[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.211.207.116. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Editorial
June 18, 2008

CETP Genes, Metabolic Effects, and Coronary Disease Risk

Author Affiliations

Author Affiliation: Emory University School of Medicine, Atlanta VAMC Epidemiology and Genetics Section, Atlanta, Georgia.

JAMA. 2008;299(23):2795-2796. doi:10.1001/jama.299.23.2795

The burden of atherosclerotic coronary heart disease (CHD) is tremendous—both genes and environment contribute to this problem. From a clinical perspective, physicians are well aware of the importance of genetic lipid abnormalities in the causation of CHD.1 The best studied genetic lipid abnormality is familial hypercholesterolemia (FH), which can cause clinical findings such as xanthomas, early atherosclerosis, and premature CHD. Approximately 1 out of 500 of the population are FH heterozygotes and 1 out of 1 000 000 are homozgotes.2 It has been estimated that FH accounts for approximately 6% of CHD on a population basis.3

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