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[PMID]:28453725
[Au] Autor:Nonhoff J; Ricke-Hoch M; Mueller M; Stapel B; Pfeffer T; Kasten M; Scherr M; von Kaisenberg C; Bauersachs J; Haghikia A; Hilfiker-Kleiner D
[Ad] Endereço:Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany.
[Ti] Título:Serelaxin treatment promotes adaptive hypertrophy but does not prevent heart failure in experimental peripartum cardiomyopathy.
[So] Source:Cardiovasc Res;113(6):598-608, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Peripartum cardiomyopathy (PPCM) is a systolic left ventricular dysfunction developing in the peripartum phase in previously healthy women. Relaxin-2 is a pregnancy hormone with potential beneficial effects in heart failure patients. We evaluated Relaxin-2 as a potential diagnostic marker and/or a therapeutic agent in PPCM. Methods and results: In healthy peripartum women, serum Relaxin-2 levels (measured by ELISA in the second half of pregnancy) were elevated showing a decreasing trend in the first postpartum week and returned to non-pregnant levels thereafter. In PPCM patients diagnosed in the first postpartum week, serum Relaxin-2 levels were lower compared to healthy postpartum stage-matched controls. In PPCM patients diagnosed later (0.5-10 months postpartum) Relaxin-2 levels were in the range of non-pregnant controls and not different from healthy postpartum stage-matched controls. In mice, serum Relaxin-1 (functional equivalent of human Relaxin-2) was increased late in pregnancy and rapidly cleared in the first postpartum week. In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or ß-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5. In vitro analyses showed that Prolactin induces cardiomyocyte hypertrophy via activation of STAT5. Conclusion: Although Relaxin-2 levels seemed lower in PPCM patients diagnosed early postpartum, we observed a high pregnancy-related variance of serum Relaxin-2 levels peripartum making it unsuitable as a biomarker for this condition. Supplementation with sRlx may contribute to angiogenesis and compensatory hypertrophy in the diseased heart, but the effects are not sufficient to prevent heart failure in an experimental PPCM model.
[Mh] Termos MeSH primário: Cardiomegalia/patologia
Cardiomiopatias/tratamento farmacológico
Fármacos Cardiovasculares/farmacologia
Insuficiência Cardíaca/prevenção & controle
Miócitos Cardíacos/efeitos dos fármacos
Período Pós-Parto/sangue
Relaxina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Animais
Biomarcadores/sangue
Cardiomegalia/sangue
Cardiomegalia/fisiopatologia
Cardiomiopatias/sangue
Cardiomiopatias/patologia
Cardiomiopatias/fisiopatologia
Estudos de Casos e Controles
Modelos Animais de Doenças
Feminino
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Camundongos Knockout
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Gravidez
Prolactina/sangue
Ratos
Proteínas Recombinantes/farmacologia
Sistema de Registros
Relaxina/sangue
Fator de Transcrição STAT3/deficiência
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT5/metabolismo
Transdução de Sinais/efeitos dos fármacos
Volume Sistólico
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiovascular Agents); 0 (RLN2 protein, human); 0 (Recombinant Proteins); 0 (Rln1 protein, mouse); 0 (STAT3 Transcription Factor); 0 (STAT5 Transcription Factor); 0 (Stat3 protein, mouse); 0 (relaxin-3 protein, mouse); 0 (serelaxin protein, human); 9002-62-4 (Prolactin); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvw245


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[PMID]:29429161
[Au] Autor:Li L; Duan XJ; Sun Y; Lu Y; Xu HY; Wang QZ; Wang HY
[Ad] Endereço:Department of Pathology, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing 100037, China.
