AIM: New ischemic lesions in the brain can be detected in approximately 50% of patients undergoing carotid artery stenting (CAS). We wished to discover the laboratory-based predictors of new infarctions in the brain after CAS. METHODS: All consecutive patients with internal carotid artery stenosis of ≥70% with indication for CAS were enrolled in a prospective study for 16 months. All patients used dual antiplatelet therapy for ≥7 days before CAS. Neurologic examination and magnetic resonance imaging (MRI) of the brain were undertaken before and at 24 h after CAS. Samples of venous blood were collected at <24 h before CAS for the evaluation of hematology, reticulocytes, coagulation markers (PT, APTT, Fbg, Clauss), vWF antigen, PAI-1 activity, PAI-1 polymorphism 4G/5G, and the multiplate (aspirin and clopidogrel) resistance test. Blood samples for the assessment of anti-Xa activity were collected during CAS. Differences in the values of laboratory markers between patients with and without new ischemic lesions of the brain on control MRI were evaluated. RESULTS: The cohort comprised 81 patients (53 males; mean age, 67.3±7.2 years). New ischemic infarctions in the brain on control MRI were found in 46 (56.8%) patients. Three of seven patients with resistance to aspirin or clopidogrel had a new ischemic infarction in the brain. No significant differences for particular markers were found between patients with and without an ischemic lesion in the brain. CONCLUSION: A high risk of a new ischemic infarction in the brain was detected in patients undergoing CAS, but a laboratory-based predictor of such an infarction could not be identified.

• MeSH
• biologické markery analýza   MeSH
• CT angiografie MeSH
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• magnetická rezonanční tomografie MeSH
• mozkový infarkt diagnóza   etiologie   metabolismus   MeSH
• prospektivní studie MeSH
• rizikové faktory MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• stenóza arteria carotis komplikace   chirurgie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

AIM: The cardio-ankle vascular index (CAVI) is a sensitive non-invasive marker of arterial stiffness and atherosclerosis. The aim of this work was to compare the CAVI values in patients with dyslipidemia (without diabetes mellitus and hypertension) and healthy controls. METHODS: A Total 248 subjects with dyslipidemia (104 men, 144 women), 55.0 (95% CI 30-70) years of age with combined hyperlipidemia or primary hypercholesterolemia and 537 healthy controls (244 men, 293 women) 40.0 (95% CI 26-62) years of age were included in this study. Fasting blood samples were collected to measure the serum total cholesterol, triglyceride, HDL-cholesterol and apolipoprotein A1 and B levels. The LDL cholesterol level was also calculated, and the CAVI was measured using the VaSera(®) 1500 system. RESULTS: The CAVI values were significantly higher in the dyslipidemic patients (8.08, 95% CI 6.00-10.05) than in the controls (7.11, 95% CI 5.77-9.05; p < 0.01). In addition, the CAVI values were elevated in both subgroups of patients with hypercholesterolemia (7.95, 95% CI 5.85-6.90; p < 0.01) and combined hyperlipidemia (8.30, 95% CI 6.60-10.15; p < 0.01) in comparison with those observed in the controls. After adopting the propensity score method in order to balance the confounding factors (age, gender, body mass index) and adjust the analysis for diastolic blood pressure, the CAVI values in the dyslipidemic patients remained significantly high (7.78, 95% CI 5.80-9.69) compared to that observed in the controls (7.31, 95% CI 5.44-9.35; p < 0.001). However, the CAVI values did not differ significantly between the controls and both subgroups of dyslipidemic patients(primary hypercholesterolemia, combined hyperlipidemia). CONCLUSIONS: The present findings demonstrated that dyslipidemia increases the CAVI values in comparison to that seen in healthy subjects.

