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[PMID]:28468836
[Au] Autor:Yoshikado T; Toshimoto K; Nakada T; Ikejiri K; Kusuhara H; Maeda K; Sugiyama Y
[Ad] Endereço:Sugiyama Laboratory, RIKEN Innovation Center, RIKEN, Kanagawa, Japan (T.Y., K.T., Y.S.); DMPK Research Laboratories Sohyaku, Innovative Research Division, Mitsubishi Tanabe Pharma, Saitama, Japan (T.N.); and Laboratory of Molecular Pharmacokinetics, Graduate School of Pharmaceutical Sciences, Univer
[Ti] Título:Comparison of Methods for Estimating Unbound Intracellular-to-Medium Concentration Ratios in Rat and Human Hepatocytes Using Statins.
[So] Source:Drug Metab Dispos;45(7):779-789, 2017 Jul.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is essential to estimate concentrations of unbound drugs inside the hepatocytes to predict hepatic clearance, efficacy, and toxicity of the drugs. The present study was undertaken to compare predictability of the unbound hepatocyte-to-medium concentration ratios (K ) by two methods based on the steady-state cell-to-medium total concentration ratios at 37°C and on ice (K ) and based on their initial uptake rates (K ). Poorly metabolized statins were used as test drugs because of their concentrative uptake via organic anion-transporting polypeptides. K values of these statins provided less interexperimental variation than the K values, because only data at longer time are required for K K values for pitavastatin, rosuvastatin, and pravastatin were 1.2- to 5.1-fold K in rat hepatocytes; K values in human hepatocytes also tended to be larger than corresponding K To explain these discrepancies, theoretical values of K and K were compared with true K (K ), considering the inside-negative membrane potential and ionization of the drugs in hepatocytes and medium. Membrane potentials were approximately -30 mV in human hepatocytes at 37°C and almost abolished on ice. Theoretical equations considering the membrane potentials indicate that K values for the statins are 0.85- to 1.2-fold K , whereas K values are 2.2- to 3.1-fold K , depending on the ratio of the passive permeability of the ionized to nonionized forms. In conclusion, K values of anions are similar to K when the inside-negative membrane potential is considered. This suggests that K is preferable for estimating the concentration of unbound drugs inside the hepatocytes.
[Mh] Termos MeSH primário: Hepatócitos/metabolismo
Inibidores de Hidroximetilglutaril-CoA Redutases/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/fisiologia
Seres Humanos
Fígado/metabolismo
Masculino
Potenciais da Membrana/fisiologia
Transportadores de Ânions Orgânicos/metabolismo
Permeabilidade
Pravastatina/metabolismo
Quinolinas/metabolismo
Ratos
Ratos Sprague-Dawley
Rosuvastatina Cálcica/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Organic Anion Transporters); 0 (Quinolines); 83MVU38M7Q (Rosuvastatin Calcium); KXO2KT9N0G (Pravastatin); M5681Q5F9P (pitavastatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.116.074823


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[PMID]:29279527
[Au] Autor:Ishikawa Y; Itoh T; Satoh M; Fusazaki T; Sugawara S; Nakajima S; Nakamura M; Morino Y
[Ad] Endereço:Division of Cardiology, Department of Internal Medicine, Iwate Medical University.
[Ti] Título:Impact of Water- and Lipid-Soluble Statins on Nonculprit Lesions in Patients with Acute Coronary Syndrome.