[Ti] Título:[Classification of cardiac amyloidosis: an immunohistochemical analysis].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):105-109, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To evaluate the sensitivity and specificity of immunohistochemistry (IHC) in the classification of cardiac amyloidosis on endomyocardial biopsy (EMB) and heart allograft. Twenty cardiac tissues from 19 patients at Fuwai Hospital from January, 1990 to April, 2017 with histopathologic features of amyloidosis and Congo red staining positivity were included. IHC was performed with monoclonal antibodies against AA amyloid and polyclonal antibodies against transthyretin (ATTR), λ-light chain (AL-λ), κ-light chain (AL-κ), ApoAâ… , ApoAâ…¡, ApoA â…£ and ß(2)-microglobin. The extent of interstitial staining was evaluated by light microscopy, and three patterns were recognized; these included diffuse pericellular pattern, discrete pericellular pattern, and nodular pattern. Two patterns of vascular deposition were also noted, including arterial pattern and venous pattern. Endocardial involvement was also assessed and recorded. Nineteen cases were divided into three groups according to the pattern of proteins expression in specimens. The first group (5 cases) only showed single protein expression on EMB. The second group (6 cases) showed more than one protein expression, but one of them was intensely stained or any staining of any protein together with ApoA â…£ co-staining. The third group (8 cases) also showed more than one protein expression and all of them had intense staining. Amyloid deposits were successfully subtyped as AL-λ, ATTR, AL-κ and ApoAâ… by IHC in the former two groups with the sensitivity of 11/19. In the third group, amyloid deposits could not be subtyped by immunohistochemistry due to their poor specificity. The pericellular pattern tended to favor AL over ATTR amyloidosis and vascular deposition tended to favor ATTR. Amyloid deposits can be reliably subtyped in diagnostic cardiac specimens using IHC. The co-deposition of chaperon proteins, the distribution of amyloid proteins and clinical features are also auxiliary to subtype cardiac amyloidosis.
[Mh] Termos MeSH primário: Amiloidose/patologia
Cardiomiopatias/patologia
[Mh] Termos MeSH secundário: Amiloide/análise
Neuropatias Amiloides Familiares/patologia
Anticorpos Monoclonais/análise
Apolipoproteína A-I/análise
Apolipoproteínas A/análise
Biópsia
Seres Humanos
Cadeias kappa de Imunoglobulina/análise
Cadeias lambda de Imunoglobulina/análise
Imuno-Histoquímica
Placa Amiloide/patologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (Amyloid); 0 (Antibodies, Monoclonal); 0 (Apolipoprotein A-I); 0 (Apolipoproteins A); 0 (Immunoglobulin kappa-Chains); 0 (Immunoglobulin lambda-Chains); 0 (apolipoprotein A-IV)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.005


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[PMID]:28449797
[Au] Autor:Florido R; Ndumele CE; Kwak L; Pang Y; Matsushita K; Schrack JA; Lazo M; Nambi V; Blumenthal RS; Folsom AR; Coresh J; Ballantyne CM; Selvin E
[Ad] Endereço:Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:Physical Activity, Obesity, and Subclinical Myocardial Damage.
[So] Source:JACC Heart Fail;5(5):377-384, 2017 May.
[Is] ISSN:2213-1787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This study sought to evaluate the association of physical activity with chronic myocardial damage, assessed by elevated high-sensitivity cardiac troponin T (hs-cTnT), in individuals with and without obesity. BACKGROUND: Physical activity is associated with reduced risk of heart failure (HF), particularly among obese people. The role of chronic myocardial damage in this association is uncertain. METHODS: We studied 9,427 participants in the Atherosclerosis Risk in Communities Study without cardiovascular disease, with body mass index >18.5 kg/m . Physical activity was categorized per American Heart Association guidelines as recommended, intermediate, or poor. We evaluated cross-sectional associations of physical activity and obesity with elevated hs-cTnT (≥14 ng/l). In prospective analyses, we quantified the association of elevated hs-cTnT with HF risk within cross-categories of baseline physical activity and obesity. RESULTS: People with poor physical activity were more likely to have elevated hs-cTnT than those with recommended levels (odds ratio [OR]: 1.39; 95% confidence interval [CI]: 1.15 to 1.68). In cross-categories of physical activity and obesity, using the non-obese/recommended activity group as the reference, individuals with obesity and poor activity were most likely to have elevated hs-cTnT (OR: 2.46; 95% CI: 1.91 to 3.19), whereas the obese/recommended activity group had a weaker association (OR: 1.68; 95% CI: 1.28 to 2.21; p < 0.001 for interaction between physical activity and obesity). In prospective analyses, elevated hs-cTnT was strongly associated (p < 0.001) with incident HF in all obesity/physical activity cross-categories (p > 0.20 for interaction). CONCLUSIONS: Physical activity is inversely associated with chronic subclinical myocardial damage. Physical activity might lessen the association between obesity and subclinical myocardial damage, which could represent a mechanism by which physical activity reduces HF risk.
