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BACKGROUND: Coadministration of any statin with ezetimibe is as effective as using high doses of the same statin in the reduction of low-density lipoprotein cholesterol (LDL-c). There may be other effects called pleiotropics. OBJECTIVE: To compare the effectiveness of 2 different treatments that obtain equivalent LDL-c reductions (80 mg of simvastatin, once a day and coadministration of 10 mg of simvastatin and 10 mg of ezetimibe, once a day) over endothelial function and inflammation. METHODS: Twenty-three randomized patients with hypercholesterolemia in a 2 x 2 crossover protocol were studied. Endothelial function was analyzed by ultrasound assessment of endothelial dependent flow-mediated vasodilation of the brachial artery, and inflammation was estimated by high-sensitivity C-reactive protein (hs-CRP). RESULTS: LDL-c reduction was similar between the 2 treatments with simvastatin/ezetimibe and with simvastatin (P < 0.001); no difference between treatments was found (P = 0.968). Both treatments improved significantly the endothelial function [3.61% with simvastatin/ezetimibe (P = 0.003) and 5.08% with simvastatin (P < 0.001)]; no difference was found between the 2 treatments (P = 0.291). hs-CRP had a 23% reduction with simvastatin/ezetimibe (P = 0.004) and a 30% reduction with simvastatin alone (P = 0.01), with no significant difference between the 2 treatments (P = 0.380). CONCLUSION: The 2 forms of treatment presented similar pleiotropic effects: improvement in endothelial function and decrease in hs-CRP levels.

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Background: Coadministration of any statin with ezetimibe is as effective as using high doses of the same statin in the reduction of low-density lipoprotein cholesterol (LDL-c). There may be other effects called pleiotropics. Objective: To compare the effectiveness of 2 different treatments that obtain equivalent LDL-c reductions (80 mg of simvastatin, once a day and coadministration of 10 mg of simvastatin and 10 mg of ezetimibe, once a day) over endothelial function and inflammation. Methods: Twenty-three randomized patients with hypercholesterolemia in a 2 3 2 crossover protocol were studied. Endothelial function was analyzed by ultrasound assessment of endothelial dependent flow-mediated vasodilation of the brachial artery, and inflammation was estimated by high-sensitivity C-reactive protein (hs-CRP). Results: LDL-c reduction was similar between the 2 treatments with simvastatin/ezetimibe and with simvastatin (P , 0.001); no difference between treatments was found (P = 0.968). Both treatments improved significantly the endothelial function [3.61% with simvastatin/

ezetimibe (P = 0.003) and 5.08% with simvastatin (P , 0.001)]; no difference was found between the 2 treatments (P = 0.291). hs-CRP had a 23% reduction with simvastatin/ezetimibe (P = 0.004) and a 30% reduction with simvastatin alone (P = 0.01), with no significant difference between the 2 treatments (P = 0.380).

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Background: Coadministration of any statin with ezetimibe is as effective as using high doses of the same statin in the reduction of low-density lipoprotein cholesterol (LDL-c). There may be othereffects called pleiotropics. Objective: To compare the effectiveness of 2 different treatments that obtain equivalent LDL-c reductions (80 mg of simvastatin, oncea day and coadministration of 10 mg of simvastatin and 10 mg of ezetimibe, once a day) over endothelial function and inflammation. Methods: Twenty-three randomized patients with hypercholesterolemia in a 2 3 2 crossover protocol were studied. Endothelial function was analyzed by ultrasound assessment of endothelialdependent flow-mediated vasodilation of the brachial artery, andinflammation was estimated by high-sensitivity C-reactive protein(hs-CRP). Results: LDL-c reduction was similar between the 2 treatments withsimvastatin/ezetimibe and with simvastatin (P , 0.001); no differencebetween treatments was found (P = 0.968). Both treatments improved significantly the endothelial function [3.61% with simvastatin/ ezetimibe (P = 0.003) and 5.08% with simvastatin (P , 0.001)]; no difference was found between the 2 treatments (P = 0.291). hs-CRP had a 23% reduction with simvastatin/ezetimibe (P = 0.004) and a 30% reduction with simvastatin alone (P = 0.01), with no significant difference between the 2 treatments (P = 0.380). Conclusion: The 2 forms of treatment presented similar pleiotropiceffects: improvement in endothelial function and decrease in hs-CRP levels.

