New Insights to HDL Therapy， Waksman
CRT at CIT， Plenary Hall A， 11.52-12.05

    There is enough evidence to say that HDL acts as a protective agent against coronary heart disease， was the opening message from Professor Ron Waksman from the Washington Hospital Center， Washington DC， and a clear indication of an inverse relationship between HDL-C and CHD. HDL functions by protecting low-density lipoproteins (LDL) from oxidation and inhibits expression of adhesion molecules in endothelial cells， preventing monocyte movement into the vessel walls. HDL removes and transports excess cholesterol from peripheral cells to the liver for removal from the body. Strategies have， and need， to be developed to increase the function of HDL or apolipoprotein A-1 to reduce the atherosclerotic progression. Current drug options to achieve this goal include use of statins， fibrates and niacin. Niacin used alone has been associated with side effects but its combination with Laropiprant attenuates the flushing effect. CETP (cholesterol ester transfer protein) inhibitors have blood pressure related adverse effects but do reduce the atheroma volume. Drug therapies take time to work， but the direct infusion of HDL (“Drano for the Heart”) is proposed to cause a rapid regression of atherosclerosis. Professor Waksman outlined observational and pre-clinical studies where infusions of recombinant apolipoprotein A1 Milano， a genetic variant isolated from a non-atherosclerotic population from an Italian village which acts as a nascent HDL-like particle， had been beneficial in animal and human trials. Another novel mechanism has been the use of autologous delipidated HDL infusions to impact on plaque volume. In trials， all reperfusion sessions were well tolerated without side effects and in association with pre-beta HDL increase was a five-fold rise in the cholesterol efflux for the delipidated plasma versus the control. Pre-beta HDL is developing as a key component in anti-atherosclerotic therapy， with clear numeric trends towards reduction in atheroma volume by IVUS. In conclusion， Professor Waksman advocated raising drugs and strategies to increase HDL-C levels as a promising move towards better therapeutic targets.