Inhibitory Effect of Polyethylene Oxide and Polypropylene Oxide Triblock Copolymers on Aggregation and Fusion of Atherogenic Low Density Lipoproteins.

Triblock copolymers of poly(ethylene oxide) and poly(propylene oxide) (so-called pluronics) were shown to influence the aggregation and fusion of atherogenic low density lipoproteins (atLDL) and be able to inhibit these processes. The character of the influence and the degree of the stabilizing effect depended on the structure, relative hydrophobicity, and concentration of the copolymer. Pluronics L61, P85, and L64 characterized by the hydrophilic-lipophilic balance (HLB) value from 3 to 16 had the greatest ability to suppress the aggregation of atLDL. Pluronic L81 with the higher hydrophobicity (HLB = 2) partially inhibited atLDL aggregation at low concentrations but stimulated it at high concentrations. The influence of pluronics did not have a direct connection with their ability for micelle formation, but it was realized through individual macromolecules. We suppose that effects of pluronics could be due to their interaction with the lipid component of LDL and to a possible influence of these copolymers on the structure and hydrophilic-lipophilic characteristics of lipoproteins.

[Conventional and novel cardiovascular risk factors and predisposition to the development of atherosclerosis].

This population-based cross-sectional study included 472 apparently healthy study participants with an increased risk of cardiovascular disease, including 300 patients with hypercholesterolemia. To assess the susceptibility to the development of atherosclerosis, an ultrasonic evaluation of common carotid arteries was used. It has been confirmed that there exists the geographical gradient of carotid intima-media thickness (cIMT), and it has been shown that this gradient is highly correlated th the known gradient of cardiovascular mortality. It was found that the combination of conventional cardiovascular risk factors can help explaining only 21% variability of cIMT, the marker of generalized atherosclerosis. It was found that a predisposition to atherosclerosis, as measured by a pathological increase in cIMT, should be due to the interaction not only conventional cardiovascular risk factors, but also to genetic and environmental factors.