[Mh] Termos MeSH primário: Índice de Massa Corporal
Cardiomiopatias/fisiopatologia
Exercício/fisiologia
Obesidade/epidemiologia
Troponina T/sangue
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Biomarcadores/sangue
Cardiomiopatias/sangue
Estudos de Coortes
Intervalos de Confiança
Feminino
Seres Humanos
Masculino
Meia-Idade
Obesidade/fisiopatologia
Razão de Chances
Prognóstico
Estudos Prospectivos
Valores de Referência
Índice de Gravidade de Doença
Fatores Sexuais
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Troponin T)
[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:170429
[St] Status:MEDLINE


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[PMID]:29424517
[Au] Autor:Karchmer-Krivitzky S; Espinosa-Fernández R; Sánchez-Aranda A; LópezRioja MJ; Monzalbo-Núñez D
[Ti] Título:[Peripartum cardiomyopathy: a case report].
[Ti] Título:Miocardiopatía periparto: reporte de un caso..
[So] Source:Ginecol Obstet Mex;84(8):542-9, 2016 08.
[Is] ISSN:0300-9041
[Cp] País de publicação:Mexico
[La] Idioma:spa
[Ab] Resumo:Background: Peripartum cardiomyopathy also known as cardiomyopathy associated with pregnancy, is rarely a cause of heart failure, it affects pregnant or puerperal women in the first 5 months. Although the first case reported was in 1849, it was recognized until 1930. In 2010 the European Society of Cardiology Working Group on peripartum cardiomyopathy, defined this pathology as an idiopathic cardiomyopathy that affects pregnant women between the third trimester and five months after delivery. Characterized by a left ventricular failure with an ejection fraction of ≤45% and an end-diastolic dimension ≥2.7 cm/m2 , in absence of an identifiable cause of heart failure. Case report: We report a case of a 39-year-old patient, diagnosed with a peripartum cardiomyopathy in the early puerperium, characterized by hypertension, tachycardia, dyspnea and oxygen desaturation. The transesophageal echocardiogram reported heart failure, a hypokinetic left ventricle and a ventricular failure with an ejection fraction <40%. We could not identify an other cause to justify heart failure. Multidisciplinary management was administered successfully. Conclusion: The importance of this article relies in the fact that eripartum cardiomyopathy has a high morbidity and mortality. The impact of this pathology is unknow in our country. Here we establish and discuss the multidisciplinary management held in our hospital with this specific patient in order to improve the prognosis on future occasions.
[Mh] Termos MeSH primário: Cardiomiopatias/diagnóstico
Insuficiência Cardíaca/diagnóstico
Complicações Cardiovasculares na Gravidez/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Cardiomiopatias/fisiopatologia
Cardiomiopatias/terapia
Ecocardiografia Transesofagiana
Feminino
Insuficiência Cardíaca/fisiopatologia
Insuficiência Cardíaca/terapia
Seres Humanos
Período Periparto
Gravidez
Complicações Cardiovasculares na Gravidez/fisiopatologia
Complicações Cardiovasculares na Gravidez/terapia
Disfunção Ventricular Esquerda/diagnóstico
Disfunção Ventricular Esquerda/fisiopatologia
Disfunção Ventricular Esquerda/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE


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[PMID]:29406038
[Au] Autor:Yatsynovich Y; Dittoe N; Petrov M; Maroz N
[Ti] Título:Cardiac Sarcoidosis: A Review of Contemporary Challenges in Diagnosis and Treatment.
[So] Source:Am J Med Sci;355(2):113-125, 2018 Feb.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sarcoidosis is a systemic disease characterized by noncaseating granulomas and is often a diagnosis of exclusion. The actual prevalence of cardiac sarcoidosis (CS) is unknown, as studies have demonstrated mixed data. CS may be asymptomatic and is likely more frequently encountered than previously thought. Sudden death may often be the presenting feature of CS. Most deaths attributed to CS are caused by arrhythmias or conduction system disease, and congestive heart failure may occur. Current expert consensus on diagnosis of CS continues to rely on endomyocardial biopsy, in the absence of which, histologic proof of extracardiac sarcoid involvement is necessitated. Emergence of newer noninvasive imaging modalities such as cardiac magnetic resonance imaging and positron emission tomography, have become increasingly popular tools utilized in patients with both clinical and asymptomatic CS, and have demonstrated good diagnostic capability. The main therapeutic approaches in patients with CS can be broadly divided into the following 2 categories: pharmacological management and invasive or device oriented. However, much remains unknown about the optimal screening protocols of asymptomatic patients with extracardiac sarcoidosis and treatment of biopsy-proven CS. Our knowledge about CS has amplified significantly over the last 30 years and the growing realization that this process is often asymptomatic is paving the way for better screening protocols and earlier detection of this serious condition.
