(Circulation. 2000;102:1877.)
© 2000 American Heart Association, Inc.
Editorials |
From the Human Genetics Center and the Institute of Molecular Medicine (E.B.), University of Texas, Houston Health Science Center, Houston, Tex.
Correspondence to Eric Boerwinkle, PhD, Human Genetics Center, University of TexasHouston Health Science Center, 6901 Bertner, S250, Houston, TX 77030. E-mail eboerwin@gsbs.gs.uth.tmc.edu
Key Words: Editorials genetics genes mapping
Family studies throughout the 1970s and 1980s documented the role of shared genetic factors in the familial aggregation of cardiovascular disease and its risk factors, including hypertension. These familial aggregation studies, however, do not identify and characterize the role of particular genes. Identification of the genes contributing to interindividual variation in disease risk may facilitate early identification of patients who are at elevated risk of cardiovascular disease before the onset of any clinical symptoms, development of more efficacious treatments by exploiting previously unidentified metabolic and physiological pathways, and the tailoring of particular treatments to patients who are most likely to respond on the basis of their genetic constitution.
Cardiovascular disease risk and risk factor
levels are controlled by complex interactions among numerous
metabolic and physiological systems, as
well as demographic and lifestyle factors. Because so many systems are
involved, variation in a large number of genes can potentially
influence interindividual variation in disease risk, and the impact of
any one gene is likely to be small to moderate in size. Before the
current revolution in genomic analyses, studies identifying
genes contributing to cardiovascular disease risk were
of 2 basic types: studies of rare inborn errors of
metabolism and association studies of a priori
biologic candidate genes. The former have proved very useful for the
identification of novel pathways, but the frequencies of these
conditions are very rare, so their contribution to the prevalence of
disease in the general population is minimal. The latter have proven
useful in a few cases,
This article has been cited by other articles:
![]() |
J. W. Knowles, T. L. Assimes, J. Li, T. Quertermous, and J. P. Cooke Genetic Susceptibility to Peripheral Arterial Disease: A Dark Corner in Vascular Biology Arterioscler Thromb Vasc Biol, October 1, 2007; 27(10): 2068 - 2078. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. K. Arnett, A. E. Baird, R. A. Barkley, C. T. Basson, E. Boerwinkle, S. K. Ganesh, D. M. Herrington, Y. Hong, C. Jaquish, D. A. McDermott, et al. Relevance of Genetics and Genomics for Prevention and Treatment of Cardiovascular Disease: A Scientific Statement From the American Heart Association Council on Epidemiology and Prevention, the Stroke Council, and the Functional Genomics and Translational Biology Interdisciplinary Working Group Circulation, June 5, 2007; 115(22): 2878 - 2901. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. N. Bella, W. Tang, A. Kraja, D. C. Rao, S. C. Hunt, M. B. Miller, V. Palmieri, M. J. Roman, D. W. Kitzman, A. Oberman, et al. Genome-Wide Linkage Mapping for Valve Calcification Susceptibility Loci in Hypertensive Sibships: The Hypertension Genetic Epidemiology Network Study Hypertension, March 1, 2007; 49(3): 453 - 460. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Rankinen, P. An, T. Rice, G. Sun, Y. C. Chagnon, J. Gagnon, A. S. Leon, J. S. Skinner, J. H. Wilmore, D. C. Rao, et al. Genomic Scan for Exercise Blood Pressure in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study Hypertension, July 1, 2001; 38(1): 30 - 37. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. C. Luft and A. Busjahn Peaks and Valleys Hypertension, July 1, 2001; 38(1): 38 - 40. [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |