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Pesquisa : A07.541.207 [Categoria DeCS]
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[PMID]:29371594
[Au] Autor:Rhee S; Chung JI; King DA; D'amato G; Paik DT; Duan A; Chang A; Nagelberg D; Sharma B; Jeong Y; Diehn M; Wu JC; Morrison AJ; Red-Horse K
[Ad] Endereço:Department of Biology, Stanford University, 371 Serra Mall, Stanford, CA, 94305, USA.
[Ti] Título:Endothelial deletion of Ino80 disrupts coronary angiogenesis and causes congenital heart disease.
[So] Source:Nat Commun;9(1):368, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During development, the formation of a mature, well-functioning heart requires transformation of the ventricular wall from a loose trabecular network into a dense compact myocardium at mid-gestation. Failure to compact is associated in humans with congenital diseases such as left ventricular non-compaction (LVNC). The mechanisms regulating myocardial compaction are however still poorly understood. Here, we show that deletion of the Ino80 chromatin remodeler in vascular endothelial cells prevents ventricular compaction in the developing mouse heart. This correlates with defective coronary vascularization, and specific deletion of Ino80 in the two major coronary progenitor tissues-sinus venosus and endocardium-causes intermediate phenotypes. In vitro, endothelial cells promote myocardial expansion independently of blood flow in an Ino80-dependent manner. Ino80 deletion increases the expression of E2F-activated genes and endothelial cell S-phase occupancy. Thus, Ino80 is essential for coronary angiogenesis and allows coronary vessels to support proper compaction of the heart wall.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
Endotélio Vascular/metabolismo
Cardiopatias Congênitas/metabolismo
Neovascularização Patológica/metabolismo
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/genética
Animais
Vasos Coronários/metabolismo
DNA Helicases/genética
DNA Helicases/metabolismo
Endocárdio/metabolismo
Endocárdio/patologia
Células Endoteliais/enzimologia
Células Endoteliais/metabolismo
Endotélio Vascular/patologia
Cardiopatias Congênitas/genética
Ventrículos do Coração/metabolismo
Ventrículos do Coração/patologia
Seres Humanos
Camundongos Knockout
Camundongos Transgênicos
Miocárdio/metabolismo
Miocárdio/patologia
Neovascularização Patológica/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (INO80 protein, mouse); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02796-3


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[PMID]:29247031
[Au] Autor:Panitchob N; Li L; Huang J; Ranjan R; Ideker RE; Dosdall DJ
[Ad] Endereço:From the Nora Eccles Harrison Cardiovascular Research and Training Institute (N.P., R.R., D.J.D.), Division of Cardiothoracic Surgery, Department of Surgery (D.J.D.), and Division of Cardiovascular Medicine, Department of Medicine (L.L., R.R., D.J.D.), University of Utah, Salt Lake City; and Divisio
[Ti] Título:Endocardial Activation Drives Activation Patterns During Long-Duration Ventricular Fibrillation and Defibrillation.
[So] Source:Circ Arrhythm Electrophysiol;10(12), 2017 Dec.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Understanding the mechanisms that drive ventricular fibrillation is essential for developing improved defibrillation techniques to terminate ventricular fibrillation (VF). Distinct organization patterns of chaotic, regular, and synchronized activity were previously demonstrated in VF that persisted over 1 to 2 minutes (long-duration VF [LDVF]). We hypothesized that activity on the endocardium may be driving these activation patterns in LDVF and that unsuccessful defibrillation shocks may alter activation patterns. METHODS AND RESULTS: The study was performed using a 64-electrode basket catheter on the left ventricle endocardium and 54 6-electrode plunge needles inserted into the left ventricles of 6 dogs. VF was induced electrically, and after short-duration VF (10 seconds) and LDVF (7 minutes), shocks of increasing strengths were delivered every 10 seconds until VF was terminated. Endocardial activation patterns were classified as chaotic (varying cycle lengths and nonsynchronous activations), regular (highly repeatable cycle lengths), and synchronized (activation that spreads rapidly over the endocardium with diastolic periods between activations). CONCLUSIONS: The results showed that the chaotic pattern was predominant in early VF, but the regular pattern emerges as VF progressed. The synchronized pattern only emerged occasionally during late VF. Failed defibrillation shocks changed chaotic and regular activation patterns to synchronized patterns in LDVF but not in short-duration VF. The regular and synchronized patterns of activation were driven by rapid activations on the endocardial surface that blocked and broke up transmurally, leading to an endocardial to epicardial activation rate gradient as LDVF progressed.
