[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.163.94.5. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Editorial
May 11, 2005

Translating the Human Genome Project Into Prevention of Myocardial Infarction and Stroke—Getting Close?

Author Affiliations
 

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.

JAMA. 2005;293(18):2277-2279. doi:10.1001/jama.293.18.2277

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 of a genetically encoded 5-lipoxygenase–activating protein (FLAP) in patients with at-risk genotypes may reduce biomarkers of cardiovascular risk—illustrates the exciting potential opportunity for rapidly translating genomics into novel diagnostics and treatments.

First Page Preview View Large
First page PDF preview
First page PDF preview
×