Entity

Time filter

Source Type


Oravec S.,Comenius University | Dostal E.,Krankenanstalten Dr. Dostal | Mikl J.,Hietzing Hospital
Neuroendocrinology Letters | Year: 2011

OBJECTIVE: The identification of a non-atherogenic and an atherogenic lipoprotein profile, non-athero phenotype A vs. athero phenotype B, in a group of hypercholesterolemic subjects reveals newly discovered non-atherogenic hypercholesterolemia. Individuals with this type of hypercholesterolemia, or hyper-betalipoproteinemia LDL1,2, are probably not at increased risk to develop a premature atherothrombosis or a sudden cardiovascular event. Examined individuals with hyper-betalipoproteinemia LDL1,2 were divided into two subgroups: individuals under 40 years of age, and older individuals between 46 and 71 years of age. Subjects in the under 40 years of age group did not have any apparent clinical or laboratory-proven impairment of the cardiovascular system. The older subjects with hyper-betalipoproteinemia and a non-atherogenic lipoprotein profile had only mild signs of clinically irrelevant aortic valve sclerosis. METHODS: A quantitative analysis of the lipoprotein spectrum in plasma in a group of hypercholesterolemic subjects was performed. An innovative electrophoresis method on Polyacrylamide gel (PAG) was used for the analysis of plasma lipoproteins and for the identification of atherogenic vs. non-atherogenic lipoproteins in plasma. With regard to lipids, total cholesterol and triglycerides in plasma 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 plasma lipoproteins in the examined subjects. RESULTS: There was a high concentration of LDL1, and LDL2 subfractions (p<0.0001), and an extremely low concentration of LDL3-7 (p<0.0001) in the nonatherogenic lipoprotein profile of hyper-betalipoproteinemia LDL1,2 compared to the control group. Higher concentrations (p<0.0001) of lipids and lipoproteins in the non-atherogenic hypercholesterolemia, compared to the control group, were also found. The hyper-betalipoproteinemia LDL1,2 was also characterized by high SAAR values. There was found a higher concentration of HDL large and HDL intermediate subfractions in hypercholesterolemic subjects. CONCLUSIONS: The advantages of this new diagnostic method include: • identification of the existence of a non-atherogenic hyper-betalipoproteinemia LDL1,2 in examined hypercholesterolemic subjects with untreated hypercholesterolemia • introduction of a new risk measure, the score for anti-atherogenic risk (SAAR), for the estimation of atherogenic/anti-atherogenic risk. • the presence of small dense LDL in plasma is decisive for the declaration of an atherogenic lipoprotein profile. It is valid for hyperlipidemia and for normolipidemia as well. ©2011 Neuroendocrinology Letters. Source


Oravec S.,Comenius University | Dostal E.,Krankenanstalten Dr. Dostal | Dukat A.,Comenius University | Gavornik P.,Comenius University | And 2 more authors.
Neuroendocrinology Letters | Year: 2011

