Current Problems in Cardiology
Volume 32, Issue 5 , Pages 268-314, May 2007

HDL Cholesterol: Physiology, Pathophysiology, and Management

  • Jeffrey J. Link, MD

      Affiliations

    • Dr. Link and Dr. Rohatgi have no conflict of interest to disclose.
  • ,
  • Anand Rohatgi, MD

      Affiliations

    • Dr. Link and Dr. Rohatgi have no conflict of interest to disclose.
  • ,
  • James A. de Lemos, MD

      Affiliations

    • Dr. de Lemos has received lecture honoraria from Merck/Schering and Pfizer and consulting fees from Pfizer.
    • Corresponding Author InformationAddress reprint requests to: James A. de Lemos, MD, UT Southwestern Medical Center, 5909 Harry Hines Blvd., HA 9.133, Dallas, TX 75390-9047.

Abstract 

Numerous epidemiological studies have identified high-density lipoprotein cholesterol (HDL) to be an independent risk factor for coronary heart disease (CHD). HDL is an emerging therapeutic target that could rival the impact of 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) on LDL and CHD risk reduction. HDL metabolism, HDL kinetics, the concentration of various HDL subclasses, and other genetic factors affecting HDL functionality may all contribute to the anti-atherogenic properties of HDL; thus, standard plasma measurement may not capture the full range of HDL effects. Algorithms have been suggested to treat low HDL levels in subgroups of patients; however, no formal HDL target goals or treatment guidelines have been implemented as there is a lack of strong clinical evidence to support effective pharmacologic therapy for primary risk reduction. Available therapies have a modest impact on serum HDL levels; however, emerging therapies could have a more significant influence.

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PII: S0146-2806(07)00005-9

doi:10.1016/j.cpcardiol.2007.01.004

Current Problems in Cardiology
Volume 32, Issue 5 , Pages 268-314, May 2007