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Embora muitos avanços tenham sido obtidos na prevenção da aterosclerose, esta doença, com suas variadas manifestações, permanece como a maior causa de morte nos países ocidentais. A principal forma de lutar contra a aterosclerose envolve o combate aos seus fatores de risco de há muito conhecidos. Entretanto, novos conceitos têm surgido e entre estes se destaca o papel das apolipoproteínas como marcadores do risco coronário. Entre suas variadas funções, as proteínas que fazem parte das lipoproteínas mostraram que a determinação de seus níveis sangüíneos pode acrescentar informações sobre a situação individual de risco, particularmente com as dosagens das apos B e A-1 e da relação entre elas. Este artigo revisa os dados disponíveis sobre o papel fisiológico e de indicador de risco dessas apolipoproteínas, sugerindo o que já fazem alguns autores que defendem a idéia da incorporação da determinação rotineira dessas proteínas ao perfil lipídico para avaliação do risco cardiovascular.

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OBJECTIVE: To evaluate the effects of soy germ isoflavones and hormone therapy on vascular reactivity, the formation of nitric oxide derivatives, and lipid peroxidation in hypercholesterolemic postmenopausal women. DESIGN: Women were treated with soy germ, 17beta-estradiol or 17beta-estradiol + noretisterone acetate for 3 months after taking placebo for 1 month. The plasma concentrations of nitrite + nitrate and S-nitrosothiols were evaluated by gaseous phase chemiluminescence; nitrotyrosine, electronegative low-density lipoprotein, and estradiol levels were determined by enzyme-linked immunosorbent assay; cholesterol oxides and isoflavones were determined by gas chromatography and high-performance liquid chromatography, respectively. Vascular reactivity was analyzed by high-resolution ultrasonography. RESULTS: Soy germ isoflavones and hormone therapy induced a decrease in nitrite + nitrate, electronegative low-density lipoprotein, and cholesterol oxides, as well as an increase in S-nitrosothiols. Soy germ isoflavones lowered electronegative low-density lipoprotein, and cholesterol oxides more efficiently than did hormone therapy. Only soy isoflavones inhibited nitrotyrosine formation. A significant improvement of vascular reactivity was only seen in women treated with 17beta-estradiol. CONCLUSIONS: The soy germ isoflavones and 17beta-estradiol, alone or associated with noretisterone acetate, in the doses and forms used here, have similar effects on the bioavailability of nitric oxide. Soy germ treatment inhibited lipid peroxidation more effectively than hormone therapy.

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Objective: To evaluate the effects of soy germ isoflavones and hormone therapy on vascular reactivity, the formation of nitric oxide derivatives, and lipid peroxidation in hypercholesterolemic postmenopausal women. Design: Women were treated with soy germ, 17A-estradiol or 17A-estradiol + noretisterone acetate for 3 months after taking placebo for 1 month. The plasma concentrations of nitrite + nitrate and S-nitrosothiols were evaluated by gaseous phase chemiluminescence; nitrotyrosine, electronegative low-density lipoprotein, and estradiol levels were determined by enzymelinked immunosorbent assay; cholesterol oxides and isoflavones were determined by gas chromatography and high-performance liquid chromatography, respectively. Vascular reactivity was analyzed by high-resolution ultrasonography. Results: Soy germ isoflavones and hormone therapy induced a decrease in nitrite + nitrate, electronegative low-density lipoprotein, and cholesterol oxides, as well as an increase in S-nitrosothiols. Soy germ isoflavones lowered electronegative low-density lipoprotein, and cholesterol oxides more efficiently than did hormone therapy. Only soy isoflavones inhibited nitrotyrosine formation. A significant improvement of vascular reactivity was only seen in women treated with 17A-estradiol. Conclusions: The soy germ isoflavones and 17A-estradiol, alone or associated with noretisterone acetate, in the doses and forms used here, have similar effects on the bioavailability of nitric oxide. Soy germ treatment inhibited lipid peroxidation more effectively than hormone therapy.

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This double blind randomized placebo controlled study assessed the effects of atorvastatin, estradiol and norethisterone, isolated and in combination, on the lipid profile and on vascular reactivity, in post-menopausal women with hypercholesterolemia and arterial hypertension. Ninety-four women aged 50–65 were selected. All have received dietary counseling (4 weeks), placebo (4 weeks), and drug therapy (12 weeks): 17- estradiol 2mg/day (E) (n = 17); E + norethisterone acetate 1 mg/day (P) (n = 18); torvastatin 10 mg/day (A) (n = 20); E + A (n = 21) and E + P + A (n = 18). All treatment modalities have significantly reduced total cholesterol (TC) (E = 8.8%, E + P = 10.1%, A = 27.9%, A + E = 29.4% and E + P + A = 35.7%) and LDL-cholesterol (LDL-c) levels (E + P + A = 46.6%, E + A = 45.9%, A = 40.2%, E = 20.3%, and E + P = 12.1%). As concerns HDL-cholesterol (HDL-c), Groups E and E + A had increases of 15.5% and 13.1%, respectively. The addition of a progesterone compound reduced its concentration (Group E + P = −9.1%, and Group E + P + A = −9.5%). By random, approximately half of the patients in each group were designated to the endothelial function evaluation (brachial artery ultrasound). We observed that in Group A (n = 10), in Group E (n = 10) and with the association (Group E + A) (n = 7), there was a significant increase in the flow-mediated vasodilatation as compared to basal measurements. The addition of a progestin has annulled these benefits. Conclusions: Atorvastatin has promoted more beneficial effects on TC and LDL-c, whereas estradiol was responsible for an increase in HDL-c. The addition of a progesterone derivative abolished these benefits. Atorvastatin, estradiol or both together improved endothelial function, an effect suppressed by the addition of norethisterone.