[So] Source:Int Heart J;59(1):27-34, 2018 Jan 27.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Statins can be differentiated into two types, based on their solubility, which have potentially differing effects on the coronary artery wall. However, suspected differences in statins' effects on plaque composition have not been systemically investigated.Sixty-seven patients with acute coronary syndrome (ACS) were randomly assigned to either atorvastatin (10 mg/day) or rosuvastatin (2.5 mg/day). Intravascular ultrasound (IVUS) and integrated backscatter (IB)-IVUS, an established tool to quantify each plaque's components, were performed immediately after emergent percutaneous coronary intervention (PCI). Follow-up IVUS was performed between 6 and 12 months after PCI. Serial changes in serum lipid profiles and plaque composition volumes were compared between the two groups.Thirty-five patients were eligible for serial IB-IVUS analyses. The mean low-density lipoprotein-cholesterol level significantly decreased in the atorvastatin and rosuvastatin groups (P < 0.001); plaque volumes were also significantly reduced from 82.0 ± 46.2 to 74.9 ± 41.3 mm (P = 0.01) and from 74.7 ± 35.3 to 67.7 ± 27.0 mm (P = 0.02), respectively. IB-IVUS revealed a significant reduction in fibrous volume from 33.8 ± 20.0 to 27.5 ± 14.9 mm (P < 0.01) and from 29.6 ± 13.6 to 24.8 ± 7.6 mm (P < 0.05), respectively; however, significant changes were not noted in the volume of the lipid pool for the atorvastatin group and the rosuvastatin group, respectively.Water- and lipid-soluble statins may be similarly effective in reducing coronary plaques in patients with ACS as judged qualitatively and quantitatively. Further study is needed to determine whether differences between water- and lipid-soluble statins affect plaque components.
[Mh] Termos MeSH primário: Síndrome Coronariana Aguda/tratamento farmacológico
Atorvastatina Cálcica/administração & dosagem
Vasos Coronários/diagnóstico por imagem
Lipídeos/sangue
Placa Aterosclerótica/tratamento farmacológico
Rosuvastatina Cálcica/administração & dosagem
[Mh] Termos MeSH secundário: Síndrome Coronariana Aguda/sangue
Síndrome Coronariana Aguda/diagnóstico por imagem
Idoso
Biomarcadores/sangue
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem
Masculino
Meia-Idade
Placa Aterosclerótica/sangue
Placa Aterosclerótica/diagnóstico por imagem
Estudos Prospectivos
Índice de Gravidade de Doença
Fatores de Tempo
Resultado do Tratamento
Ultrassonografia de Intervenção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipids); 48A5M73Z4Q (Atorvastatin Calcium); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-587


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[PMID]:28450350
[Au] Autor:Khera AV; Demler OV; Adelman SJ; Collins HL; Glynn RJ; Ridker PM; Rader DJ; Mora S
[Ad] Endereço:From Cardiology Division and Center for Genomic Medicine, Massachusetts General Hospital, Boston (A.V.K.); Harvard Medical School, Boston, MA (A.V.K., O.V.D., P.MR., S.M.); Center for Lipid Metabolomics and Division of Preventive Medicine (A.V.K., O.V.D., R.J.G., P.MR., S.M.), Division of Cardiovasc
[Ti] Título:Cholesterol Efflux Capacity, High-Density Lipoprotein Particle Number, and Incident Cardiovascular Events: An Analysis From the JUPITER Trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin).
