Abstract
Limited ability of prediction of CAD lead to the definition of novel risk factors including both molecular-genetic factors and novel molecules. It is known that the statin treatment does not alleviate in some patients the burden of residual risk for CAD.
The part of the residual risk is caused by high TAG and low HDL-C concentrations. Increased level of basal cholesterol biosynthesis (high concentrations of cholesterol precursors) and decreased cholesterol absorption (high concentrations of phytosterols) are connected with high profit from statin treatment, whereas the opposite is characteristic for the patients with CVD.
The absorption of phytosterols is also linked with diabetes mellitus. Experimental models point at the crosstalk between endothelial dysfunction, high blood pressure and phytosterol levels.
Although retrospective studies proved the efficacy of statins in the cessation of progression of degenerative aortal stenosis, the prospective studies produced controversial results. In conclusion, the noncholesterol sterols take part in the etiology and pathogenesis of human atherosclerosis, at least in the patients with lowered activity of of ABCG5/G8.
Therapeutic implications could involve on one side the selection of individuals, whose cardiovascular risk is increased or whose profit from the control of conventional risk factors for CVD is eliminated by phytosterol supplementation, and on the other side the patients who profit considerably from statin treatment.