[Mh] Termos MeSH primário: Cardiomiopatias
Imagem por Ressonância Magnética
Miocárdio/patologia
Tomografia por Emissão de Pósitrons
Sarcoidose
[Mh] Termos MeSH secundário: Biópsia
Cardiomiopatias/diagnóstico por imagem
Cardiomiopatias/patologia
Cardiomiopatias/terapia
Seres Humanos
Sarcoidose/diagnóstico por imagem
Sarcoidose/patologia
Sarcoidose/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:28458167
[Au] Autor:Fan TT; Feng XY; Yang YZ; Gao F; Liu Q
[Ad] Endereço:Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China; Department of Emergency, Chengdu First People's Hospital, Sichuan 610016, PR China.
[Ti] Título:Downregulation of PI3K-γ in a mouse model of sepsis-induced myocardial dysfunction.
[So] Source:Cytokine;96:208-216, 2017 08.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A key component during sepsis is the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, of which the PI3K-γ isoform is a major regulator in many inflammatory responses. However, the role of PI3K-γ in the development of sepsis-induced myocardial dysfunction (SIMD) is unknown. In this study, we established a model of SIMD induced by lipopolysaccharide (LPS), subsequently used the selective inhibitor LY294002 and AS605240 to block the effect of PI3K and PI3K-γ, respectively. Cardiac function was evaluated by echocardiography, hearts were obtained for histological and protein expression examinations. ELISA was used to measure the serum levels of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), cardiac troponin I (cTnI) and heart-type fatty acid binding protein (H-FABP). LPS-treated mice showed an increase to cardiac inflammation, myocardial damage and production of TNF-α, IL-6, NF-κB, cTnI and H-FABP. Administration of AS605240 to LPS-treated mice reduced some patho-physiological characteristics of SIMD and reduced TNF-α, IL-6, cTnI and H-FABP production. However, administration of LY294002 did not improve those same conditions. The results showed that PI3K-γ is likely a crucial element in SIMD by regulating the PI3K/Akt pathway, and become a new marker of myocardial injury. Inhibition of PI3K-γ might be a potential therapeutic target in SIMD.
[Mh] Termos MeSH primário: Cardiomiopatias/metabolismo
Classe II de Fosfatidilinositol 3-Quinases/metabolismo
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Cardiomiopatias/genética
Cardiomiopatias/fisiopatologia
Cromonas/administração & dosagem
Classe II de Fosfatidilinositol 3-Quinases/genética
Citocinas/sangue
Modelos Animais de Doenças
Regulação para Baixo
Interleucina-6/biossíntese
Lipopolissacarídeos/administração & dosagem
Camundongos
Morfolinas/administração & dosagem
Miocárdio/patologia
Quinoxalinas/administração & dosagem
Quinoxalinas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
Tiazolidinedionas/administração & dosagem
Tiazolidinedionas/uso terapêutico
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-quinoxalin-6-ylmethylenethiazolidine-2,4-dione); 0 (Chromones); 0 (Cytokines); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Morpholines); 0 (Quinoxalines); 0 (Thiazolidinediones); 0 (Tumor Necrosis Factor-alpha); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.137 (Class II Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29197877
[Au] Autor:Gerbino A; Bottillo I; Milano S; Lipari M; Zio R; Morlino S; Mola MG; Procino G; Re F; Zachara E; Grammatico P; Svelto M; Carmosino M
[Ad] Endereço:Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
[Ti] Título:Functional Characterization of a Novel Truncating Mutation in Lamin A/C Gene in a Family with a Severe Cardiomyopathy with Conduction Defects.
[So] Source:Cell Physiol Biochem;44(4):1559-1577, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Truncating LMNA gene mutations occur in many inherited cardiomyopathy cases, but the molecular mechanisms involved in the disease they cause have not yet been systematically investigated. Here, we studied a novel frameshift LMNA variant (p.D243Gfs*4) identified in three members of an Italian family co-segregating with a severe form of cardiomyopathy with conduction defects. METHODS: HEK293 cells and HL-1 cardiomyocytes were transiently transfected with either Lamin A or D243Gfs*4 tagged with GFP (or mCherry). D243Gfs*4 expression, cellular localization and its effects on diverse cellular mechanisms were evaluated with western blotting, laser-scanning confocal microscopy and video-imaging analysis in single cells. RESULTS: When expressed in HEK293 cells, GFP- (or mCherry)-tagged LMNA D243Gfs*4 colocalized with calnexin within the ER. ER mislocalization of LMNA D243Gfs*4 did not significantly induce ER stress response, abnormal Ca2+ handling and apoptosis when compared with HEK293 cells expressing another truncated mutant of LMNA (R321X) which similarly accumulates within the ER. Of note, HEK293-LMNA D243Gfs*4 cells showed a significant reduction of connexin 43 (CX43) expression level, which was completely rescued by activation of the WNT/ß-catenin signaling pathway. When expressed in HL-1 cardiomyocytes, D243Gfs*4 significantly impaired the spontaneous Ca2+ oscillations recorded in these cells as result of propagation of the depolarizing waves through the gap junctions between non-transfected cells surrounding a cell harboring the mutation. Furthermore, mCh-D243Gfs*4 HL-1 cardiomyocytes showed reduced CX43-dependent Lucifer Yellow (LY) loading and propagation. Of note, activation of ß-catenin rescued both LY loading and LMNA D243Gfs*4 -HL-1 cells spontaneous activity propagation. CONCLUSION: Overall, the present results clearly indicate the involvement of the aberrant CX43 expression/activity as a pathogenic mechanism for the conduction defects associated to this LMNA truncating alteration.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/genética
Cardiomiopatias/genética
Lamina Tipo A/genética
[Mh] Termos MeSH secundário: Apoptose
Sequência de Bases
Cálcio/metabolismo
Calnexina/metabolismo
Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/patologia
Cardiomiopatias/complicações
Cardiomiopatias/patologia
Linhagem Celular
Conexina 43
Retículo Endoplasmático/metabolismo
Feminino
Junções Comunicantes/metabolismo
Células HEK293
Seres Humanos
Lamina Tipo A/metabolismo
Repetições de Microssatélites/genética
Microscopia Confocal
Meia-Idade
Mutagênese Sítio-Dirigida
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Linhagem
Polimorfismo de Nucleotídeo Único
Imagem com Lapso de Tempo
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (LMNA protein, human); 0 (Lamin Type A); 139873-08-8 (Calnexin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485651


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[PMID]:29304122
[Au] Autor:Leon Rodriguez DA; Acosta-Herrera M; Carmona FD; Dolade N; Vargas S; Echeverría LE; González CI; Martin J
[Ad] Endereço:Instituto de Parasitología y Biomedicina 'López-Neyra', IPBLN-CSIC, PTS Granada, Granada, Spain.
[Ti] Título:Comprehensive analysis of three TYK2 gene variants in the susceptibility to Chagas disease infection and cardiomyopathy.
[So] Source:PLoS One;13(1):e0190591, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tyrosine kinase 2 (TYK2) is a member of the Janus kinases family implicated in the signal transduction of type I interferons and several interleukins. It has been described that genetic mutations within TYK2 lead to multiple deleterious effects in the immune response. In this work, we have analyzed three functional independent variants from the frequency spectrum on the TYK2 gene (common and low-frequency variants) suggested to reduce the function of the gene in mediating cytokine signaling and the susceptibility to infections by Trypanosoma cruzi and/or the development of Chagas cardiomyopathy in the Colombian population. A total of 1,323 individuals from a Colombian endemic region for Chagas disease were enrolled in the study. They were classified as seronegative (n = 445), seropositive asymptomatic (n = 336), and chronic Chagas Cardiomyopathy subjects (n = 542). DNA samples were genotyped using TaqMan probes. Our results showed no statistically significant differences between the allelic frequencies of the three analyzed variants when seropositive and seronegative individuals were compared, therefore these variants were not associated with susceptibility to Chagas disease. Moreover, when Chagas cardiomyopathy patients were compared to asymptomatic patients, no significant associations were found. Previous reports highlighted the association of this gene in immune-related disorders under an autoimmunity context, but not predisposing patients to infectious diseases, which is consistent with our findings. Therefore, according to our results, TYK2 gene variants do not seem to play an important role in Chagas disease susceptibility and/or chronic Chagas cardiomyopathy.
