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[PMID]:29324623
[Au] Autor:Hussar DA
[Ad] Endereço:Remington Professor of Pharmacy Philadelphia College of Pharmacy University of the Sciences Philadelphia, Pa.
[Ti] Título:New Drugs 2018, part 1.
[So] Source:Nursing;48(2):36-44, 2018 Feb.
[Is] ISSN:1538-8689
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Aprovação de Drogas
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Anticorpos Neutralizantes/uso terapêutico
Antipirina/análogos & derivados
Antipirina/uso terapêutico
Benzamidas/uso terapêutico
Benzimidazóis/uso terapêutico
Carbamatos/uso terapêutico
Combinação de Medicamentos
Compostos Heterocíclicos de 4 ou mais Anéis/uso terapêutico
Seres Humanos
Compostos Macrocíclicos/uso terapêutico
Naltrexona/análogos & derivados
Naltrexona/uso terapêutico
Peptídeos Natriuréticos/uso terapêutico
Piridinas/uso terapêutico
Quinoxalinas/uso terapêutico
Sofosbuvir/uso terapêutico
Sulfonamidas/uso terapêutico
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-493); 0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Benzamides); 0 (Benzimidazoles); 0 (Carbamates); 0 (Drug Combinations); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Macrocyclic Compounds); 0 (Natriuretic Peptides); 0 (Pyridines); 0 (Quinoxalines); 0 (Sulfonamides); 0 (bezlotoxumab); 0 (naldemedine); 0 (pibrentasvir); 0 (voxilaprevir); 5S6W795CQM (Naltrexone); 74RWP7W0J9 (betrixaban); 7IK8Z952OK (plecanatide); KCU0C7RS7Z (velpatasvir); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine); WJ6CA3ZU8B (Sofosbuvir)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1097/01.NURSE.0000529803.83288.e1


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[PMID]:29180454
[Au] Autor:Engeli S; Stinkens R; Heise T; May M; Goossens GH; Blaak EE; Havekes B; Jax T; Albrecht D; Pal P; Tegtbur U; Haufe S; Langenickel TH; Jordan J
[Ad] Endereço:From the Institute of Clinical Pharmacology (S.E., M.M., S.H., J.J.), Institute of Sports Medicine (U.T.), Hannover Medical School, Germany; Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism (R.S., G.H.G., E.E.B.), Division of Endocrinology, Department
[Ti] Título:Effect of Sacubitril/Valsartan on Exercise-Induced Lipid Metabolism in Patients With Obesity and Hypertension.
[So] Source:Hypertension;71(1):70-77, 2018 01.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sacubitril/valsartan (LCZ696), a novel angiotensin receptor-neprilysin inhibitor, was recently approved for the treatment of heart failure with reduced ejection fraction. Neprilysin degrades several peptides that modulate lipid metabolism, including natriuretic peptides. In this study, we investigated the effects of 8 weeks' treatment with sacubitril/valsartan on whole-body and adipose tissue lipolysis and lipid oxidation during defined physical exercise compared with the metabolically neutral comparator amlodipine. This was a multicenter, randomized, double-blind, active-controlled, parallel-group study enrolling subjects with abdominal obesity and moderate hypertension (mean sitting systolic blood pressure ≥130-180 mm Hg). Lipolysis during rest and exercise was assessed by microdialysis and [1,1,2,3,3- H]-glycerol tracer kinetics. Energy expenditure and substrate oxidation were measured simultaneously using indirect calorimetry. Plasma nonesterified fatty acids, glycerol, insulin, glucose, adrenaline and noradrenaline concentrations, blood pressure, and heart rate were also determined. Exercise elevated plasma glycerol, free fatty acids, and interstitial glycerol concentrations and increased the rate of glycerol appearance. However, exercise-induced stimulation of lipolysis was not augmented on sacubitril/valsartan treatment compared with amlodipine treatment. Furthermore, sacubitril/valsartan did not alter energy expenditure and substrate oxidation during exercise compared with amlodipine treatment. In conclusion, sacubitril/valsartan treatment for 8 weeks did not elicit clinically relevant changes in exercise-induced lipolysis or substrate oxidation in obese patients with hypertension, implying that its beneficial cardiovascular effects cannot be explained by changes in lipid metabolism during exercise. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01631864.
