Physicians' Academy for Cardiovascular Education

HDL & Residual Risk

3' education - Aug. 31, 2011

The potential role of HDL in further reduction of residual risk

Prof. John Kastelein in discussion with prof Chris Packard, R&D Director of NHS Greater Glasgow & Clyde Health BoardWestern Infirmary, Glasgow, United Kingdom, on the role of HDL in further reducing residual risk.

Questions to be addressed in this PACE expert opinion are
  • Residual risk: What is it exactly?
  • Reducing residual risk: What is the potential role of HDL?
  • Raising HDL: Are there new ways of more robustly influencing HDL?
  • What is the role of CETP as a target
  • What about the development of drugs to focus on CETP?
  • Dalcetrapib / anacetrapib: What is the efficacy in terms of the lipoproteins of these two drugs?

View prof Kastelein in discusion with prof Packard

More about the speakers

Professor John Kastelein
Professor of Medicine, Chairman, Department of Vascular Medicine, University of Amsterdam, The Netherlands

Prof Kastelein’s current research interests are in the aetiology, diagnosis, prevention and treatment of hypertriglyceridaemia, hypercholesterolaemia and low HDL cholesterol, all conditions associated with atherosclerosis and cardiovascular disease. Recently Dr. Kastelein has developed the use of non-invasive B-mode ultrasound studies of the carotid arteries for the diagnosis and assessment of novel treatments for atherosclerosis.

Professsor Chris Packard
Prof Packard is R&D Director, NHS Greater Glasgow & Clyde Health Board, Honorary Professor of Vascular Biochemistry, University of Glasgow, Consultant Clinical Scientist, Dept of Biochemistry NHS Greater Glasgow & Clyde Health Board

Professor Packard research career has focussed on two aspects of atherosclerosis research:
lipoprotein metabolism and how it is affected by diets and drugs & large scale clinical trials of lipid lowering agents

HDL Cholesterol

The clinical utility of elevating high-density lipoprotein cholesterol (HDL-C) to reduce risk for cardiovascular morbidity and mortality remains the subject of much debate. Low serum levels of HDL-C or of apolipoprotein A-1 (ApoA-1), the major protein of HDL particles, are consistently associated with increased risk for all forms of atherosclerotic disease and its clinical sequelae, including myocardial infarction, stroke, and sudden death. Although statins efficaciously reduce low-density lipoprotein cholesterol (LDL-C) levels, they are not normally adequate as monotherapy to raise HDL-C or to correct HDL-associated cardiovascular risk in low subjects with low HDL-C because of their modest effect on HDL-C levels. The principal therapies used for the management of low HDL-C include niacin and fibrates. Another approach for elevating HDL-C is through the inhibition of cholesterol ester transfer protein (CETP). CETP plays an important role in cholesterol metabolism because it is responsible for the transfer of cholesteryl esters from HDL to very low-density lipoproteins (VLDL) and LDLs. The first agent in that class, torcetrapib, was studied in clinical trials, but a risk for dose-dependent increases in blood pressure and an increase in all-cause mortality associated with torcetrapib resulted in discontinuance of the trial. Although CETP inhibition with torcetrapib did not prove efficacious, the concept of CETP inhibition represents a possible area of focus to modulate CETP activity to alter atherogenesis, and development of several investigational agents is ongoing.


View the Powerpoint files presented

The information and data provided in this program were updated and correct at the time of the program development, but may be subject to change.

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