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UNLABELLED: This double blind randomized placebo controlled study assessed the effects of atorvastatin, estradiol and norethisterone, isolated and in combination, on the lipid profile and on vascular reactivity, in post-menopausal women with hypercholesterolemia and arterial hypertension. Ninety-four women aged 50-65 were selected. All have received dietary counseling (4 weeks), placebo (4 weeks), and drug therapy (12 weeks): 17-beta estradiol 2mg/day (E) (n=17); E + norethisterone acetate 1mg/day (P) (n=18); Atorvastatin 10mg/day (A) (n=20); E + A (n=21) and E + P + A (n=18). All treatment modalities have significantly reduced total cholesterol (TC) (E=8.8%, E + P=10.1%, A=27.9%, A + E=29.4% and E + P + A=35.7%) and LDL-cholesterol (LDL-c) levels (E + P + A=46.6%, E + A=45.9%, A=40.2%, E=20.3%, and E + P=12.1%). As concerns HDL-cholesterol (HDL-c), Groups E and E + A had increases of 15.5% and 13.1%, respectively. The addition of a progesterone compound reduced its concentration (Group E + P=-9.1%, and Group E + P + A=-9.5%). By random, approximately half of the patients in each group were designated to the endothelial function evaluation (brachial artery ultrasound). We observed that in Group A (n=10), in Group E (n=10) and with the association (Group E + A) (n=7), there was a significant increase in the flow-mediated vasodilatation as compared to basal measurements. The addition of a progestin has annulled these benefits. CONCLUSIONS: Atorvastatin has promoted more beneficial effects on TC and LDL-c, whereas estradiol was responsible for an increase in HDL-c. The addition of a progesterone derivative abolished these benefits. Atorvastatin, estradiol or both together improved endothelial function, an effect suppressed by the addition of norethisterone.

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Em estudo aberto, näo comparativo, foram avaliados 25 pacientes portadores de hiperlipidemia primária. Deste total, 13 pacientes apresentavam hiperlipiproteinemia do tipo IIA de Fredrickson com níveis plasmáticos de colesterol acima de 220 mg/dl e 12 pacientes do tipo IIB com colesterol maior que 220 mg/dl e triglicérides acima de 250 mg/dl. Antes do início do tratamento o uso de medicamentos hipolipeniantes foi suspenso e os pacientes submetidos durante 60 dias à uma orientaçäo dietética. Durante os primeiros 30 dias os pacientes receberam placebo na posologia de um comprimido ao dia, seguido por um tratamento de 90 dias, durante o qual foi administrado um comprimido (400 mg) de bezafibrato retard ao dia. Ao término do tratamento houve uma reduçäo média da taxa de colesterol total (-17,1%), dos níveis de triglicérides (-38,6%) bem como um aumento de HDL-colesterol (+39,5%);-observou-se também uma queda de LDL-colesterol (-25,3%). Reaçöes colaterais ocorreram em nove casos sendo na maioria de intensidade leve, näo levando à suspensäo do tratamento

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A lovastatina potente inibidor competitivo da 3-Hidróxi-3-Metilglutari coenzima A redutase, foi utilizada no tratamento de 20 pacientes portadores de Hipercolesterolemia Primária. Os pacientes foram acompanhados por um período de 16 semanas, sendo as quatro iniciais sob uso de placebo e 12 semanas de tratamento ativo com lovastatina 20 a 40 mg ao dia. Análise de variância mostrou ao final do tratamento ativo reduçöes estatisticamente significativas (p < ou = 0.01) para: colesterol total (27%), LDL-colesterol (33%) e SF 0-12(27%). As variaçöes de HDL-colesterol mostraram tendência a elevaçäo, näo considerada significante. Tambem näo significantes foram as variaçöes observadas para: triglicérides, SF 20-100 e Sf 100-400. Näo foram observadas alteraçöes clínicas, laboratoriais, nem efeitos colaterais significativos durante a duraçäo do tratamento. Conclui-se ter a lovastatina boa atuaçäo sobre os níveis lipídicos e lipoprotéicos plasmáticos, apresentando boa tolerabilidade

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