[Mh] Termos MeSH primário: Aminobutiratos
Anlodipino/administração & dosagem
Exercício/fisiologia
Hipertensão
Neprilisina
Obesidade Abdominal
Tetrazóis
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Aminobutiratos/administração & dosagem
Aminobutiratos/efeitos adversos
Aminobutiratos/farmacocinética
Antagonistas de Receptores de Angiotensina/administração & dosagem
Antagonistas de Receptores de Angiotensina/efeitos adversos
Antagonistas de Receptores de Angiotensina/farmacocinética
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/administração & dosagem
Método Duplo-Cego
Monitoramento de Medicamentos/métodos
Feminino
Seres Humanos
Hipertensão/diagnóstico
Hipertensão/tratamento farmacológico
Hipertensão/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Metabolismo dos Lipídeos/fisiologia
Masculino
Meia-Idade
Peptídeos Natriuréticos/metabolismo
Neprilisina/antagonistas & inibidores
Neprilisina/metabolismo
Obesidade Abdominal/diagnóstico
Obesidade Abdominal/tratamento farmacológico
Obesidade Abdominal/metabolismo
Tetrazóis/administração & dosagem
Tetrazóis/efeitos adversos
Tetrazóis/farmacocinética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (Calcium Channel Blockers); 0 (LCZ 696); 0 (Natriuretic Peptides); 0 (Tetrazoles); 1J444QC288 (Amlodipine); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.10224


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[PMID]:29263167
[Au] Autor:Menzaghi C; Trischitta V
[Ad] Endereço:Research Unit of Diabetes and Endocrine Diseases, IRCCS Casa Sollievo della Sofferenza, Sapienza University of Rome, Rome, Italy c.menzaghi@operapadrepio.it vincenzo.trischitta@uniroma1.it.
[Ti] Título:The Adiponectin Paradox for All-Cause and Cardiovascular Mortality.
[So] Source:Diabetes;67(1):12-22, 2018 Jan.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Basic science studies have shown beneficial effects of adiponectin on glucose homeostasis, chronic low-grade inflammation, apoptosis, oxidative stress, and atherosclerotic processes, so this molecule usually has been considered a salutary adipokine. It was therefore quite unexpected that large prospective human studies suggested that adiponectin is simply a marker of glucose homeostasis, with no direct favorable effect on the risk of type 2 diabetes and cardiovascular disease. But even more unforeseen were data addressing the role of adiponectin on the risk of death. In fact, a positive, rather than the expected negative, relationship was reported between adiponectin and mortality rate across many clinical conditions, comprising diabetes. The biology underlying this paradox is unknown. Several explanations have been proposed, including adiponectin resistance and the confounding role of natriuretic peptides. In addition, preliminary genetic evidence speaks in favor of a direct role of adiponectin in increasing the risk of death. However, none of these hypotheses are based on robust data, so further efforts are needed to unravel the elusive role of adiponectin on cardiometabolic health and, most important, its paradoxical association with mortality rate.
[Mh] Termos MeSH primário: Adiponectina/metabolismo
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/mortalidade
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/metabolismo
Diabetes Mellitus Tipo 2/mortalidade
Seres Humanos
Peptídeos Natriuréticos/metabolismo
Estresse Oxidativo/fisiologia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Natriuretic Peptides)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.2337/dbi17-0016


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[PMID]:29025575
[Au] Autor:McMahon TJ; Bryan NS
[Ad] Endereço:Duke University, Durham, North Carolina. Electronic address: tim.mcmahon@duke.edu.
[Ti] Título:Biomarkers in Pulmonary Vascular Disease: Gauging Response to Therapy.
