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Bruce M. Psaty, MD, PhD; Donna Arnett, PhD; Gregory Burke, MD, MS

JAMA. 2007;298(17):2060-2062.

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

Cardiovascular epidemiology has a rich, collaborative, and productive history. Beginning in 1948, the Framingham Heart Study was instrumental in identifying, for instance, high blood pressure and dyslipidemia as major risk factors for coronary heart disease and stroke.¹ Subsequent clinical trials identified safe and effective treatments for these conditions. In the last several decades, the widespread use of medications for hypertension and dyslipidemia have prevented or delayed the onset of cardiovascular disease for millions of US residents. At the 60th anniversary of the Framingham study, a new approach to cardiovascular disease epidemiology is about to be tested.

In October 2007, data from approximately 9000 Framingham participants, not only extensive phenotype data but also 500 000 single nucleotide polymorphisms (SNPs) from a whole-genome scan on each individual, became accessible to the scientific community under the SHARe (SNP Health Association Resource) program.² . . . [Full Text of this Article]

Author Affiliations: Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology and Health Services, University of Washington and Center for Health Studies, Group Health, Seattle (Dr Psaty); Department of Epidemiology, University of Alabama at Birmingham, Birmingham (Dr Arnett); and Division of Public Health Sciences, Wake Forest University, Winston-Salem, North Carolina (Dr Burke).

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