[Mh] Termos MeSH primário: Cardioversão Elétrica
Endocárdio/fisiopatologia
Fibrilação Ventricular/prevenção & controle
Fibrilação Ventricular/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Cães
Eletrocardiografia
Eletrodos Implantados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:29038101
[Au] Autor:Samanta R; Kumar S; Chik W; Qian P; Barry MA; Al Raisi S; Bhaskaran A; Farraha M; Nadri F; Kizana E; Thiagalingam A; Kovoor P; Pouliopoulos J
[Ad] Endereço:From the Department of Cardiology, Westmead Hospital, New South Wales, Australia (R.S., S.K., W.C., P.Q., M.A.B., S.A.R., A.B., F.N., E.K., A.T., P.K., J.P.); and Sydney Medical School, University of Sydney, Australia (R.S., W.C., S.A.R., A.B., M.F., E.K., A.T., P.K., J.P.).
[Ti] Título:Influence of Intramyocardial Adipose Tissue on the Accuracy of Endocardial Contact Mapping of the Chronic Myocardial Infarction Substrate.
[So] Source:Circ Arrhythm Electrophysiol;10(10), 2017 Oct.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent studies have demonstrated that intramyocardial adipose tissue (IMAT) may contribute to ventricular electrophysiological remodeling in patients with chronic myocardial infarction. Using an ovine model of myocardial infarction, we aimed to determine the influence of IMAT on scar tissue identification during endocardial contact mapping and optimal voltage-based mapping criteria for defining IMAT dense regions. METHOD AND RESULTS: In 7 sheep, left ventricular endocardial and transmural mapping was performed 84 weeks (15-111 weeks) post-myocardial infarction. Spearman rank correlation coefficient was used to assess the relationship between endocardial contact electrogram amplitude and histological composition of myocardium. Receiver operator characteristic curves were used to derive optimal electrogram thresholds for IMAT delineation during endocardial mapping and to describe the use of endocardial mapping for delineation of IMAT dense regions within scar. Endocardial electrogram amplitude correlated significantly with IMAT (unipolar =-0.48±0.12, <0.001; bipolar =-0.45±0.22, =0.04) but not collagen (unipolar =-0.36±0.24, =0.13; bipolar =-0.43±0.31, =0.16). IMAT dense regions of myocardium reliably identified using endocardial mapping with thresholds of <3.7 and <0.6 mV, respectively, for unipolar, bipolar, and combined modalities (single modality area under the curve=0.80, <0.001; combined modality area under the curve=0.84, <0.001). Unipolar mapping using optimal thresholding remained significantly reliable (area under the curve=0.76, <0.001) during mapping of IMAT, confined to putative scar border zones (bipolar amplitude, 0.5-1.5 mV). CONCLUSIONS: These novel findings enhance our understanding of the confounding influence of IMAT on endocardial scar mapping. Combined bipolar and unipolar voltage mapping using optimal thresholds may be useful for delineating IMAT dense regions of myocardium, in postinfarct cardiomyopathy.