OBJECTIVE: The HDL family forms a protective part of plasma lipoproteins. It consists of large HDL, intermediate HDL, and small HDL subclasses. The large HDL and intermediate HDL subclasses are considered anti-atherogenic parts of the HDL family. The atherogenicity of the small HDL subclass is currently the subject of much discussion. In the patient group with the diagnosis of cardiovascular disease (arterial hypertension, coronary heart disease) and in individuals with a non-atherogenic hypercholesterolemia, a type of lipoprotein profile (either a non-atherogenic phenotype A, or an atherogenic phenotype B) was identified, and a concentration of small dense LDL (sdLDL) was analyzed. The aim of this study was to identify the major representative of the HDL subclasses in the individuals with cardiovascular diseases, who had an atherogenic lipoprotein phenotype B, and in the individuals with the diagnosis of non-atherogenic hyperbetalipoproteinemia LDL1,2, who had a non-atherogenic lipoprotein phenotype A. METHODS: Identification of the specific lipoprotein phenotype and a quantitative analysis of small dense LDL was performed by an electrophoresis method on Polyacrylamide gel (PAG), using the Lipoprint LDL system. For a quantitative analysis of HDL subclasses, i.e., large HDL, intermediatete HDL, and small HDL, in subjects with newly diagnosed cardiovascular diseases (arterial hypertension and coronary heart disease), and in subjects with a non-atherogenic hypercholesterolemia (hyper- betalipoproteinemia LDL1,2), we used an innovative electrophoresis method on Polyacrylamide gel (PAG), the Lipoprint HDL system. With regard to lipids, total cholesterol and triglycerides in plasma were analyzed by an enzymatic CHOD PAP method. A control group consisted of a group of healthy normolipidemic volunteers without signs of clinically manifested impairment of the cardiovascular system. RESULTS: In the patient group with the diagnosis of arterial hypertension (p<0.0002) and coronary heart disease (p<0.0001), (both are classified as cardiovascular diseases), the large HDL subclass was significantly decreased and the small HDL subclass was increased (p<0.0001). The concentration of the intermediate HDL subclass did not differ from that of the control group. These results were in accordance with an atherogenic lipoprotein phenotype B in individuals with the diagnosis of cardiovascular diseases, where, using a Lipoprint LDL analysis, a high concentration of atherogenic small dense LDL (p<0.0001) was found. Thus, it seems that the small HDL subclass represents an atherogenic part of the HDL family. Conversely, an increased concentration of total HDL (p<0.0001), large HDL (p<0.005), and intermediate HDL subclasses (p<0.0001) was found in a group of subjects with a non-atherogenic hyper-betalipoproteinemia LDL1,2. The concentration of the small HDL subclass did not differ from that of the control group. In this non-atherogenic lipoprotein profile, only traces of atherogenic small dense LDL were identified. CONCLUSIONS: The advantages of this new method includes: (i) Identification of ten HDL subfractions with Lipoprint HDL analysis (large HDL1-3, intermediate HDL 4-7, and small HDL 8-10). (ii) Discovery of a high concentration of smal HDL in plasma lipoproteins in patients with cardovascular diseases with an atherogenic lipoprotein phenotype B, confirmes that the atherogenic subclass of HDL family is attributable to small HDL. (iii) Presence of a low concentration of small HDL in non-atherogenic hypercholesterolemia also confirms the atherogenic characteristics of the small HDL subclass per se. (iv) Presence of small dense LDL is definitive to diagnose an atherogenic lipoprotein profile. It is valid for hyperlipidemia and for normolipidemia as well. © 2011 Neuroendocrinology Letters. Source


Goliasch G.,Medical University of Vienna | Oravec S.,University of Bratislava | Blessberger H.,Medical University of Vienna | Dostal E.,Krankenanstalten Dr. Dostal | And 6 more authors.
European Journal of Clinical Investigation | Year: 2012

Background Low-density lipoprotein (LDL) cholesterol lowering has been established as one of the principal targets in preventive cardiology. Recently, assessment of LDL particle size and number as well as other lipid moieties has been presented as a more reliable method to quantify atherogenicity of the lipoprotein fractions. Thus, it was our aim to assess the influence of different lipoprotein fractions on premature myocardial infarction (≤40years of age). Methods and results We enrolled 302 patients into our multicentre case-control study, including 102 patients with myocardial infarction and 200 age-, gender- and centre-matched controls. The LDL and HDL Lipoprint ® System were used for lipid subfraction quantification. The lipid risk factors most strongly associated with premature acute myocardial infarction (AMI) in the adjusted model were non-HDL C (OR 5·02, 95% CI 2·75-9·15, P-value=0·001), LDL-C (OR 4·35, 95% CI 2·5-7·57, P-value=0·001), VLDL-C (OR 3·66, 95% CI 2·14-6·28, P-value=0·001), large IDL-C (OR 3·15, 95% CI 1·94-5·12, P-value=0·001), large LDL-C (OR 3·67, 95% CI 2·19-6·15, P-value=0·001) and intermediate LDL-C (OR 1·96, 95% CI 1·25-3·06, P-value=0·003). In contrast, small dense LDL was not significantly associated with premature myocardial infarction. Conclusion Non-HDL cholesterol is most strongly associated with premature coronary artery disease and could serve as preferred risk predictor and therapeutic target in this young patient population (≤40years). Besides, VLDL, LDL-C, large LDL, intermediate LDL and large IDL were significantly associated with premature myocardial infarction. Furthermore, our data suggest that risk prediction using small dense LDL particles might not be useful in young AMI survivors. © 2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation. Source


