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Christopher J. O’Donnell, MD, MPH

JAMA. 2005;293:2277-2279.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

With a nearly completed Human Genome Project,¹ it is hoped that the road from the complete genome sequence of 2.85 billion nucleotides containing up to 25 000 genes will lead to a promised land of new and better patient-tailored diagnostics and treatments. Some have even predicted the end of common complex diseases such as myocardial infarction (MI) as a major public health problem in the near future.² Risks for MI and stroke are conferred by established major modifiable risk factors, including hyperlipidemia and hypertension, as well as other factors, such as inflammation. Cardiovascular disease risks are also substantially increased in those with disease occurrence in twin siblings³ or parents.⁴ This suggests that genetic variation may lead to increased risk, although to date few genetic variants have emerged as strong candidates. The randomized trial described by Hakonarson et al⁵ in this issue of JAMA—suggesting that inhibition . . . [Full Text of this Article]

Author Affiliations: National Heart, Lung, and Blood Institute, Framingham Heart Study Cardiology Division, and Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston.

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