[Mh] Termos MeSH primário: Tecido Adiposo/patologia
Cicatriz/diagnóstico
Técnicas Eletrofisiológicas Cardíacas
Endocárdio/patologia
Infarto do Miocárdio/diagnóstico
Miocárdio/patologia
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Área Sob a Curva
Biópsia
Cicatriz/metabolismo
Cicatriz/patologia
Cicatriz/fisiopatologia
Colágeno/metabolismo
Modelos Animais de Doenças
Endocárdio/metabolismo
Endocárdio/fisiopatologia
Frequência Cardíaca
Masculino
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/metabolismo
Valor Preditivo dos Testes
Curva ROC
Reprodutibilidade dos Testes
Carneiro Doméstico
Processamento de Sinais Assistido por Computador
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9007-34-5 (Collagen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


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[PMID]:29018165
[Au] Autor:Maurer T; Metzner A; Ho SY; Wohlmuth P; Reißmann B; Heeger C; Lemes C; Hayashi K; Saguner AM; Riedl J; Sohns C; Mathew S; Kuck KH; Wissner E; Ouyang F
[Ad] Endereço:From the Department of Cardiology, Asklepios-Klinik St Georg, Hamburg, Germany (T.M., A.M., B.R., C.H., C.L., K.H., A.M.S., J.R., C.S., S.M., K.-H.K., F.O.); Royal Brompton Hospital and Harefield NHS Trust, London, United Kingdom (S.Y.H.); Asklepios Proresearch, Hamburg, Germany (P.W.); and Division
[Ti] Título:Catheter Ablation of the Superolateral Mitral Isthmus Line: A Novel Approach to Reduce the Need for Epicardial Ablation.
[So] Source:Circ Arrhythm Electrophysiol;10(10), 2017 Oct.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The mitral isthmus is a critical part of perimitral reentrant tachycardia, as well as an important substrate of persistent atrial fibrillation. Deployment of an endocardial mitral isthmus line (MIL) with the end point of bidirectional block may be challenging and often requires additional epicardial ablation within the coronary sinus. METHODS AND RESULTS: The study population comprised 114 patients with perimitral flutter who underwent de novo ablation of an MIL. The initial 57 patients (group A) underwent catheter ablation using a novel superolateral MIL design, connecting the left-sided pulmonary veins with the mitral annulus along the posterior base of the left atrial appendage visualized by selective angiography. The next 57 patients (group B) served as a control group and underwent ablation using a conventional MIL design, connecting the left inferior pulmonary vein with the mitral annulus. Bidirectional block was achieved in 56 of 57 patients in group A (98.2%) and 50 of 57 patients in group B (87.7%; =0.06). Deployment of a superolateral MIL required significantly less ablation from within the coronary sinus (7.0% versus 71.9%; <0.01). Predictors for unsuccessful bidirectional mitral isthmus blockade were the need for epicardial ablation from within the coronary sinus ( <0.01) and the total length of the MIL (29.3±6.35 mm versus 40.8±7.29 mm; =0.005). A higher rate of pericardial tamponade was observed in group A (5.2% versus 0%; =0.24). CONCLUSIONS: The superolateral MIL is associated with a high acute success rate to achieve bidirectional block using endocardial ablation only with minimal need for epicardial ablation from within the coronary sinus.
[Mh] Termos MeSH primário: Flutter Atrial/cirurgia
Ablação por Cateter/métodos
Valva Mitral/cirurgia
[Mh] Termos MeSH secundário: Idoso
Fibrilação Atrial/diagnóstico por imagem
Fibrilação Atrial/fisiopatologia
Fibrilação Atrial/cirurgia
Flutter Atrial/diagnóstico por imagem
Flutter Atrial/fisiopatologia
Angiografia Coronária
Seio Coronário/diagnóstico por imagem
Seio Coronário/fisiopatologia
Seio Coronário/cirurgia
Ecocardiografia
Eletrocardiografia
Endocárdio/fisiopatologia
Endocárdio/cirurgia
Mapeamento Epicárdico
Feminino
Seres Humanos
Masculino
Meia-Idade
Valva Mitral/diagnóstico por imagem
Valva Mitral/fisiopatologia
Veias Pulmonares/diagnóstico por imagem
Veias Pulmonares/cirurgia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[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:171012
[St] Status:MEDLINE


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[PMID]:28890073
[Au] Autor:Sharma B; Ho L; Ford GH; Chen HI; Goldstone AB; Woo YJ; Quertermous T; Reversade B; Red-Horse K
[Ad] Endereço:Department of Biology, Stanford University, Stanford, CA 94305, USA.