[So] Source:Am J Cardiol;120(8S):S89-S95, 2017 Oct 15.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biomarkers are increasingly being investigated in the treatment of pulmonary vascular disease. In particular, the signaling pathways targeted by therapies for pulmonary arterial hypertension provide biomarkers that potentially can be used to guide therapy and to assess clinical response as an alternative to invasive procedures such as right-sided cardiac catheterization. Moreover, the growing use of combination therapy for both the initial and subsequent treatment of pulmonary arterial hypertension highlights the need for biomarkers in this treatment approach. Currently approved therapies for pulmonary arterial hypertension target 3 major signaling pathways: the nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate pathway, the endothelin pathway, and the prostacyclin pathway. Although the main biomarker used in practice and evaluated in clinical trials is N-terminal pro-brain natriuretic peptide, other putative biomarkers include the endogenous nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine, NO metabolites including S-nitrosothiols and nitrite, exhaled NO, endothelins, cyclic guanosine monophosphate, cyclic adenosine monophosphate, and atrial natriuretic peptide. This review describes accessible biomarkers, related to the actual molecules targeted by current therapies, for measuring and predicting response to the individual pulmonary arterial hypertension treatment classes as well as combination therapy.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/metabolismo
Óxido Nítrico/fisiologia
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
GMP Cíclico/fisiologia
Seres Humanos
Hipertensão Pulmonar/fisiopatologia
Hipertensão Pulmonar/terapia
Peptídeos Natriuréticos/metabolismo
Avaliação de Resultados (Cuidados de Saúde)
Transdução de Sinais
Guanilil Ciclase Solúvel/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Natriuretic Peptides); 31C4KY9ESH (Nitric Oxide); EC 4.6.1.2 (Soluble Guanylyl Cyclase); H2D2X058MU (Cyclic GMP)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


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[PMID]:28964433
[Au] Autor:Griffin EA; Wonderling D; Ludman AJ; Al-Mohammad A; Cowie MR; Hardman SMC; McMurray JJV; Kendall J; Mitchell P; Shote A; Dworzynski K; Mant J
[Ad] Endereço:National Clinical Guideline Centre, Royal College of Physicians, London, UK. Electronic address: ed@igriffin.co.uk.
[Ti] Título:Cost-Effectiveness Analysis of Natriuretic Peptide Testing and Specialist Management in Patients with Suspected Acute Heart Failure.
[So] Source:Value Health;20(8):1025-1033, 2017 Sep.
[Is] ISSN:1524-4733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine the cost-effectiveness of natriuretic peptide (NP) testing and specialist outreach in patients with acute heart failure (AHF) residing off the cardiology ward. METHODS: We used a Markov model to estimate costs and quality-adjusted life-years (QALYs) for patients presenting to hospital with suspected AHF. We examined diagnostic workup with and without the NP test in suspected new cases, and we examined the impact of specialist heart failure outreach in all suspected cases. Inputs for the model were derived from systematic reviews, the UK national heart failure audit, randomized controlled trials, expert consensus from a National Institute for Health and Care Excellence guideline development group, and a national online survey. The main benefit from specialist care (cardiology ward and specialist outreach) was the increased likelihood of discharge on disease-modifying drugs for people with left ventricular systolic dysfunction, which improve mortality and reduce re-admissions due to worsened heart failure (associated with lower utility). Costs included diagnostic investigations, admissions, pharmacological therapy, and follow-up heart failure care. RESULTS: NP testing and specialist outreach are both higher cost, higher QALY, cost-effective strategies (incremental cost-effectiveness ratios of £11,656 and £2,883 per QALY gained, respectively). Combining NP and specialist outreach is the most cost-effective strategy. This result was robust to both univariate deterministic and probabilistic sensitivity analyses. CONCLUSIONS: NP testing for the diagnostic workup of new suspected AHF is cost-effective. The use of specialist heart failure outreach for inpatients with AHF residing off the cardiology ward is cost-effective. Both interventions will help improve outcomes for this high-risk group.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/diagnóstico
Modelos Econômicos
Peptídeos Natriuréticos/sangue
Anos de Vida Ajustados por Qualidade de Vida
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Idoso de 80 Anos ou mais
Análise Custo-Benefício
Feminino
Insuficiência Cardíaca/economia
Insuficiência Cardíaca/terapia
Hospitalização/economia
Seres Humanos
Masculino
Cadeias de Markov
Ensaios Clínicos Controlados Aleatórios como Assunto
Disfunção Ventricular/economia
Disfunção Ventricular/mortalidade
Disfunção Ventricular/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Natriuretic Peptides)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:28916678
[Au] Autor:Li P; Wuthrick E; Rappaport JA; Kraft C; Lin JE; Marszalowicz G; Snook AE; Zhan T; Hyslop TM; Waldman SA
[Ad] Endereço:Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, The University of Florida, Gainesville, Florida.