[So] Source:Circulation;135(25):2494-2504, 2017 Jun 20.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent failures of drugs that raised high-density lipoprotein (HDL) cholesterol levels to reduce cardiovascular events in clinical trials have led to increased interest in alternative indices of HDL quality, such as cholesterol efflux capacity, and HDL quantity, such as HDL particle number. However, no studies have directly compared these metrics in a contemporary population that includes potent statin therapy and low low-density lipoprotein cholesterol. METHODS: HDL cholesterol levels, apolipoprotein A-I, cholesterol efflux capacity, and HDL particle number were assessed at baseline and 12 months in a nested case-control study of the JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin), a randomized primary prevention trial that compared rosuvastatin treatment to placebo in individuals with normal low-density lipoprotein cholesterol but increased C-reactive protein levels. In total, 314 cases of incident cardiovascular disease (CVD) (myocardial infarction, unstable angina, arterial revascularization, stroke, or cardiovascular death) were compared to age- and gender-matched controls. Conditional logistic regression models adjusting for risk factors evaluated associations between HDL-related biomarkers and incident CVD. RESULTS: Cholesterol efflux capacity was moderately correlated with HDL cholesterol, apolipoprotein A-I, and HDL particle number (Spearman = 0.39, 0.48, and 0.39 respectively; <0.001). Baseline HDL particle number was inversely associated with incident CVD (adjusted odds ratio per SD increment [OR/SD], 0.69; 95% confidence interval [CI], 0.56-0.86; <0.001), whereas no significant association was found for baseline cholesterol efflux capacity (OR/SD, 0.89; 95% CI, 0.72-1.10; =0.28), HDL cholesterol (OR/SD, 0.82; 95% CI, 0.66-1.02; =0.08), or apolipoprotein A-I (OR/SD, 0.83; 95% CI, 0.67-1.03; =0.08). Twelve months of rosuvastatin (20 mg/day) did not change cholesterol efflux capacity (average percentage change -1.5%, 95% CI, -13.3 to +10.2; =0.80), but increased HDL cholesterol (+7.7%), apolipoprotein A-I (+4.3%), and HDL particle number (+5.2%). On-statin cholesterol efflux capacity was inversely associated with incident CVD (OR/SD, 0.62; 95% CI, 0.42-0.92; =0.02), although HDL particle number again emerged as the strongest predictor (OR/SD, 0.51; 95% CI, 0.33-0.77; <0.001). CONCLUSIONS: In JUPITER, cholesterol efflux capacity was associated with incident CVD in individuals on potent statin therapy but not at baseline. For both baseline and on-statin analyses, HDL particle number was the strongest of 4 HDL-related biomarkers as an inverse predictor of incident events and biomarker of residual risk. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00239681.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/prevenção & controle
HDL-Colesterol/sangue
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Lipoproteínas HDL/sangue
Rosuvastatina Cálcica/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Doenças Cardiovasculares/epidemiologia
Estudos de Casos e Controles
HDL-Colesterol/antagonistas & inibidores
Método Duplo-Cego
Feminino
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Incidência
Lipoproteínas HDL/antagonistas & inibidores
Masculino
Meia-Idade
Rosuvastatina Cálcica/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Cholesterol, HDL); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipoproteins, HDL); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.116.025678


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[PMID]:28838366
[Au] Autor:Stein EA; Dann EJ; Wiegman A; Skovby F; Gaudet D; Sokal E; Charng MJ; Mohamed M; Luirink I; Raichlen JS; Sundén M; Carlsson SC; Raal FJ; Kastelein JJP
[Ad] Endereço:Metabolic and Atherosclerosis Research Center, Cincinnati, Ohio. Electronic address: esteinmrl@aol.com.
[Ti] Título:Efficacy of Rosuvastatin in Children With Homozygous Familial Hypercholesterolemia and Association With Underlying Genetic Mutations.