[Ti] Título:Alternative Progenitor Cells Compensate to Rebuild the Coronary Vasculature in Elabela- and Apj-Deficient Hearts.
[So] Source:Dev Cell;42(6):655-666.e3, 2017 Sep 25.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Organogenesis during embryonic development occurs through the differentiation of progenitor cells. This process is extraordinarily accurate, but the mechanisms ensuring high fidelity are poorly understood. Coronary vessels of the mouse heart derive from at least two progenitor pools, the sinus venosus and endocardium. We find that the ELABELA (ELA)-APJ signaling axis is only required for sinus venosus-derived progenitors. Because they do not depend on ELA-APJ, endocardial progenitors are able to expand and compensate for faulty sinus venosus development in Apj mutants, leading to normal adult heart function. An upregulation of endocardial SOX17 accompanied compensation in Apj mutants, which was also seen in Ccbe1 knockouts, indicating that the endocardium is activated in multiple cases where sinus venosus angiogenesis is stunted. Our data demonstrate that by diversifying their responsivity to growth cues, distinct coronary progenitor pools are able to compensate for each other during coronary development, thereby providing robustness to organ development.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Vasos Coronários/embriologia
Neovascularização Fisiológica
Receptores Acoplados a Proteínas-G/deficiência
Células-Tronco/citologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Receptores de Apelina
Vasos Coronários/metabolismo
Embrião de Mamíferos/metabolismo
Embrião de Mamíferos/patologia
Endocárdio/metabolismo
Proteínas HMGB/metabolismo
Hipóxia/metabolismo
Hipóxia/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mutação/genética
Miocárdio/patologia
Receptores Acoplados a Proteínas-G/metabolismo
Fatores de Transcrição SOXF/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apela protein, mouse); 0 (Apelin Receptors); 0 (Aplnr protein, mouse); 0 (Carrier Proteins); 0 (HMGB Proteins); 0 (Receptors, G-Protein-Coupled); 0 (SOXF Transcription Factors); 0 (Sox17 protein, mouse)
[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:170912
[St] Status:MEDLINE


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[PMID]:28798020
[Au] Autor:Venlet J; Piers SRD; Kapel GFL; de Riva M; Pauli PFG; van der Geest RJ; Zeppenfeld K
[Ad] Endereço:From the Departments of Cardiology (J.V., S.R.D.P., G.F.L.K., M.d.R., P.F.G.P., K.Z.) and Image Processing (R.J.v.d.G.), Leiden University Medical Center, The Netherlands.
[Ti] Título:Unipolar Endocardial Voltage Mapping in the Right Ventricle: Optimal Cutoff Values Correcting for Computed Tomography-Derived Epicardial Fat Thickness and Their Clinical Value for Substrate Delineation.
[So] Source:Circ Arrhythm Electrophysiol;10(8), 2017 Aug.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Low endocardial unipolar voltage (UV) at sites with normal bipolar voltage (BV) may indicate epicardial scar. Currently applied UV cutoff values are based on studies that lacked epicardial fat information. This study aimed to define endocardial UV cutoff values using computed tomography-derived fat information and to analyze their clinical value for right ventricular substrate delineation. METHODS AND RESULTS: Thirty-three patients (50±14 years; 79% men) underwent combined endocardial-epicardial right ventricular electroanatomical mapping and ablation of right ventricular scar-related ventricular tachycardia with computed tomographic image integration, including computed tomography-derived fat thickness. Of 6889 endocardial-epicardial mapping point pairs, 547 (8%) pairs with distance <10 mm and fat thickness <1.0 mm were analyzed for voltage and abnormal (fragmented/late potential) electrogram characteristics. At sites with endocardial BV >1.50 mV, the optimal endocardial UV cutoff for identification of epicardial BV <1.50 mV was 3.9 mV (area under the curve, 0.75; sensitivity, 60%; specificity, 79%) and cutoff for identification of abnormal epicardial electrogram was 3.7 mV (area under the curve, 0.88; sensitivity, 100%; specificity, 67%). The majority of abnormal electrograms (130 of 151) were associated with transmural scar. Eighty-six percent of abnormal epicardial electrograms had corresponding endocardial sites with BV <1.50 mV, and the remaining could be identified by corresponding low endocardial UV <3.7 mV. CONCLUSIONS: For identification of epicardial right ventricular scar, an endocardial UV cutoff value of 3.9 mV is more accurate than previously reported cutoff values. Although the majority of epicardial abnormal electrograms are associated with transmural scar with low endocardial BV, the additional use of endocardial UV at normal BV sites improves the diagnostic accuracy resulting in identification of all epicardial abnormal electrograms at sites with <1.0 mm fat.