[Mh] Termos MeSH primário: Cardiomiopatias/genética
Doença de Chagas/genética
Predisposição Genética para Doença
TYK2 Quinase/genética
[Mh] Termos MeSH secundário: Adulto
Doença de Chagas/epidemiologia
Colômbia/epidemiologia
Feminino
Seres Humanos
Masculino
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (TYK2 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190591


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[PMID]:28453909
[Au] Autor:Rotz SJ; Ryan TD; Hlavaty J; George SA; El-Bietar J; Dandoy CE
[Ad] Endereço:Division of Bone Marrow Transplantation and Immune Deficiency, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
[Ti] Título:Cardiotoxicity and cardiomyopathy in children and young adult survivors of hematopoietic stem cell transplant.
[So] Source:Pediatr Blood Cancer;64(11), 2017 Nov.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiomyopathy is common in long-term survivors of pediatric hematopoietic stem cell transplant (HSCT). Events occurring before and after HSCT when combined with specific insults during HSCT likely contribute to long-term risk. Strategies for detecting subclinical cardiomyopathy prior to patients developing overt heart failure are under investigation. Changes in HSCT preparative regimens and cardioprotective medications administered during chemotherapy may alter the risk for cardiomyopathy. Interventions in long-term survivors such as lifestyle modification and cardioactive medications are of increasing importance. Herein we review the causes of cardiac injury, discuss strategies for detection of cardiomyopathy, and evaluate therapeutic options for long-term HSCT survivors.
[Mh] Termos MeSH primário: Cardiomiopatias/etiologia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Sobreviventes/estatística & dados numéricos
[Mh] Termos MeSH secundário: Adulto
Cardiomiopatias/diagnóstico
Cardiomiopatias/prevenção & controle
Cardiotoxicidade
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26600


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[PMID]:28456755
[Au] Autor:Grogan M; Dispenzieri A; Gertz MA
[Ad] Endereço:Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
[Ti] Título:Light-chain cardiac amyloidosis: strategies to promote early diagnosis and cardiac response.
[So] Source:Heart;103(14):1065-1072, 2017 07.
[Is] ISSN:1468-201X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Amyloid light chain (AL) amyloidosis is a systemic disease characterised by the aggregation of misfolded immunoglobulin light chain (LC), predominantly in the heart and kidneys, causing organ failure. If untreated, the median survival of patients with cardiac AL amyloidosis is 6 months from the onset of heart failure. Protracted time to establish a diagnosis, often lasting >1 year, is a frequent factor in poor treatment outcomes. Cardiologists, to whom patients are often referred, frequently miss the opportunity to diagnose cardiac AL amyloidosis. Nearly all typical cardiac support measures, with the exception of diuretics, are ineffective and may even worsen clinical symptoms, emphasising the need for accurate diagnosis. Patients with severe cardiac involvement face poor outcomes; heart transplantation is rarely an option because of multiorgan involvement, rapid clinical decline and challenges in predicting which patients will respond to treatment of the underlying plasma cell disorder. Early diagnosis and prompt treatment with ââ'¬ËÅ“source therapiesââ'¬â"¢ that limit the production of amyloidogenic LC are associated with better survival and improvement in organ function after a median of 2.4 months following haematological complete response. However, organ recovery is often incomplete because these source therapies do not directly target deposited amyloid. Emerging amyloid-directed therapies may attenuate, and potentially reverse, organ dysfunction by clearing existing amyloid and inhibiting fibril formation of circulating aggregates. Improved recognition of AL amyloidosis by cardiologists allows for earlier treatment and improved outcomes.
[Mh] Termos MeSH primário: Amiloidose/diagnóstico
Cardiomiopatias/diagnóstico
Diagnóstico Precoce
Insuficiência Cardíaca/etiologia
Cadeias Leves de Imunoglobulina/metabolismo
Guias de Prática Clínica como Assunto
[Mh] Termos MeSH secundário: Amiloidose/complicações
Cardiomiopatias/complicações
Insuficiência Cardíaca/diagnóstico
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunoglobulin Light Chains)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1136/heartjnl-2016-310704



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