Association of lipoprotein subfractions with endothelial function and arterial stiffness in acute ischemic stroke.

Hypercholesterolemia represents a risk factor for the development of atherosclerosis. Lipoprotein research has recently been focused on the phenomenon of atherogenic and non-atherogenic lipoproteins. The aim of this study was to explore the association of lipoprotein subfractions with a measure for endothelial function (represented by reactive hyperemia index [RHI]) and arterial stiffness (represented by augmentation index [AI]) in patients with acute ischemic stroke. We enrolled 51 patients with acute ischemic stroke. Blood samples were obtained within 24 h after the stroke onset in a fasting condition. Electrophoresis method on polyacrylamide gel was used for the analysis of plasma lipoproteins. RHI and AI was measured by peripheral arterial tonometry (EndoPAT2000 device). We failed to find any significant correlation between RHI and baseline characteristics of the population. Significant correlation was found between AI and age, hypertension, low density lipoprotein cholesterol (LDL) 1, LDL 3-7, score for anti-atherogenic risk and atherogenic profile. Age (beta = .362, p = .006) and LDL1 (beta = -0.283, p = .031) were the only independent variables significantly associated with AI in regression analysis. Significantly higher AI was found in an atherogenic lipoprotein profile compared to a non-atherogenic profile population (median 25% vs. median 11.5%, p = .043). In conclusion, our results suggest significant inverse correlation between levels of LDL 1 subfraction and measures of AI in patients with acute ischemic stroke. Significantly higher values of AI were observed in the population with an atherogenic lipoprotein profile.

Lipoprotein profile in patients who survive a stroke.

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.

Oxidative Stress Markers and Their Dynamic Changes in Patients after Acute Ischemic Stroke.

We have focused on determining the range of oxidative stress biomarkers and their dynamic changes in patients at different time points after the acute ischemic stroke (AIS). 82 patients with AIS were involved in our study and were tested: within 24 h from the onset of the attack (group A); at 7-day follow-up (group B); and at 3-month follow-up (group C). 81 gender and age matched volunteers were used as controls. Stroke patients in group A had significantly higher concentrations of plasma lipid peroxides and urine 8-isoprostanes when compared with controls. Protein carbonyls were not significantly different in any experimental group compared to controls. Antioxidant capacity of plasma was increased only in experimental group C. Activities of superoxide dismutase and catalase were elevated in all three experimental AIS groups compared to controls. Paraoxonase activity was reduced in groups A and B and unchanged in group C when compared to controls. Glutathione peroxide activity was elevated only in group A. Our results suggest that free radical damage is the highest within 24 h after the attack. During the next 3 months oxidative damage to lipids caused by free radicals is reduced due to activated antioxidant system.