[Mh] Termos MeSH primário: Tecido Adiposo/diagnóstico por imagem
Tecido Adiposo/fisiopatologia
Cicatriz/diagnóstico por imagem
Mapeamento Epicárdico/métodos
Taquicardia Ventricular/cirurgia
Tomografia Computadorizada por Raios X
Disfunção Ventricular Direita/cirurgia
[Mh] Termos MeSH secundário: Cicatriz/fisiopatologia
Eletrocardiografia
Endocárdio/diagnóstico por imagem
Endocárdio/fisiopatologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Pericárdio/diagnóstico por imagem
Pericárdio/fisiopatologia
Sensibilidade e Especificidade
Taquicardia Ventricular/diagnóstico por imagem
Taquicardia Ventricular/fisiopatologia
Disfunção Ventricular Direita/diagnóstico por imagem
Disfunção Ventricular Direita/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


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[PMID]:28778856
[Au] Autor:Bulava A; Mokracek A; Hanis J; Eisenberger M; Kurfirst V; Dusek L
[Ad] Endereço:From the Department of Cardiology (A.B., J.H., M.E.) and Department of Cardiac Surgery (A.M., V.K.), Budweis Hospital, Ceské Budejovice, Czech Republic; Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic (A.B.); Faculty of Health and Social Sciences, University of South Bo
[Ti] Título:Correlates of Arrhythmia Recurrence After Hybrid Epi- and Endocardial Radiofrequency Ablation for Persistent Atrial Fibrillation.
[So] Source:Circ Arrhythm Electrophysiol;10(8), 2017 Aug.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long-term efficacy of catheter-based treatment of persistent atrial fibrillation is unsatisfactory. Minimally invasive surgical ablation techniques have been developed recently, but their efficacy has never been systematically tested. METHODS AND RESULTS: Seventy patients (median age, 63.5 years) with persistent atrial fibrillation underwent epicardial thoracoscopic radiofrequency pulmonary vein isolation, linear ablation, Marshal ligament disruption, and exclusion of the left atrial appendage. The procedure was followed by electroanatomic mapping and ablation (EAM) 2 to 3 months later. Only 76% of patients were in normal sinus rhythm at the beginning of EAM. All 4 pulmonary veins and the left atrium posterior wall were found isolated in 69% and 23% of patients, respectively. Arrhythmia-free survival off antiarrhythmic drugs 12 months after EAM was 77%. Using previously ineffective antiarrhythmic drugs and reablation procedures, arrhythmia free-survival increased to 97% during follow-up (mean, 936±432 days; range, 346-1509 days). The majority of arrhythmia recurrences occurred during the first 12 months after EAM. In a multivariable-adjusted estimates, left atrium volume >165 mL, absent normal sinus rhythm at admission for EAM, and inducibility of any sustained tachyarrhythmia at the end of EAM procedure were identified as independent correlates of atrial fibrillation recurrence. CONCLUSIONS: Our report demonstrated that the majority of patients after epicardial ablation, using bipolar radiofrequency instruments, required endocardial catheter ablation to complete the linear ablation lesions and a significant proportion of patients required spot-ablations to complete electric pulmonary vein isolation. Noninducibility of any arrhythmia after a staged hybrid procedure seemed to be the strongest correlate of long-term arrhythmia-free survival. CLINICAL TRIAL REGISTRATION: URL: www.ablace.cz. Unique identifier: cz-060520121617.