[Ti] Título:GUCY2C Signaling Opposes the Acute Radiation-Induced GI Syndrome.
[So] Source:Cancer Res;77(18):5095-5106, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High doses of ionizing radiation induce acute damage to epithelial cells of the gastrointestinal (GI) tract, mediating toxicities restricting the therapeutic efficacy of radiation in cancer and morbidity and mortality in nuclear disasters. No approved prophylaxis or therapy exists for these toxicities, in part reflecting an incomplete understanding of mechanisms contributing to the acute radiation-induced GI syndrome (RIGS). Guanylate cyclase C (GUCY2C) and its hormones guanylin and uroguanylin have recently emerged as one paracrine axis defending intestinal mucosal integrity against mutational, chemical, and inflammatory injury. Here, we reveal a role for the GUCY2C paracrine axis in compensatory mechanisms opposing RIGS. Eliminating GUCY2C signaling exacerbated RIGS, amplifying radiation-induced mortality, weight loss, mucosal bleeding, debilitation, and intestinal dysfunction. Durable expression of GUCY2C, guanylin, and uroguanylin mRNA and protein by intestinal epithelial cells was preserved following lethal irradiation inducing RIGS. Oral delivery of the heat-stable enterotoxin (ST), an exogenous GUCY2C ligand, opposed RIGS, a process requiring p53 activation mediated by dissociation from MDM2. In turn, p53 activation prevented cell death by selectively limiting mitotic catastrophe, but not apoptosis. These studies reveal a role for the GUCY2C paracrine hormone axis as a novel compensatory mechanism opposing RIGS, and they highlight the potential of oral GUCY2C agonists (Linzess; Trulance) to prevent and treat RIGS in cancer therapy and nuclear disasters. .
[Mh] Termos MeSH primário: Raios gama/efeitos adversos
Trato Gastrointestinal/efeitos da radiação
Síndrome do Intestino Irritável/prevenção & controle
Lesões Experimentais por Radiação/prevenção & controle
Receptores Acoplados a Guanilato Ciclase/metabolismo
Receptores de Peptídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos da radiação
Proliferação Celular/efeitos da radiação
Neoplasias do Colo/enzimologia
Neoplasias do Colo/patologia
Neoplasias do Colo/radioterapia
Feminino
Hormônios Gastrointestinais/metabolismo
Seres Humanos
Síndrome do Intestino Irritável/enzimologia
Síndrome do Intestino Irritável/etiologia
Linfoma/enzimologia
Linfoma/patologia
Linfoma/radioterapia
Masculino
Melanoma Experimental/enzimologia
Melanoma Experimental/patologia
Melanoma Experimental/radioterapia
Camundongos
Camundongos Endogâmicos C57BL
Peptídeos Natriuréticos/metabolismo
Comunicação Parácrina/efeitos da radiação
Lesões Experimentais por Radiação/enzimologia
Lesões Experimentais por Radiação/etiologia
Receptores de Enterotoxina
Transdução de Sinais/efeitos da radiação
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastrointestinal Hormones); 0 (Natriuretic Peptides); 0 (Receptors, Peptide); 140653-38-9 (guanylin); 152175-68-3 (uroguanylin); EC 4.6.1.2 (GUCY2C protein, human); EC 4.6.1.2 (Gucy2c protein, mouse); EC 4.6.1.2 (Receptors, Enterotoxin); EC 4.6.1.2 (Receptors, Guanylate Cyclase-Coupled)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0859


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[PMID]:28865890
[Au] Autor:Darkner S; Goetze JP; Chen X; Henningsen K; Pehrson S; Svendsen JH
[Ad] Endereço:Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. Electronic address: stinedarkner@hotmail.com.
