[Recent progresses in the treatment of dyslipidemia]

There is a linear relationship between LDLcholesterol plasma concentration and coronary events, both in patients with stable angina pectoris and after an acute event. All medications that affect the lipid profile do not have a favorable effect on cardiovascular events (i.e. niacin, inhibitors of the cholesteryl ester transfer protein). Statins increase slightly the risk of type II diabetes in subjects at risk. We have also learnt that statins activate a transcription factor that increases LDL-cholesterol receptors, as well as a protein named " PCSK9 ". This latter protein reduces the number of LDL-cholesterol receptors on the hepatocyte and hampers thereby the LDLcholesterol lowering effects of statins. Spontaneous mutations that render PCSK9 ineffective reduce the LDL-cholesterol, and prevent coronary heart disease. Similar observations have been reproduced with numerous mutations that affect LDL-cholesterol levels. If a monoclonal antibody against PSCK9 is provided in addition to statin therapy, LDLcholesterol plasma concentration falls at unprecedented low concentrations of 30 mg/dl. 4.4% of these patients present a myocardial infarction, as compared to 6.3% in the placebo group. This new class of medication seems therefore promising for the secondary prevention in patients at risk of recurrent ischemic events.