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(Circulation. 2004;110:2074-2076.)
© 2004 American Heart Association, Inc.

Editorial

Family History, Subclinical Atherosclerosis, and Coronary Heart Disease Risk

Barriers and Opportunities for the Use of Family History Information in Risk Prediction and Prevention

Christopher J. O’Donnell, MD, MPH

From the National Heart, Lung and Blood Institute, Bethesda, Md; the National Heart, Lung and Blood Institute’s Framingham Heart Study, Framingham, Mass; and the Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston Mass.

Correspondence to Christopher J. O’Donnell, MD, MPH, Framingham Heart Study, 73 Mount Wayte Ave, Suite #2, Framingham, MA 01702. E-mail codonnell@nih.gov

Key Words: Editorials • genetics • risk factors • coronary disease • prevention

An extract of the first 250 words of the full text is provided, because this article has no abstract.

With completion of the human genome sequence, expectations are rising that a detailed catalogue will soon be available of all important common genetic susceptibility variants for human diseases, including coronary heart disease (CHD) and related atherosclerotic cardiovascular disease (CVD).¹ In light of this seminal event in medical research, it is curious that the family history of CHD has not been accorded a more central role in risk prediction and disease prevention by clinicians and public health professionals. A positive family history of CHD is present in the majority of cases of premature-onset CHD.² In cases of familial hypercholesterolemia and other rare forms of premature-onset CVD, CHD clearly segregates in a mendelian fashion. For most cases of premature-onset CHD, the mode of genetic transmission in families is less clear. Although the family history of CHD has been considered a putative risk factor for decades, it has not been incorporated along with other established risk factors such as hyperlipidemia, hypertension, and cigarette smoking in some widely applied multivariable risk algorithms,³ though other risk algorithms do incorporate family history information.⁴

See p 2150

This cautious approach to widespread application of family history information is not due to insufficient evidence. Risks for CHD death are greatest in monozygotic (identical) compared with dizygotic (nonidentical) twins, particularly when there is a premature (eg, <65 years) age of onset in the initially affected twin.⁵ In multiple prospective studies involving hundreds of thousands of men and women, a parental history of premature CHD is a significant risk factor . . . [Full Text of this Article]

Related Article:

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Circulation 2004 110: 2150-2156. [Abstract] [Full Text]

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