941-2948
Publication Type
Article
Date
Jun-20-2017
Author
Mehdi Afshar
Kevin Luk
Ron Do
Line Dufresne
David S Owens
Tamara B Harris
Gina M Peloso
Kathleen F Kerr
Quenna Wong
Albert V Smith
Mathew J Budoff
Jerome I Rotter
L Adrienne Cupples
Stephen S Rich
James C Engert
Vilmundur Gudnason
Christopher J O'Donnell
Wendy S Post
George Thanassoulis
Source
J Am Coll Cardiol. 2017 Jun 20;69(24):2941-2948
Date
Jun-20-2017
Language
English
Publication Type
Article
Abstract
Mitral annular calcium (MAC), commonly identified by cardiac imaging, is associated with cardiovascular events and predisposes to the development of clinically important mitral valve regurgitation and mitral valve stenosis. However, its biological determinants remain largely unknown.
The authors sought to evaluate whether a genetic predisposition to elevations in plasma lipids is associated with the presence of MAC.
The authors used 3 separate Mendelian randomization techniques to evaluate the associations of lipid genetic risk scores (GRS) with MAC in 3 large patient cohorts: the Framingham Health Study, MESA (Multiethnic European Study of Atherosclerosis), and the AGE-RS (Age, Gene/Environment Susceptibility-Reykjavik Study). The authors provided cross-ethnicity replication in the MESA Hispanic-American participants.
MAC was present in 1,149 participants (20.4%). In pooled analyses across all 3 cohorts, a triglyceride GRS was significantly associated with the presence of MAC (odds ratio [OR] per triglyceride GRS unit: 1.73; 95% confidence interval [CI]: 1.24 to 2.41; p = 0.0013). Neither low- nor high-density lipoprotein cholesterol GRS was significantly associated with MAC. Results were consistent in cross-ethnicity analyses among the MESA Hispanic-Americans cohort (OR per triglyceride GRS unit: 2.04; 95% CI: 1.03 to 4.03; p = 0.04). In joint meta-analysis across all included cohorts, the triglyceride GRS was associated with MAC (OR per triglyceride GRS unit: 1.79; 95% CI: 1.32 to 2.41; p = 0.0001). The results were robust to several sensitivity analyses that limit both known and unknown forms of genetic pleiotropy.
Genetic predisposition to elevated triglyceride levels was associated with the presence of MAC, a risk factor for clinically significant mitral valve disease, suggesting a causal association. Whether reducing triglyceride levels can lower the incidence of clinically significant mitral valve disease requires further study.
PubMed ID
28619195 View in PubMed
Less detail

Changing attitudes in health promotion.

https://arctichealth.org/en/permalink/ahliterature237468
Source
Can Nurse. 1986 Feb;82(2):34-7
Publication Type
Article
Date
Feb-1986

Dimensions talks to Shirley Post. Interview by Nancy Sandrin.

https://arctichealth.org/en/permalink/ahliterature244133
Source
Dimens Health Serv. 1981 Oct;58(10):28-9
Publication Type
Article
Date
Oct-1981

Do pediatric units' school programs make the grade?

https://arctichealth.org/en/permalink/ahliterature233529
Source
Dimens Health Serv. 1988 Feb;65(1):30-1
Publication Type
Article
Date
Feb-1988
Author
S. Post
J. Power
W. Baskerville
Author Affiliation
Canadian Institute of Child Health.
Source
Dimens Health Serv. 1988 Feb;65(1):30-1
Date
Feb-1988
Language
English
Publication Type
Article
Keywords
Child
Child Advocacy
Education, Special
Hospital Units - organization & administration
Humans
Ontario
Pediatrics
Schools
PubMed ID
3342950 View in PubMed
Less detail

Familial defective apolipoprotein B-100 and increased low-density lipoprotein cholesterol and coronary artery calcification in the old order amish.

https://arctichealth.org/en/permalink/ahliterature139444
Source
Arch Intern Med. 2010 Nov 8;170(20):1850-5
Publication Type
Article
Date
Nov-8-2010
Author
Haiqing Shen
Coleen M Damcott
Evadnie Rampersaud
Toni I Pollin
Richard B Horenstein
Patrick F McArdle
Patricia A Peyser
Lawrence F Bielak
Wendy S Post
Yen-Pei C Chang
Kathleen A Ryan
Michael Miller
John A Rumberger
Patrick F Sheedy
John Shelton
Jeffrey R O'Connell
Alan R Shuldiner
Braxton D Mitchell
Author Affiliation
Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Source
Arch Intern Med. 2010 Nov 8;170(20):1850-5
Date
Nov-8-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Apolipoprotein B-100 - blood - genetics
Calcinosis - blood - ethnology - genetics
Cholesterol, LDL - blood
Coronary Artery Disease - blood - ethnology - genetics
DNA - genetics
Denmark - ethnology
Female
Genome-Wide Association Study
Genotype
Humans
Male
Middle Aged
Mutation
Pennsylvania - epidemiology
Polymorphism, Single Nucleotide
Prevalence
Retrospective Studies
Risk factors
Young Adult
Abstract
Elevated low-density lipoprotein cholesterol (LDL-C) levels are a major cardiovascular disease risk factor. Genetic factors are an important determinant of LDL-C levels.
To identify single nucleotide polymorphisms associated with LDL-C and subclinical coronary atherosclerosis, we performed a genome-wide association study of LDL-C in 841 asymptomatic Amish individuals aged 20 to 80 years, with replication in a second sample of 663 Amish individuals. We also performed scanning for coronary artery calcification (CAC) in 1018 of these individuals.
From the initial genome-wide association study, a cluster of single nucleotide polymorphisms in the region of the apolipoprotein B-100 gene (APOB) was strongly associated with LDL-C levels (P
Notes
Cites: Circulation. 1996 Nov 1;94(9):2159-708901667
Cites: Am J Epidemiol. 2004 Sep 1;160(5):407-2015321837
Cites: J Lipid Res. 1997 Jul;38(7):1361-739254062
Cites: J Clin Invest. 1998 Mar 1;101(5):1084-939486979
Cites: N Engl J Med. 1998 May 28;338(22):1577-849603795
Cites: J Am Coll Cardiol. 2005 Jul 5;46(1):158-6515992651
Cites: J Am Soc Nephrol. 2005 Nov;16 Suppl 2:S115-916251246
Cites: Hum Mol Genet. 2006 Aug 15;15(16):2468-7816835261
Cites: Circulation. 2007 Feb 13;115(6):717-2417261661
Cites: Genet Epidemiol. 2000;19 Suppl 1:S36-4211055368
Cites: J Biol Chem. 2001 Mar 23;276(12):9214-811115503
Cites: Twin Res. 2002 Apr;5(2):87-9711931686
Cites: Atherosclerosis. 2007 Mar;191(1):40-716730014
Cites: J Am Coll Cardiol. 2007 May 22;49(20):2013-2017512357
Cites: Am Heart J. 2008 May;155(5):823-818440328
Cites: Atherosclerosis. 2009 Jan;202(1):289-9518452924
Cites: Bioinformatics. 2003 Jan;19(1):149-5012499305
Cites: Arterioscler Thromb Vasc Biol. 1997 Apr;17(4):741-79108789
Cites: Clin Chem. 1972 Jun;18(6):499-5024337382
Cites: Science. 1986 Apr 4;232(4746):34-473513311
Cites: Proc Natl Acad Sci U S A. 1989 Jan;86(2):587-912563166
Cites: J Am Coll Cardiol. 1990 Mar 15;15(4):827-322407762
Cites: J Lipid Res. 1994 Apr;35(4):574-838006512
Comment In: Arch Intern Med. 2011 Jun 13;171(11):1039-40; author reply 104021670376
PubMed ID
21059979 View in PubMed
Less detail

Family-centered care for children: is it a reality?

https://arctichealth.org/en/permalink/ahliterature234596
Source
Hosp Trustee. 1987 Nov-Dec;11(6):15-7
Publication Type
Article
Author
S. Post
J. Powers
W. Baskerville
Source
Hosp Trustee. 1987 Nov-Dec;11(6):15-7
Language
English
Publication Type
Article
Keywords
Canada
Child
Child, Hospitalized
Family
Hospital Units
Humans
Questionnaires
PubMed ID
10284822 View in PubMed
Less detail

18 records – page 1 of 2.