[Mh] Termos MeSH primário: Fibrilação Atrial/cirurgia
Ablação por Cateter/métodos
Endocárdio/cirurgia
Veias Pulmonares/cirurgia
[Mh] Termos MeSH secundário: Fibrilação Atrial/fisiopatologia
Técnicas Eletrofisiológicas Cardíacas
Endocárdio/fisiopatologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Procedimentos Cirúrgicos Minimamente Invasivos
Ondas de Rádio
Recidiva
Reoperação
Fatores de Risco
Toracoscopia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE


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[PMID]:28705792
[Au] Autor:Prakash S; Borreguero LJJ; Sylva M; Flores Ruiz L; Rezai F; Gunst QD; de la Pompa JL; Ruijter JM; van den Hoff MJB
[Ad] Endereço:From the Department of Medical Biology, Academic Medical Center, Amsterdam, The Netherlands (S.P., M.S., F.R., Q.D.G., J.M.R., M.J.B.v.d.H.); Cardiovascular Imaging Laboratory, Centro Nacional de Investigación Cardiovascular, Madrid, Spain (L.J.J.B., L.F.R.); and Intercellular Signaling in Cardiovas
[Ti] Título:Deletion of Fstl1 (Follistatin-Like 1) From the Endocardial/Endothelial Lineage Causes Mitral Valve Disease.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):e116-e130, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Fstl1 (Follistatin-like 1) is a secreted protein that is expressed in the atrioventricular valves throughout embryonic development, postnatal maturation, and adulthood. In this study, we investigated the loss of Fstl1 in the endocardium/endothelium and their derived cells. APPROACH AND RESULTS: We conditionally ablated Fstl1 from the endocardial lineage using a transgenic Tie2-Cre mouse model. These mice showed a sustained Bmp and Tgfß signaling after birth. This resulted in ongoing proliferation and endocardial-to-mesenchymal transition and ultimately in deformed nonfunctional mitral valves and a hypertrophic dilated heart. Echocardiographic and electrocardiographic analyses revealed that loss of Fstl1 leads to mitral regurgitation and left ventricular diastolic dysfunction. Cardiac function gradually deteriorated resulting in heart failure with preserved ejection fraction and death of the mice between 2 and 4 weeks after birth. CONCLUSIONS: We report on a mouse model in which deletion of Fstl1 from the endocardial/endothelial lineage results in deformed mitral valves, which cause regurgitation, heart failure, and early cardiac death. The findings provide a potential molecular target for the clinical research into myxomatous mitral valve disease.
[Mh] Termos MeSH primário: Linhagem da Célula
Endocárdio/metabolismo
Células Endoteliais/metabolismo
Proteínas Relacionadas à Folistatina/deficiência
Insuficiência Cardíaca/metabolismo
Insuficiência da Valva Mitral/metabolismo
Prolapso da Valva Mitral/metabolismo
Valva Mitral/metabolismo
Disfunção Ventricular Esquerda/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Proliferação Celular
Modelos Animais de Doenças
Progressão da Doença
Endocárdio/patologia
Células Endoteliais/patologia
Transição Epitelial-Mesenquimal
Proteínas Relacionadas à Folistatina/genética
Predisposição Genética para Doença
Sistema de Condução Cardíaco/metabolismo
Sistema de Condução Cardíaco/fisiopatologia
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/patologia
Insuficiência Cardíaca/fisiopatologia
Integrases/genética
Camundongos Knockout
Valva Mitral/patologia
Valva Mitral/fisiopatologia
Insuficiência da Valva Mitral/genética
Insuficiência da Valva Mitral/patologia
Insuficiência da Valva Mitral/fisiopatologia
Prolapso da Valva Mitral/genética
Prolapso da Valva Mitral/patologia
Prolapso da Valva Mitral/fisiopatologia
Fenótipo
Receptor TIE-2/genética
Transdução de Sinais
Fatores de Tempo
Fatores de Transcrição/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Disfunção Ventricular Esquerda/genética
Disfunção Ventricular Esquerda/patologia
Disfunção Ventricular Esquerda/fisiopatologia
Função Ventricular Esquerda
Remodelação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Follistatin-Related Proteins); 0 (Fstl1 protein, mouse); 0 (Transcription Factors); 0 (Transforming Growth Factor beta); EC 2.7.10.1 (Receptor, TIE-2); EC 2.7.10.1 (Tek protein, mouse); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309089


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[PMID]:28555404
[Au] Autor:Grotenhuis HB; Nyns ECA; Kantor PF; Dipchand AI; Greenway SC; Yoo SJ; Tomlinson G; Chaturvedi RR; Grosse-Wortmann L
[Ad] Endereço:Department of Paediatrics, Labatt Family Heart Centre, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, ON, M5G 1X8, Canada. hgrotenhuis@hotmail.com.
