on November 14, 2005
Published online before print November 14, 2005, doi: 10.1161/01.HYP.0000191706.41980.29
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Submitted on June 1, 2005
From the Division of Epidemiology and Community Health (S.J.B., A.I.L., M.B.M., D.K.A.), University of Minnesota, Minneapolis; University of Michigan Hospitals (A.W.), Ann Arbor; Loyola University Medical Center (R.C.), Maywood, Ill; UAB Division of Preventive Medicine (A.O.), Birmingham, Ala; Cedars-Sinai Medical Center (Y.-D.I.C., M.P.), Los Angles, Calif; Division of Nephrology and Hypertension (S.T.T.), Mayo Clinic, Rochester, Minn; Institute of Molecular Medicine (M.F.), Houston, Tex; Division of Biostatistics (M.P.), Washington University School of Medicine, St. Louis, Mo; and Department of Epidemiology (D.K.A.), University of Alabama, Birmingham. * To whom correspondence should be addressed. E-mail: Arnett{at}ms.soph.uab.edu.
Abstract--Pulse pressure, the difference between systolic and diastolic blood pressure, is an independent risk factor for cardiovascular disease. Increased pulse pressure reflects reduced compliance of arteries and is a marker of atherosclerosis. To locate genes that affect pulse pressure, a genome-wide linkage scan for quantitative trait loci influencing pulse pressure was performed using variance components methods as implemented in sequential oligogenic linkage analysis routines. The analysis sample included 10 798 participants in 3320 families who were recruited as part of the Family Blood Pressure Program and were phenotyped with an oscillometric blood pressure measurement device using a consistent protocol across centers. Pulse pressure was adjusted for the effects of sex, age, age2, age-by-sex interaction, age2-by-sex interaction, body mass index, and field center to remove sources of variation other than the genetic effects related to pulse pressure. Significant linkage was observed on chromosome 18 (logarithm of odds [LOD]=3.2) in a combined racial sample, chromosome 20 (LOD=4.4), and 17 (LOD=3.6) in Hispanics, chromosome 21 (LOD=4.3) in whites, chromosome 19 (LOD=3.1) in a combined sample of blacks and whites, and chromosome 7 (logarithm of odds [LOD]=3.1) in blacks from the GenNet Network. Our genome scan shows significant evidence for linkage for pulse pressure in multiple areas of the genome, supporting previous published linkage studies. The identification of these loci for pulse pressure and the apparent congruence with other blood pressure phenotypes provide increased support that these regions contain genes influencing blood pressure phenotypes.
Revised on July 1, 2005
Genome-Wide Linkage Analysis for Loci Affecting Pulse Pressure. The Family Blood Pressure Program
Suzette J. Bielinski;
Key words: blood pressure • genetics • hypertension, genetics
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