[So] Source:J Am Coll Cardiol;70(9):1162-1170, 2017 Aug 29.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Homozygous familial hypercholesterolemia (HoFH), a rare genetic disorder, is characterized by extremely elevated levels of low-density lipoprotein cholesterol (LDL-C) and accelerated atherosclerotic cardiovascular disease. Statin treatment starts at diagnosis, but no statin has been formally evaluated in, or approved for, HoFH children. OBJECTIVES: The authors sought to assess the LDL-C efficacy of rosuvastatin versus placebo in HoFH children, and the relationship with underlying genetic mutations. METHODS: This was a randomized, double-blind, 12-week, crossover study of rosuvastatin 20 mg versus placebo, followed by 12 weeks of open-label rosuvastatin. Patients discontinued all lipid-lowering treatment except ezetimibe and/or apheresis. Clinical and laboratory assessments were performed every 6 weeks. The relationship between LDL-C response and genetic mutations was assessed by adding children and adults from a prior HoFH rosuvastatin trial. RESULTS: Twenty patients were screened, 14 randomized, and 13 completed the study. The mean age was 10.9 years; 8 patients were on ezetimibe and 7 on apheresis. Mean LDL-C was 481 mg/dl (range: 229 to 742 mg/dl) on placebo and 396 mg/dl (range: 130 to 700 mg/dl) on rosuvastatin, producing a mean 85.4 mg/dl (22.3%) difference (p = 0.005). Efficacy was similar regardless of age or use of ezetimibe or apheresis, and was maintained for 12 weeks. Adverse events were few and not serious. Patients with 2 defective versus 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5% (p = 0.0044) and 14% (p = 0.038), respectively. CONCLUSIONS: This first-ever pediatric HoFH statin trial demonstrated safe and effective LDL-C reduction with rosuvastatin 20 mg alone or added to ezetimibe and/or apheresis. The LDL-C response in children and adults was related to underlying genetic mutations. (A Study to Evaluate the Efficacy and Safety of Rosuvastatin in Children and Adolescents With Homozygous Familial Hypercholesterolemia [HYDRA]; NCT02226198).
[Mh] Termos MeSH primário: LDL-Colesterol/genética
DNA/genética
Hiperlipoproteinemia Tipo II/tratamento farmacológico
Mutação
Rosuvastatina Cálcica/administração & dosagem
[Mh] Termos MeSH secundário: Adolescente
Anticolesterolemiantes/administração & dosagem
Criança
LDL-Colesterol/sangue
Estudos Cross-Over
Análise Mutacional de DNA
Relação Dose-Resposta a Droga
Método Duplo-Cego
Feminino
Seguimentos
Homozigoto
Seres Humanos
Hiperlipoproteinemia Tipo II/sangue
Hiperlipoproteinemia Tipo II/genética
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, LDL); 83MVU38M7Q (Rosuvastatin Calcium); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


  5 / 2053 MEDLINE  
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[PMID]:28822563
[Au] Autor:Longenecker CT; Margevicius S; Liu Y; Schluchter MD; Yun CH; Bezerra HG; McComsey GA
[Ad] Endereço:Case Western Reserve University School of Medicine, Cleveland, Ohio; University Hospitals Cleveland Medical Center, Cleveland, Ohio. Electronic address: cxl473@case.edu.
[Ti] Título:Effect of Pericardial Fat Volume and Density on Markers of Insulin Resistance and Inflammation in Patients With Human Immunodeficiency Virus Infection.
[So] Source:Am J Cardiol;120(8):1427-1433, 2017 Oct 15.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treated human immunodeficiency virus (HIV) infection is characterized by ectopic fat deposition, a persistent inflammatory state, and increased cardiometabolic risk. In this secondary analysis of a placebo controlled trial of rosuvastatin among 147 HIV+ subjects (median age 46; 78% men) on stable antiretroviral therapy, we aimed to evaluate longitudinal associations between computed tomography (CT) measures of pericardial fat (PCF) volume and density, insulin resistance, and inflammation. We measured PCF volume and density (mean attenuation in Hounsfield units) by noncontrast gated CT at baseline and week 96. Homeostatic model of insulin resistance was calculated from fasting insulin and glucose at entry, 24, 48, and 96 weeks. At baseline, insulin resistance correlated positively with PCF volume and negatively with density. Similarly divergent correlations of volume and density were observed with waist:hip ratio, nadir CD4+ count, and duration of antiretroviral therapy. In a linear mixed model, PCF density was associated with insulin resistance independent of PCF volume, body mass index, metabolic syndrome, and biomarkers of immune activation and systemic inflammation; however, baseline PCF measures were not associated with longitudinal changes in insulin resistance. Soluble CD163, a marker of monocyte activation, positively correlated with PCF volume and was associated with insulin resistance in linear models. Statin treatment assignment did not affect PCF volume or density change (both p > 0.8). In conclusion, the quantity and quality (i.e., radiodensity) of PCF are differentially related to insulin resistance and inflammation in patients with treated HIV infection.
