Update on HDLc, HDLp, HDL functonality

Benjamin J. Ansell, MD, FACP, FACC, FNLA
Professor of Medicine
Division of Cardiology and General Internal Medicine
UCLA School of Medicine
Los Angeles, CA

The last eight years have tempered the enthusiasm directed toward development and clinical utility of HDL-based therapies to mitigate CVD risk.
 In clinical trials employing contemporary statin treatment, high-risk patients with CHD have not been shown to benefit from the addition of niacin, fenofibrate, and two CETP-inhibitors, all of which significantly raise HDL-C.
 Studies of other developmental compounds have been similarly underwhelming, in some cases limited by study size, practicality of the approach, and possibly patient selection.

 While HDL-C, and even better, HDL-P and/or ApoA-1 levels have demonstrated clear utility in identifying individuals at increased risk for CVD, their role as targets of therapy remains elusive.

 A greater understanding of HDL’s role in
1-innate immunity, and as
2-a target and mediator of systemic inflammation,
 has led to an appreciation that HDL functionality in modulating
1- lipid transport,
2-inflammation,
3-oxidation,
4- thrombosis,
5-glycemia, and
6-endothelial function
 may be as or even more important than quantitative measures of HDL. 

However, there is no consensus as to which function(s) of HDL is/are most relevant or how they are best measured.
 Several potential therapeutic pathways involving HDL remain the subject of active clinical investigation, and these will be discussed. (At NLA Spring meeting)