[Ti] Título:Natriuretic Propeptides as Markers of Atrial Fibrillation Burden and Recurrence (from the AMIO-CAT Trial).
[So] Source:Am J Cardiol;120(8):1309-1315, 2017 Oct 15.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natriuretic peptides are established plasma markers of systolic heart failure, but their usefulness for the evaluation of atrial fibrillation (AF) is unknown. We examined mid-regional pro-atrial natriuretic peptide (MR-proANP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients undergoing ablation for AF. A subpopulation of 102 patients (median age 60 [52;65], 82% male) from the AMIO-CAT trial (Recurrence of arrhythmia following short-term oral AMIOdarone after CATheter ablation for atrial fibrillation: a double-blind, randomized, placebo-controlled study) undergoing ablation for paroxysmal (n = 55) or persistent (n = 47) AF was studied. MR-proANP and NT-proBNP were measured before ablation and at 1, 3, and 6 months' follow-up. Three-day Holter monitoring was performed before ablation, and 6 to 8 weeks and 6 months after ablation. Plasma MR-proANP and NT-proBNP concentrations were higher during AF than during sinus rhythm before ablation (188 pmol/L [131;260] vs 94 pmol/L [64;125], p <0.001; 78 pmol/L [43;121] vs 10.3 pmol/L [5.9;121], p <0.001) and at 1, 3, and 6 months' follow-up. Categories of AF burden on 3-day Holter monitoring (0%, 0% to 99%, and 99% to 100%) were associated with plasma concentrations of both MR-proANP (94 pmol/L [55;127] vs 117 pmol/L [88;185] vs 192 pmol/L [127;261], p <0.001) and NT-proBNP (10 pmol/L [5.9;22] vs 22 pmol/L [8.9;53] vs 81 pmol/L [45;116], p <0.001). In a multivariate regression analysis, however, there was no significant association between baseline propeptide concentrations and recurrence of AF at 6 months' follow-up. In conclusion, AF was associated with higher plasma concentrations of MR-proANP and NT-proBNP than sinus rhythm. Moreover, AF burden was associated with subsequent concentrations of both MR-proANP and NT-proBNP. The results suggest that natriuretic propeptide measurement reflects functional cardiac dysfunction during AF, and that AF burden should be included in biochemical assessment of left ventricular dysfunction.
[Mh] Termos MeSH primário: Amiodarona/administração & dosagem
Fibrilação Atrial/sangue
Ablação por Cateter/métodos
Peptídeos Natriuréticos/sangue
[Mh] Termos MeSH secundário: Administração Oral
Idoso
Antiarrítmicos/administração & dosagem
Fibrilação Atrial/terapia
Biomarcadores/sangue
Método Duplo-Cego
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Recidiva
Reprodutibilidade dos Testes
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Biomarkers); 0 (Natriuretic Peptides); N3RQ532IUT (Amiodarone)
[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:170904
[St] Status:MEDLINE


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[PMID]:28727835
[Au] Autor:Fukumoto R; Kawai M; Minai K; Ogawa K; Yoshida J; Inoue Y; Morimoto S; Tanaka T; Nagoshi T; Ogawa T; Yoshimura M
[Ad] Endereço:Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
[Ti] Título:Conflicting relationship between age-dependent disorders, valvular heart disease and coronary artery disease by covariance structure analysis: Possible contribution of natriuretic peptide.
