Increasing HDL Cholesterol

It is true that "STATINS " had revolutionised the treatment of atherosclerotic heart disease. It has allowed us to medically, regress atherosclerosis (medical angioplasty). True, the percentage stenosis reduction is only in the order of 3-5% points but these translated to a 25-30% reduction in major adverse cardiac events, preventing more heart attacks, cardiac deaths and strokes than percutaneous coronary intervention. Statins have been so well studied, low dose, high dose, primary prevention, secondary prevention, in patients with normal LDL-C, patients with high LDL-C, low LDL-C levels that we seem to have run out of things to study with statins.

Therefore, we will soon be seeing many studies with HDL-C (good cholesterol) raisers. The reknowned team in Oxford (clinical trial service unit) has just announced the launching of a study of of Niacin (HDL-C raiser) to reduce CVS events in patients with known vascular disease (secondary prevention). The study called by the acronym HPS2-THRIVE or Heart Protection Study 2 Treatment of HDL to Reduce the Incidence of Vascular Events. This study is funded by Merck and Co and led by Dr Jane Amirtage. It will enroll 20,000 patients, from UK, China and the Scandinavian countries of Denmark, Sweden, Norway and Finland. It will study the effect of tablet MK-0254A, a combo pill of Niacin and a prostaglandin D2 (to reduce the problems of flushing). One of Niacins problems is severe flushing. The prostaglandin D2 is an attempt to make niacin more tolerable. The follow-up is 4 years.

We will have some results in 2010 or thereabouts. It is important to note that there are no less than 6 other studies in various stages of completion, studying the anti-atherosclerotic effects of raising HDL-C. Some of the many includes, AIM-HIGH (testing a combo of Niacin+simvastatin), HATS (again testing combo of simvastatin+niacin), ARBITER2 (testing statins against Niacin), VA-HIT (testing gemfibrozil), Apo A1 milano study, ILLUMINATE and ILLUSTRATE (both testing torceprib and atorvastatin against atorvastatin). Torceprib is a CETP inhibitor that show a lot of promise. If Fibrates raise HDL-C by 10-15%, and Niacin increases HDL-C by 20%, Torceprib at the standard dose can increase HDL-C by 50-60%. Can you imagine the impact that this will have on the plaque volume. I only hope that this reduction in plaque volume as already been shown by IVUS study in patients on Torceprib, will translate to greater event reduction, over and on top of the events reduction presently seen with statins.

The future for management of CAD certainly looks good. Perhaps there will be no further need for angioplasty. My dream.