• MeSH
• dospělí MeSH
• hyperlipidemie komplikace   patofyziologie   MeSH
• hypertenze komplikace   MeSH
• komplikace diabetu patofyziologie   MeSH
• kotník krevní zásobení   MeSH
• lidé MeSH
• mladý dospělý MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

AIM: The cardio-ankle vascular index (CAVI) is a novel non-invasive marker of arterial stiffness and atherosclerosis. The aim of this work was to examine whether the CAVI value in patients with dyslipidaemia (DLP) is increased by the presence of other cardiovascular risk factors: hypertension, diabetes mellitus, and smoking. METHODS: A total of 392 subjects with DLP (166 male, 226 female), with a median age of 58.5 and 5-95 percentile range 32.2-73.9 years were examined. CAVI was measured using the VaSera 1500 system. RESULTS: CAVI correlated significantly with age (p<0.001) and both systolic (p<0.001) and diastolic (p=0.002) blood pressure; higher values were found in men (p=0.034) than in women in the 56-65 age group. There was no significant difference in CAVI between smokers and non-smokers (p= 0.217) and between subjects with and without diabetes mellitus (p= 0.424). CAVI was significantly higher in subjects with hypertension than in the normotensive group (p<0.001) and in statin-treated subjects than in those without statins (p<0.001); however, CAVI values adjusted for age and sex did not differ significantly between these groups. Adjusted CAVI values were higher only in smokers than in non-smokers (former smokers) (p<0.001). CONCLUSION: The study proves conclusively that the CAVI value in DLP patients is not significantly affected by hypertension and diabetes mellitus, but it is increased by smoking.

• MeSH
• ateroskleróza etiologie   patofyziologie   MeSH
• dospělí MeSH
• dyslipidemie komplikace   patofyziologie   MeSH
• kardiovaskulární nemoci etiologie   patofyziologie   MeSH
• kotník krevní zásobení   MeSH
• krevní tlak MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipidy krev   MeSH
• rizikové faktory MeSH
• senioři MeSH
• srdce patofyziologie   MeSH
• tuhost cévní stěny MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

AIM: The cardio-ankle vascular index (CAVI) is a new non-invasive marker of arterial stiffness and atherosclerosis. The purpose of this study was to compare CAVI in patients with heterozygous familial hypercholesterolemia (FH) and in healthy controls. METHODS: 82 FH subjects (27 males, 65 females), aged 53.7±13.6 years without clinical symptoms of cardiovascular diseases and 359 healthy controls (121 males, 238 females), aged 43.9±14.9 years, were examined. CAVI was measured using the system VaSera® 1500. RESULTS: CAVI in FH patients was significantly higher (8.0±1.4) than in healthy subjects (7.5±1.3) p = 0.002; however, age, sex and BMI adjusted CAVI did not differ significantly (p = 0.061) between the FH group (7.5, CI: 7.3; 7.7) and control group (7.7, CI: 7.6; 7.7). CONCLUSION: The study showed no significant difference in CAVI between heterozygous FH and healthy controls.

• MeSH
• dospělí MeSH
• hyperlipoproteinemie typ II patofyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• srdce patofyziologie   MeSH
• tlakový index kotník-paže MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

AIM: Transforming growth factor-beta (TGF-β) plays important role in atherogenesis via TGF-β receptors and Smad proteins, which determine its signaling activity. In this study, we hypothesized, whether non-lipid related effects of atorvastatin, affect both endoglin/ALK-5/Smad2/eNOS and/or endoglin/ALK-1/Smad1/VEGF previously proposed pathways in ApoE/LDLR double knockout mice. METHODS: ApoE/LDLR double knockout mice were divided into two groups. The chow group (CHOW) (n =8) was fed with chow diet, while in the atorvastatin group (ATV) (n =8) atorvastatin was added to the chow diet at dose 50 mg/kg/day. Biochemical analyses of lipid profile, lesion area measurement, immunohistochemistry and Western blot analysis of endoglin, ALK-1, 5, phosphorylated and non-phosphorylated forms Smad-1, 2, VEGF and eNOS proteins in mice aorta were performed. RESULTS: Biochemical analysis of blood serum and morphometric analysis of aortic lesion size showed that atorvastatin treatment resulted in a significant increase of cholesterol levels and simultaneously in reduced lesion size in aortic sinus when compared to CHOW mice. Western blot analysis revealed that atorvastatin treatment significantly increase the expressions of endoglin by 102%, ALK-1 by 113%, ALK-5 by 296%, pSmad-1 by 202%, pSmad-2 by 34%, VEGF by 68% and eNOS by 687% as compared with CHOW mice. Immunofluorescence staining revealed endoglin coexpression with all studied markers that were increased by atorvastatin treatment mainly in endothelial cells covering atherosclerotic plaques. CONCLUSION: This study shows that atorvastatin treatment increases the expression of endoglin, ALK-1, ALK-5, phosphorylated forms of Smad1 and Smad2, VEGF and eNOS and reduces atherosclerotic lesion size beyond its lipid lowering effects. Therefore, we propose that endoglin related receptors and signal transducers might play protective role in atherogenesis.

