**3. Analytic system**

**1. Introduction**

42 Cholesterol Lowering Therapies and Drugs

[7].

**2. Plasma atherogenic biomarkers**

including that of the detailed lipid profile.

Abnormal lipid metabolism preceding overt atherosclerosis is associated with increased cardiovascular risk. In atherogenic dyslipidaemia, the lipoprotein abnormalities include increased small dense LDL particles (sdLDL), elevations of VLDL and low HDL-cholesterol usually occur together [1, 2]. Over the last two decades, it has been demonstrated that routine measurement of total cholesterol, LDL-C and HDL-C fails to distinguish all lipoprotein abnormalities associated with cardiovascular diseases [3]. There is a need to find new biomarkers for this. By contrast, the analysis of lipoprotein subfractions appears more important in assessing the risk of cardiovascular complications [4]. LDL-C remains the primary focus for cardiovascular risk assessment and evaluation of pharmacologic effectiveness, but not based on LDL targets instead on LDL lowering [5]. Yet, a large body of evidence indicates that a narrow focus on LDL-C assessment and treatment alone is not the optimal strategy for patient care [6]. Examining individual lipoprotein subpopulations/subfractions provides opportunities for risk stratification, independent of commonly determined lipid parameters

The term "lipid triad" has been introduced to describe a common form of dyslipidaemia, characterized by three lipid abnormalities: increased plasma triglyceride levels, decreased HDL-cholesterol concentrations and the presence of sdLDL particles [8]. Apolipoprotein B (apo B) is the major protein of all lipoproteins except for high-density lipoprotein. Estimation of apo B reflects the total number of sdLDL particles. It is notable that LDL particles can vary

Haematological parameters, mainly red cell distribution width (RDW) and mean platelet volume (MPV) have gained great interest in cardiovascular research. This has been reported to be a strong and independent predictor of adverse cardiovascular outcomes in the general population [9]. In the last few years, MPV, respected an effective marker of platelet activation, has also created much interest in cardiovascular research. This stems from the fact that platelets undergo a dramatic change in shape from quiescent discs to swollen spheres, with an increased MPV, during the activation process. It is well-known that large platelets are more adhesive and prone to aggregate than smaller ones [10], and elevated MPV values have been reported in cardiovascular diseases [11]. "Another haematological parameter which seems to play a role is RDW, a measure of the variability of red cell size. RDW has been reported to be a strong and independent predictor of adverse cardiovascular outcomes in the general population" [12].

The aim of our study was to compare different methods in the evaluation of atherogenicity,

in size, cholesterol content and number, for a given concentration of LDL-C.

Various methods have been developed such as gradient gel electrophoresis, ultracentrifugation, magnetic resonance spectroscopy, endothelial models for testing lipoprotein cytotoxicity to identify atherogenic lipoproteins [13], but because of technical and financial limitations, long-term analyses and high operating costs, the previously mentioned methods were used primarily in basic research. Electrophoresis of plasma lipoproteins on the polyacrylamide gel (PAG) Lipoprint LDL system is a new method, which has become a milestone in routine laboratory analysis and in diagnosing disorders of lipoproteins, for the identification and quantitative evaluation of lipoprotein subfractions, i.e., the atherogenic and non-atherogenic lipoproteins [14]. The benefits of Lipoprint LDL method are in unique identification of an atherogenic and non-atherogenic lipoprotein spectrum in case of hyperlipoproteinaemia with the possibility of a better assessment of the adequacy of lipid-lowering interventions. Another important aspect is to identify the atherogenic lipoprotein profile in patients with normolipidaemia after lipid-lowering therapy [15].