Distelmaier K.,Medical University of Vienna | Wiesbauer F.,Medical University of Vienna | Blessberger H.,Johannes Kepler University | Oravec S.,University of Bratislava | And 10 more authors.
European Journal of Clinical Investigation | Year: 2015

Background: There is growing evidence that the predictive value of HDL cholesterol levels for cardiovascular risk stratification is limited in patients with coronary artery disease (CAD). HDL function seems to be a more sensitive surrogate of cardiovascular risk estimation than simple serum levels. Therefore, we aimed to assess whether impaired antioxidant HDL function is involved in the development of premature acute myocardial infarction (AMI). Methods: In this multicentre case-control study, we compared the antioxidant function of HDL, measured by the HDL inflammatory index (HII), and HDL particle size in 184 patients comprising 92 patients with AMI at a very young age (≤40 years of age) and 92 age- and gender-matched controls. Results: Antioxidant capacities of HDL were significantly impaired in the acute phase of AMI (HII of 1·50 [IQR 1·10-1·74] vs. 0·56 [IQR 0·41-0·86] in controls, P < 0·001 as well as in the chronic stable phase 1 year after the event (HII of 0·85 [IQR 0·72-1·03] vs. 0·56 [IQR 0·41-0·86], P < 0·001) compared to controls. Moreover, HDL function in the stable phase remained significantly associated with premature MI in adjusted logistic regression analysis with an OR of 2·24 per SD increase of HII (95% CI 1·28-3·91; P = 0·005). Analyses of HDL size revealed a significant correlation between all HDL subfractions and HDL function in controls, whereas this correlation was lost for large and intermediate HDL in AMI patients. Conclusion: Impaired antioxidant function of HDL is independently associated with the development of premature AMI. The maintenance of HDL function might evolve into a significant therapeutic target, especially in patients with premature CAD. © 2015 Stichting European Society for Clinical Investigation Journal Foundation. Source


Krychtiuk K.A.,Medical University of Vienna | Krychtiuk K.A.,Ludwig Boltzmann Cluster for Cardiovascular Research | Kastl S.P.,Medical University of Vienna | Hofbauer S.L.,Medical University of Vienna | And 14 more authors.
Journal of Clinical Lipidology | Year: 2015

Background Lipoprotein(a) (Lp(a)) is a proatherogenic plasma lipoprotein currently established as an independent risk factor for the development of atherosclerotic disease and as a predictor for acute thrombotic complications. In addition, Lp(a) is the major carrier of proinflammatory oxidized phospholipids (OxPL). Today, atherosclerosis is considered to be an inflammatory disease of the vessel wall in which monocytes and monocyte-derived macrophages are crucially involved. Circulating monocytes can be divided according to their surface expression pattern of CD14 and CD16 into at least 3 subsets with distinct inflammatory and atherogenic potential. Objective The aim of this study was to examine whether elevated levels of Lp(a) and OxPL on apolipoprotein B-100-containing lipoproteins (OxPL/apoB) are associated with changes in monocyte subset distribution. Methods We included 90 patients with stable coronary artery disease. Lp(a) and OxPL/apoB were measured, and monocyte subsets were identified as classical monocytes (CMs; CD14++CD16-), intermediate monocytes (IMs; CD14++CD16+), and nonclassical monocytes (NCMs; CD14+CD16++) by flow cytometry. Results In patients with elevated levels of Lp(a) (>50 mg/dL), monocyte subset distribution was skewed toward an increase in the proportion of IM (7.0 ± 3.8% vs 5.2 ± 3.0%; P =.026), whereas CM (82.6 ± 6.5% vs 82.0 ± 6.8%; P =.73) and NCM (10.5 ± 5.3 vs 12.8 ± 6.0; P =.10) were not significantly different. This association was independent of clinical risk factors, choice of statin treatment regime, and inflammatory markers. In addition, OxPL/apoB was higher in patients with elevated Lp(a) and correlated with IM but not CM and NCM. Conclusions In conclusion, we provide a potential link between elevated levels of Lp(a) and a proatherogenic distribution of monocyte subtypes in patients with stable atherosclerotic disease. © 2015 National Lipid Association. All rights reserved. Source

Discover hidden collaborations