[So] Source:PLoS One;12(7):e0181206, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It is conceivable that contemporary valvular heart disease (VHD) is affected largely by an age-dependent atherosclerotic process, which is similar to that observed in coronary artery disease (CAD). However, a comorbid condition of VHD and CAD has not been precisely examined. The first objective of this study was to examine a possible comorbid condition. Provided that there is no comorbidity, the second objective was to search for the possible reasons by using conventional risk factors and plasma B-type natriuretic peptide (BNP) because BNP has a potentiality to suppress atherosclerotic development. METHODS: The study population consisted of 3,457 patients consecutively admitted to our institution. The possible comorbid condition of VHD and CAD and the factors that influence the comorbidity were examined by covariance structure analysis and multivariate analysis. RESULTS: The distribution of the patients with VHD and those with CAD in the histograms showed that the incidence of VHD and the severity of CAD rose with seniority in appearance. The real statistical analysis was planned by covariance structure analysis. The current path model revealed that aging was associated with VHD and CAD severity (P < 0.001 for each); however, as a notable result, there was an inverse association regarding the comorbid condition between VHD and CAD (Correlation coefficient [ß]: -0.121, P < 0.001). As the second objective, to clarify the factors leading to this inverse association, the contribution of conventional risk factors, such as age, gender, hypertension, smoking, diabetes, obesity and dyslipidemia, to VHD and CAD were examined by multivariate analysis. However, these factors did not exert an opposing effect on VHD and CAD, and the inverse association defied explanation. Since different pathological mechanisms may contribute to the formation of VHD and CAD, a differentially proposed path model using plasma BNP revealed that an increase in plasma BNP being drawn by VHD suppressed the progression of CAD (ß: -0.465, P < 0.001). CONCLUSIONS: The incidence of VHD and CAD showed a significant conflicting relationship. This result supported the likely presence of unknown diverse mechanisms on top of the common cascade of atherosclerosis. Among them, the continuous elevation of plasma BNP due to VHD might be one of the explicable factors suppressing the progression of CAD.
[Mh] Termos MeSH primário: Envelhecimento
Doença da Artéria Coronariana/complicações
Doenças das Valvas Cardíacas/complicações
Peptídeos Natriuréticos/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Aterosclerose/metabolismo
Aterosclerose/patologia
Doença da Artéria Coronariana/epidemiologia
Doença da Artéria Coronariana/metabolismo
Feminino
Doenças das Valvas Cardíacas/epidemiologia
Doenças das Valvas Cardíacas/metabolismo
Seres Humanos
Incidência
Masculino
Meia-Idade
Análise Multivariada
Peptídeos Natriuréticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Natriuretic Peptides)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181206


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[PMID]:28689178
[Au] Autor:Singh JSS; Burrell LM; Cherif M; Squire IB; Clark AL; Lang CC
[Ad] Endereço:Division of Molecular and Clinical Medicine, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
[Ti] Título:Sacubitril/valsartan: beyond natriuretic peptides.
[So] Source:Heart;103(20):1569-1577, 2017 Oct.