[Mh] Termos MeSH primário: Tecido Adiposo/diagnóstico por imagem
Aterosclerose/tratamento farmacológico
Biomarcadores/sangue
Infecções por HIV/complicações
Inflamação/metabolismo
Resistência à Insulina
Pericárdio/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Aterosclerose/etiologia
Aterosclerose/metabolismo
Método Duplo-Cego
Feminino
HIV
Infecções por HIV/diagnóstico
Infecções por HIV/metabolismo
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Inflamação/diagnóstico
Masculino
Meia-Idade
Rosuvastatina Cálcica/uso terapêutico
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


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[PMID]:28774497
[Au] Autor:Sanfelice RA; Machado LF; Bosqui LR; Miranda-Sapla MM; Tomiotto-Pellissier F; de Alcântara Dalevedo G; Ioris D; Reis GF; Panagio LA; Navarro IT; Bordignon J; Conchon-Costa I; Pavanelli WR; Almeida RS; Costa IN
[Ad] Endereço:Laboratório de Protozoologia Experimental - Departamento de Ciências Patológicas, Universidade Estadual de Londrina, Paraná CEP 86051-990, Brazil.
[Ti] Título:Activity of rosuvastatin in tachyzoites of Toxoplasma gondii (RH strain) in HeLa cells.
[So] Source:Exp Parasitol;181:75-81, 2017 Oct.
[Is] ISSN:1090-2449
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Due to the toxicity of conventional medication in toxoplasmosis, some drugs are being studied for treating this infection, such as statins, especially rosuvastatin compound, which is efficient in inhibiting the initial isoprenoid biosynthesis processes in humans and the parasite. The goal of this study was to assess the activity of rosuvastatin in HeLa cells infected with the RH strain of T. gondii. In the experiment, HeLa cells (1 × 10 ) were infected with tachyzoites of T. gondii (5 × 10 ). After the experimental infection, we assessed the number of infected cells and the amount of intracellular tachyzoites. In addition, culture supernatants were collected to determine the amount of cytokines by cytometric bead array. We observed that there was no cytotoxicity in the concentrations tested in this cell line. The effect of rosuvastatin showed a significant reduction in both the number of infected cells and the proliferation index of the intracellular parasite, when compared with the conventional treatment combining sulfadiazine and pyrimethamine for toxoplasmosis. There were also reduced levels of cytokines IL-6 and IL-17. Therefore, it was concluded that rosuvastatin exhibited antiproliferative activity. The data presented are significant to promote further studies and the search for alternative treatment for toxoplasmosis.
[Mh] Termos MeSH primário: Células HeLa/parasitologia
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Rosuvastatina Cálcica/farmacologia
Toxoplasma/efeitos dos fármacos
[Mh] Termos MeSH secundário: Análise de Variância
Antiprotozoários/farmacologia
Meios de Cultura
Células HeLa/efeitos dos fármacos
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/toxicidade
Interleucina-17/metabolismo
Interleucina-6/metabolismo
Pirimetamina/farmacologia
Rosuvastatina Cálcica/toxicidade
Sulfadiazina/farmacologia
Toxoplasma/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiprotozoal Agents); 0 (Culture Media); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Interleukin-17); 0 (Interleukin-6); 0N7609K889 (Sulfadiazine); 83MVU38M7Q (Rosuvastatin Calcium); Z3614QOX8W (Pyrimethamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


  7 / 2053 MEDLINE  
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[PMID]:28682890
[Au] Autor:Liang M; Yang S; Fu N
[Ad] Endereço:aGraduate School of Tianjin Medical University bDepartment of Cardiology, Tianjin Chest Hospital, Tianjin, China.
[Ti] Título:Efficacy of short-term moderate or high-dose rosuvastatin in preventing contrast-induced nephropathy: A meta-analysis of 15 randomized controlled trials.
[So] Source:Medicine (Baltimore);96(27):e7384, 2017 Jul.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The prophylactic efficacy of statin pretreatment for the prevention of contrast-induced nephropathy (CIN) in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) remains controversial. The aim of the study was to perform a meta-analysis of randomized controlled trials (RCTs) to assess the effectiveness of short-term moderate or high-dose rosuvastatin pretreatment in preventing CIN. METHODS: We included RCTs comparing short-term moderate or high-dose rosuvastatin treatment versus low-dose rosuvastatin treatment or placebo for preventing CIN. The primary endpoint was the incidence of CIN within 2 to 5 days after contrast administration, and related-parameters including serum creatinine (SCr), cystatin C (CysC), hypersensitive C-reactive protein (hs-CRP), urine microalbumin (mALB) were also extracted. RESULTS: Fifteen RCTs with a total of 2673 patients were identified and analyzed. Patients who received moderate or high-dose rosuvastatin pretreatment had a 55% lower risk of CIN compared with low-dose rosuvastatin pretreatment or placebo group based on a fixed effect model (RR = 0.45, 95% CI 0.35-0.58, P < .0001). The benefit of moderate or high-dose rosuvastatin was consistent in both comparisons with low-dose rosuvastatin (RR = 0.40, 95% CI 0.27-0.59, P < .0001) or placebo (RR = 0.45, 95% CI 0.35-0.58, P < .0001). And moderate (20 mg) or high dose (≥40 mg) rosuvastatin significantly reduced the incidence of CIN compared with the control (RR = 0.39, 95% CI 0.29-0.54, P < .0001, RR = 0.56, 95% CI 0.37-0.85, P = .006, respectively). Subgroup analysis showed that moderate or high-dose rosuvastatin pretreatment could decrease the incidence of CIN in patients with chronic kidney disease (CKD) (RR = 0.53, 95% CI 0.30-0.93, P = .03) or diabetes mellitus (DM) (RR = 0.51, 95% CI 0.31-0.86, P = .01) or acute coronary syndrome (ACS) patients undergoing PCI (RR = 0.52, 95% CI 0.35-0.76, P = .0009) or in studies which received mean contrast volume ≥110 mL (RR = 0.43, 95% CI 0.32-0.58, P < .0001). The SCr, CysC, hs-CRP, and mALB after the operation in the moderate or high-dose rosuvastatin group were lower than those of low-dose rosuvastatin group. CONCLUSION: This meta-analysis demonstrated that moderate or high-dose rosuvastatin treatment could reduce the incidence of CIN in patients undergoing CAG or PCI. Moreover, moderate or high-dose rosuvastatin would be beneficial in high-risk patients with CKD or DM or undergoing PCI.
[Mh] Termos MeSH primário: Meios de Contraste/efeitos adversos
Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem
Nefropatias/induzido quimicamente
Nefropatias/prevenção & controle
Rosuvastatina Cálcica/administração & dosagem
[Mh] Termos MeSH secundário: Angiografia Coronária/efeitos adversos
Seres Humanos
Intervenção Coronária Percutânea/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Contrast Media); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007384


  8 / 2053 MEDLINE  
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[PMID]:28679524
[Au] Autor:Kwon O; Kang SJ; Kang SH; Lee PH; Yun SC; Ahn JM; Park DW; Lee SW; Kim YH; Lee CW; Han KH; Park SW; Park SJ
[Ad] Endereço:From the Department of Cardiology (O.K., S.-J.K., S.H.K., P.H.L., J.-M.A., D.-W.P., S.-W.L., Y.-H.K., C.W.L., K.H.H., S.-W.P., S.-J.P.) and Department of Biostatistics (S.-C.Y.), University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
[Ti] Título:Relationship Between Serum Inflammatory Marker Levels and the Dynamic Changes in Coronary Plaque Characteristics After Statin Therapy.
[So] Source:Circ Cardiovasc Imaging;10(7), 2017 Jul.
[Is] ISSN:1942-0080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The mechanism of statin for atheroma stabilization remains unclear. We aimed to assess the relationship between on-treatment changes in serum inflammatory biomarker levels and plaque composition in differed nonculprit coronary lesions. METHODS AND RESULTS: The changes in serum biochemical values, and intravascular ultrasound data were evaluated in 218 patients with virtual histology (VH)-intravascular ultrasound-defined fibroatheroma-containing segments after 12-month rosuvastatin treatment. When stratifying patients into quartiles according to the change in high-sensitivity C-reactive protein (hsCRP), there was a significant positive linear relationship for the changes in %necrotic core (coefficient, 1.31; standard error, 0.54) and %dense calcium volumes (coefficient, 0.80; standard error, 0.27), but a negative linear relationship for the changes in %fibrous (coefficient, -0.94; standard error, 0.45) and %fibrofatty volumes (coefficient, -1.17; standard error, 0.56; all <0.05). The decrease in hsCRP (-1.2±3.9 versus 0.5±3.4 mg/L; =0.02) was greater in those without VH-defined thin-cap fibroatheroma (TCFA, defined as >30° of necrotic core abutting the lumen in 3 consecutive slices) than those with VH-TCFA at follow-up. Diabetes mellitus, a larger normalized total atheroma volume, and the presence of VH-TCFA at baseline predicted the presence of VH-TCFA at follow-up (odds ratio, 4.01, 1.18, and 9.21, respectively; all <0.05), whereas the change in hsCRP showed a trend (odds ratio, 1.19; =0.07). The change in low-density lipoprotein-cholesterol had no relationship with the changes in hsCRP or plaque compositions. CONCLUSIONS: With 12-month rosuvastatin therapy, a greater hsCRP reduction (not low-density lipoprotein-cholesterol) was associated with a greater decrease in %necrotic core volume and the absence of VH-TCFA, indicating a link between the anti-inflammatory action of statin and plaque stabilization by reducing NC and reinforcing fibrous cap. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT00997880.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Doença da Artéria Coronariana/tratamento farmacológico
Vasos Coronários/efeitos dos fármacos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Mediadores da Inflamação/sangue
Placa Aterosclerótica
Rosuvastatina Cálcica/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Distribuição de Qui-Quadrado
Doença da Artéria Coronariana/sangue
Doença da Artéria Coronariana/diagnóstico por imagem
Vasos Coronários/diagnóstico por imagem
Método Duplo-Cego
Feminino
Fibrose
Seres Humanos
Modelos Lineares
Modelos Logísticos
Masculino
Meia-Idade
Análise Multivariada
Necrose
Razão de Chances
Valor Preditivo dos Testes
Estudos Prospectivos
Fatores de Risco
Seul
Fatores de Tempo
Resultado do Tratamento
Ultrassonografia de Intervenção
Calcificação Vascular/sangue
Calcificação Vascular/diagnóstico por imagem
Calcificação Vascular/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Biomarkers); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Inflammation Mediators); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE


  9 / 2053 MEDLINE  
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[PMID]:28596414
[Au] Autor:Athyros VG; Katsiki N; Mikhailidis DP
[Ad] Endereço:Second Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Hippocration Hospital, Thessaloniki, Greece; and.
[Ti] Título:Letter to the editor: Treating nonalcoholic fatty liver disease with statins. Are all statins equal?
[So] Source:Am J Physiol Gastrointest Liver Physiol;312(6):G681-G682, 2017 06 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Atorvastatina Cálcica/administração & dosagem
Doença das Coronárias/epidemiologia
Doença das Coronárias/prevenção & controle
Hepatopatia Gordurosa não Alcoólica/epidemiologia
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Rosuvastatina Cálcica/administração & dosagem
[Mh] Termos MeSH secundário: Comorbidade
Medicina Baseada em Evidências
Seres Humanos
Estudos Longitudinais
Prevalência
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
48A5M73Z4Q (Atorvastatin Calcium); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00101.2017


  10 / 2053 MEDLINE  
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[PMID]:28592434
[Au] Autor:Braamskamp MJAM; Langslet G; McCrindle BW; Cassiman D; Francis GA; Gagne C; Gaudet D; Morrison KM; Wiegman A; Turner T; Miller E; Kusters DM; Raichlen JS; Martin PD; Stein EA; Kastelein JJP; Hutten BA
[Ad] Endereço:From Department of Vascular Medicine (M.J.A.M.B., D.M.K., J.J.P.K.), Department of Pediatrics (M.J.A.M.B., A.W.), and Department of Clinical Epidemiology, Biostatistics and Bioinformatics (B.A.H.), Academic Medical Center, Amsterdam, the Netherlands; Lipid Clinic, Medical Department, Oslo University
[Ti] Título:Effect of Rosuvastatin on Carotid Intima-Media Thickness in Children With Heterozygous Familial Hypercholesterolemia: The CHARON Study (Hypercholesterolemia in Children and Adolescents Taking Rosuvastatin Open Label).
[So] Source:Circulation;136(4):359-366, 2017 Jul 25.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Heterozygous familial hypercholesterolemia (HeFH) is an autosomal dominant disorder leading to premature atherosclerosis. Children with HeFH exhibit early signs of atherosclerosis manifested by increased carotid intima-media thickness (IMT). In this study, we assessed the effect of 2-year treatment with rosuvastatin on carotid IMT in children with HeFH. METHODS: Children with HeFH (age, 6-<18 years) and low-density lipoprotein cholesterol >4.9 mmol/L or >4.1 mmol/L in combination with other risk factors received rosuvastatin for 2 years, starting at 5 mg once daily, with uptitration to 10 mg (age, 6-<10 years) or 20 mg (age, 10-<18 years). Carotid IMT was assessed by ultrasonography at baseline and 12 and 24 months in all patients and in age-matched unaffected siblings. Carotid IMT was measured at 3 locations (common carotid artery, carotid bulb, internal carotid artery) in both the left and right carotid arteries. A linear mixed-effects model was used to evaluate differences in carotid IMT between children with HeFH and the unaffected siblings. values were adjusted for age, sex, carotid artery site, and family relations. RESULTS: At baseline, mean±SD carotid IMT was significantly greater for the 197 children with HeFH compared with the 65 unaffected siblings (0.397±0.049 and 0.377±0.045 mm, respectively; =0.001). During 2 years of follow-up, the change in carotid IMT was 0.0054 mm/y (95% confidence interval, 0.0030-0.0082) in children with HeFH and 0.0143 mm/y (95% confidence interval, 0.0095-0.0192) in unaffected siblings ( =0.002). The end-of-study difference in mean carotid IMT between children with HeFH and unaffected siblings after 2 years was no longer significant (0.408±0.043 and 0.402±0.042 mm, respectively; =0.2). CONCLUSIONS: In children with HeFH who were ≥6 years of age, carotid IMT was significantly greater at baseline compared with unaffected siblings. Rosuvastatin treatment for 2 years resulted in significantly less progression of increased carotid IMT in children with HeFH than untreated unaffected siblings. As a result, no difference in carotid IMT could be detected between the 2 groups after 2 years of rosuvastatin. These findings support the value of early initiation of statin treatment for low-density lipoprotein cholesterol reduction in children with HeFH. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01078675.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Espessura Intima-Media Carotídea/tendências
Heterozigoto
Hiperlipoproteinemia Tipo II/diagnóstico
Hiperlipoproteinemia Tipo II/tratamento farmacológico
Rosuvastatina Cálcica/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Criança
Feminino
Seguimentos
Seres Humanos
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 83MVU38M7Q (Rosuvastatin Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.116.025158



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