OBJECTIVE: In the subjects, who survived a stroke, an atherogenic lipoprotein profile phenotype B, was identified and a predominance of atherogenic lipoproteins of the lipoprotein families, VLDL and LDL, in the lipoprotein spectrum, was confirmed. The higher total cholesterol, triglycerides, and low HDL concentrations were accompanied by high serum levels of small dense LDL - strong atherogenic subfractions of the LDL family. High LDL2 also contributes to the creation of the atherogenic lipoprotein profile. Conversely, decreased serum concentration of LDL1 suggests, that the LDL1 subfraction does not contribute to the creation of an atherogenic lipoprotein profile of specific individuals, i.e., those who survived a stroke.
MATERIALS AND METHODS: A quantitative analysis of serum lipoproteins in a group of stroke patients, and in a group of healthy normolipidemic volunteers, without signs of clinically manifested impairment of the cardiovascular system, was performed. For the analysis of plasma lipoproteins, an innovative electrophoresis method was used, on polyacrylamide gel (PAG) - the Lipoprint LDL system, (Quantimetrix corp., CA, USA). With regard to lipids, total cholesterol and triglycerides in serum were analyzed with an enzymatic CHOD PAP method (Roche Diagnostics, FRG). A new parameter, the score for anti-atherogenic risk (SAAR), was calculated as the ratio between non-atherogenic to atherogenic serum lipoproteins in examined subjects.
RESULTS: An atherogenic lipoprotein profile phenotyp B was identified in the individuals who survived a stroke. There were increased concentrations of total cholesterol, triglycerides (p<0.001), and atherogenic lipoproteins: VLDL (p<0.001), total LDL, LDL2 (p<0.0001) and LDL3-7 (p<0.01), in the group of stroke patients, compared to the control group. The LDL1 subfraction, like HDL, was decreased and did not contribute to the formation of the atherogenic lipoprotein spectrum in stroke-surviving individuals. Therefore, it can be assumed that the LDL1 subfraction is not an atherogenic part of the LDL family, which was usually considered to be an atherogenic lipoprotein part of the lipoprotein spectrum. Decreased SAAR values - score of anti-atherogenic risk, was confirmed in the stroke surviving individuals, compared to the controls, with high statistical significance (p<0.0001).
CONCLUSIONS: The advantages of this new method include: (i) Identification of an atherogenic and a non-atherogenic lipoprotein profile, in the serum of examined individuals. (ii) Identification of an atherogenic normopidemic lipoprotein profile; phenotype B in subjects who survived a stroke. (iii) Introduction of new risk measure, the score for anti-atherogenic risk (SAAR), to estimate the atherogenic risk of examined individuals. (iv) Declaration of an atherogenic lipoprotein profile is definitive when small dense LDL are present in serum. It is valid for hyperlipidemia and for normolipidemia as well. (v) Selection of optimal therapeutic measures, including removal of atherogenic lipoproteins, as a part of a complex therapeutic approach, and the secondary prevention of a relapsing ischemic cerebral-vascular event.