• MeSH
• anticholesteremika terapeutické užití   MeSH
• apolipoproteiny E fyziologie   MeSH
• ateroskleróza metabolismus   prevence a kontrola   MeSH
• cholesterol metabolismus   MeSH
• imunoenzymatické techniky MeSH
• intracelulární signální peptidy a proteiny metabolismus   MeSH
• kyseliny heptylové terapeutické užití   MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• myši MeSH
• protein Smad1 metabolismus   MeSH
• protein Smad2 metabolismus   MeSH
• protein-serin-threoninkinasy metabolismus   MeSH
• pyrroly terapeutické užití   MeSH
• receptory LDL fyziologie   MeSH
• receptory transformujícího růstového faktoru beta metabolismus   MeSH
• synthasa oxidu dusnatého, typ III metabolismus   MeSH
• vaskulární endoteliální růstový faktor A metabolismus   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

AIM: The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice. METHODS: The experiments were performed on ApoE-/--deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3-4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods. RESULTS: Conventionally reared ApoE-/- mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE-/- mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls. CONCLUSION: In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE-/- mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE-/- mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development.

• MeSH
• aorta abdominalis metabolismus   patologie   MeSH
• aorta thoracica metabolismus   patologie   MeSH
• apolipoproteiny E fyziologie   MeSH
• ateroskleróza etiologie   metabolismus   prevence a kontrola   MeSH
• cholesterol dietní aplikace a dávkování   MeSH
• cholesterol krev   MeSH
• gnotobiologické modely MeSH
• messenger RNA genetika   MeSH
• metagenom * MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• myši MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• střevní sliznice mikrobiologie   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

AIM: Endoglin is a homodimeric transmembrane glycoprotein that has been demonstrated to affect transforming growth factor beta (TGF-beta) signaling and endothelial nitric oxide synthase (eNOS) expression by affecting SMAD proteins in vitro. Thus, in this study we stepped forward to elucidate whether endoglin is co-expressed with SMAD2, phosphorylated SMAD2/3 proteins and eNOS in vivo in atherosclerotic lesions in ApoE/LDLR double knockout mice. In addition, we sought whether endoglin expression as well as the expression of SMAD2, phosphorylated SMAD2/3 and eNOS is affected by atorvastatin treatment. METHODS: Two-month-old female ApoE/LDLR double knockout mice were divided into two groups. The control group was fed with the western type diet whereas in the atorvastatin group, atorvastatin at dose 100 mg/kg per day was added to the same diet. Immunohistochemical and western blot analysis of endoglin, SMAD2, phosphorylated SMAD2/3 and eNOS expressions in aorta were performed. RESULTS: The biochemical analysis showed that administration of atorvastatin significantly decreased level of total cholesterol, VLDL, LDL, TAG, and significantly increased level of HDL cholesterol. Fluorescence immunohistochemistry showed endoglin co-expression with SMAD2, phosphorylated SMAD2/3 and eNOS in aortic endothelium covering atherosclerotic lesions in both control and atorvastatin treated mice. Western blot analysis demonstrated that atorvastatin significantly increased expression of endoglin, SMAD2, phosphorylated SMAD2/3, and eNOS in mice aorta. CONCLUSION: These findings suggest, that endoglin might be interesting marker of endothelial dysfunction and/or atherogenesis which is upregulated by statins implicating potential beneficial role of endoglin and its pathway in atherosclerosis.

• MeSH
• anticholesteremika farmakologie   MeSH
• aorta chemie   MeSH
• apolipoproteiny E genetika   MeSH
• ateroskleróza metabolismus   MeSH
• cévní endotel chemie   MeSH
• fosforylace MeSH
• imunohistochemie MeSH
• intracelulární signální peptidy a proteiny analýza   MeSH
• kyseliny heptylové farmakologie   MeSH
• myši knockoutované MeSH
• myši MeSH
• protein Smad2 analýza   MeSH
• protein Smad3 analýza   MeSH
• pyrroly farmakologie   MeSH
• receptory LDL genetika   MeSH
• synthasa oxidu dusnatého, typ III analýza   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH