Heritability and a Genome-Wide Linkage Scan for Arterial Stiffness, Wave Reflection, and Mean Arterial Pressure. The Framingham Heart Study

2005 ◽  
Vol 14 (11) ◽  
pp. 21
Author(s):  
G.F. Mitchell ◽  
A.L. DeStefano ◽  
M.G. Larson
Circulation ◽  
2005 ◽  
Vol 112 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Gary F. Mitchell ◽  
Anita L. DeStefano ◽  
Martin G. Larson ◽  
Emelia J. Benjamin ◽  
Ming-Huei Chen ◽  
...  

2012 ◽  
Vol 129 (3) ◽  
pp. 840-845.e21 ◽  
Author(s):  
Mark Granada ◽  
Jemma B. Wilk ◽  
Marina Tuzova ◽  
David P. Strachan ◽  
Stephan Weidinger ◽  
...  

2007 ◽  
Vol 8 (Suppl 1) ◽  
pp. S6 ◽  
Author(s):  
Joanne M Murabito ◽  
Carol L Rosenberg ◽  
Daniel Finger ◽  
Bernard E Kreger ◽  
Daniel Levy ◽  
...  

2007 ◽  
Vol 8 (Suppl 1) ◽  
pp. S10 ◽  
Author(s):  
Shih-Jen Hwang ◽  
Qiong Yang ◽  
James B Meigs ◽  
Elizabeth N Pearce ◽  
Caroline S Fox

2007 ◽  
Vol 8 (Suppl 1) ◽  
pp. S3 ◽  
Author(s):  
Daniel Levy ◽  
Martin G Larson ◽  
Emelia J Benjamin ◽  
Christopher Newton-Cheh ◽  
Thomas J Wang ◽  
...  

2007 ◽  
Vol 8 (Suppl 1) ◽  
pp. S17 ◽  
Author(s):  
Sekar Kathiresan ◽  
Alisa K Manning ◽  
Serkalem Demissie ◽  
Ralph B D'Agostino ◽  
Aarti Surti ◽  
...  

Author(s):  
Leroy L. Cooper ◽  
Jian Rong ◽  
Martin G. Larson ◽  
Emelia J. Benjamin ◽  
Naomi M. Hamburg ◽  
...  

Community-based studies have evaluated cross-sectional age relations of aortic stiffness measures, which are not often recapitulated in longitudinal studies. We examined baseline and longitudinal change in aortic stiffness in 5491 participants (mean age, 49.5±14.5 years; 54% women) who attended 2 sequential examinations (6.0±0.6 years apart) of the Framingham Heart Study. Cross-sectional relations of central hemodynamics (mean arterial pressure, central pulse pressure, carotid-femoral pulse wave velocity, and characteristic impedance) with age and risk factors were assessed at visits 1 and 2 (models 1 and 2). We used model 1 coefficients (M 1 ), visit 1 risk factor levels (R 1 ), and age at each visit (A 1 , A 2 ) to estimate values at visits 1 (M 1 R 1 A 1 ) and 2 (M 1 R 1 A 2 ). While using model 1 coefficients, we accounted for age and risk factor level (R 2 ) changes to predict values at visit 2 (M 1 R 2 A 2 ). Using model 2 coefficients (M 2 ) and visit 2 age and risk factor levels, we predicted visit 2 values (M 2 R 2 A 2 ). We calculated predicted change 3 ways: delta1=M 1 R 1 A 2 −M 1 R 1 A 1 , delta2=M 1 R 2 A 2 −M 1 R 1 A 1 , and delta3=M 2 R 2 A 2 −M 1 R 1 A 1 . Delta1 values were biased and correlated poorly with actual changes ( r =−0.02–0.14). For mean arterial pressure, delta1=1.9±0.8 mm Hg ( r =0.14), observed change=−3.3±10.3 mm Hg, and discrepancy=5.2±10.2 mm Hg ( P <0.0001). For characteristic impedance, delta1=7.2±14.7 dyne×sec/cm 5 ( r =0.07), observed change=20.5±68.2 dyne×sec/cm 5 , and discrepancy=−13.3±68.7 dyne×sec/cm 5 ( P <0.0001). Delta2 values were moderately correlated with change ( r =0.17–0.54) but remained biased whereas delta3 values were moderately correlated with change with no bias. Projected change in hemodynamic measures extrapolated from cross-sectional age relations may differ substantially from actual change, particularly for variables with nonlinear age relations.


BMC Genetics ◽  
2003 ◽  
Vol 4 (Suppl 1) ◽  
pp. S97 ◽  
Author(s):  
Roxana Moslehi ◽  
Alisa M Goldstein ◽  
Michael Beerman ◽  
Lynn Goldin ◽  
Andrew W Bergen

2019 ◽  
Vol 28 (15) ◽  
pp. 2615-2633 ◽  
Author(s):  
Yun Ju Sung ◽  
Lisa de las Fuentes ◽  
Thomas W Winkler ◽  
Daniel I Chasman ◽  
Amy R Bentley ◽  
...  

Abstract Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene–smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene–smoking interaction analysis and 38 were newly identified (P < 5 × 10−8, false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.


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