[Is] ISSN:1468-201X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Natriuretic peptides, especially B-type natriuretic peptide (BNP), have primarily been regarded as biomarkers in heart failure (HF). However, they are also possible therapeutic agents due to their potentially beneficial physiological effects. The angiotensin receptor-neprilysin inhibitor, sacubitril/valsartan, simultaneously augments the natriuretic peptide system (NPS) by inhibiting the enzyme neprilysin (NEP) and inhibits the renin-angiotensin-aldosterone system (RAAS) by blocking the angiotensin II receptor. It has been shown to improve mortality and hospitalisation outcomes in patients with HF due to left ventricular systolic dysfunction. The key advantage of sacubitril/valsartan has been perceived to be its ability to augment BNP, while its other effects have largely been overlooked. This review highlights the important effects of sacubitril/valsartan, beyond just the augmentation of BNP. First we discuss how NPS physiology differs between healthy individuals and those with HF by looking at mechanisms like the overwhelming effects of RAAS on the NPS, natriuretic peptide receptor desensitisation and absolute natriuretic deficiency. Second, this review explores other hormones that are augmented by sacubitril/valsartan such as bradykinin, substance P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF. We also discuss concerns that sacubitril/valsartan may interfere with amyloid-ß homeostasis with potential implications on Alzheimer's disease and macular degeneration. Finally, we explore the concept of 'autoinhibition' which is a recently described observation that humans have innate NEP inhibitory capability when natriuretic peptide levels rise above a threshold. There is speculation that autoinhibition may provide a surge of natriuretic and other vasoactive peptides to rapidly reverse decompensation. We contend that by pre-emptively inhibiting NEP, sacubitril/valsartan is inducing this surge earlier during decompensation, resulting in the better outcomes observed.
[Mh] Termos MeSH primário: Aminobutiratos/farmacologia
Antagonistas de Receptores de Angiotensina/farmacologia
Insuficiência Cardíaca/tratamento farmacológico
Tetrazóis/farmacologia
[Mh] Termos MeSH secundário: Insuficiência Cardíaca/metabolismo
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Peptídeos Natriuréticos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (LCZ 696); 0 (Natriuretic Peptides); 0 (Tetrazoles)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE
[do] DOI:10.1136/heartjnl-2017-311295


  10 / 1345 MEDLINE  
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[PMID]:28668839
[Au] Autor:Otsuka T; Nojiri T; Minami S; Hosoda H; Kuroyama M; Hirata H; Nakanishi K; Yamamoto S; Komuta K; Kangawa K; Kijima T
[Ad] Endereço:Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka, Japan.
[Ti] Título:Evaluation of Natriuretic Peptide in Non-small Cell Lung Cancer Patients Treated with Bevacizumab Together with Carboplatin-Paclitaxel: A Prospective Study.
[So] Source:Anticancer Res;37(7):3505-3512, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: To identify predictive markers for efficacy of combination bevacizumab and carboplatin-paclitaxel treatment in patients with advanced non-squamous non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Twenty patients received carboplatin (area under the concentration-time curve (AUC) 6 mg/ml×min) and paclitaxel (200 mg/m ) with bevacizumab (15 mg/kg) on day 1 of a 21-day cycle. After four cycles of induction therapy, patients received bevacizumab maintenance therapy until disease progression or unacceptable toxicity occurred. Plasma and serum samples (baseline, day 8 and before cycle 2) were analyzed for natriuretic peptide content. RESULTS: Plasma brain natriuretic peptide (BNP) levels were significantly decreased at day 8 (20.1±4.0 pg/ml vs. 9.1±1.8 pg/ml, p=0.0002). Patients whose plasma BNP level was reduced to <50% of the baseline at day 8 had a longer progression-free survival (PFS) than those with a less decrease (9.73 versus 2.63 months, p=0.00013). In multivariate Cox analysis, decrease of plasma BNP concentration was associated with a longer PFS (p=0.0022). CONCLUSION: Decrease of plasma BNP concentration correlated with PFS after a treatment of combination bevacizumab plus carboplatin-paclitaxel.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
Peptídeos Natriuréticos/metabolismo
[Mh] Termos MeSH secundário: Idoso
Bevacizumab/administração & dosagem
Biomarcadores Tumorais/metabolismo
Carboplatina/administração & dosagem
Carcinoma Pulmonar de Células não Pequenas/mortalidade
Carcinoma Pulmonar de Células não Pequenas/patologia
Progressão da Doença
Intervalo Livre de Doença
Feminino
Seres Humanos
Neoplasias Pulmonares/mortalidade
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Paclitaxel/administração & dosagem
Plasma/metabolismo
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Natriuretic Peptides); 2S9ZZM9Q9V (Bevacizumab); BG3F62OND5 (Carboplatin); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE



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