[Ti] Título:Abnormal Myocardial Contractility After Pediatric Heart Transplantation by Cardiac MRI.
[So] Source:Pediatr Cardiol;38(6):1198-1205, 2017 Aug.
[Is] ISSN:1432-1971
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute cellular rejection (ACR) compromises graft function after heart transplantation (HTX). The purpose of this study was to describe systolic myocardial deformation in pediatric HTX and to determine whether it is impaired during ACR. Eighteen combined cardiac magnetic resonance imaging (CMR)/endomyocardial biopsy (EMBx) examinations were performed in 14 HTX patients (11 male, age 13.9 ± 4.7 years; 1.2 ± 1.3 years after HTX). Biventricular function and left ventricular (LV) circumferential strain, rotation, and torsion by myocardial tagging CMR were compared to 11 controls as well as between patients with and without clinically significant ACR. HTX patients showed mildly reduced biventricular systolic function when compared to controls [LV ejection fraction (EF): 55 ± 8% vs. 61 ± 3, p = 0.02; right ventricular (RV) EF: 48 ± 7% vs. 53 ± 6, p = 0.04]. Indexed LV mass was mildly increased in HTX patients (67 ± 14 g/m vs. 55 ± 13, p = 0.03). LV myocardial deformation indices were all significantly reduced, expressed by global circumferential strain (-13.5 ± 2.3% vs. -19.1 ± 1.1%, p < 0.01), basal strain (-13.7 ± 3.0% vs. -17.5 ± 2.4%, p < 0.01), mid-ventricular strain (-13.4 ± 2.7% vs. -19.3 ± 2.2%, p < 0.01), apical strain (-13.5 ± 2.8% vs. -19.9 ± 2.0%, p < 0.01), basal rotation (-2.0 ± 2.1° vs. -5.0 ± 2.0°, p < 0.01), and torsion (6.1 ± 1.7° vs. 7.8 ± 1.1°, p < 0.01). EMBx demonstrated ACR grade 0 R in 3 HTX cases, ACR grade 1 R in 11 HTX cases and ACR grade 2 R in 4 HTX cases. When comparing clinically non-significant ACR (grades 0-1 R vs. ACR 2 R), basal rotation, and apical rotation were worse in ACR 2 R patients (-1.4 ± 1.8° vs. -4.2 ± 1.4°, p = 0.01 and 10.2 ± 2.9° vs. 2.8 ± 1.9°, p < 0.01, respectively). Pediatric HTX recipients demonstrate reduced biventricular systolic function and decreased myocardial contractility. Myocardial deformation indices by CMR may serve as non-invasive markers of graft function and, perhaps, rejection in pediatric HTX patients.
[Mh] Termos MeSH primário: Rejeição de Enxerto/fisiopatologia
Transplante de Coração/efeitos adversos
Imagem por Ressonância Magnética/métodos
Contração Miocárdica
Disfunção Ventricular Esquerda/fisiopatologia
[Mh] Termos MeSH secundário: Adolescente
Biópsia por Agulha
Criança
Pré-Escolar
Estudos Transversais
Endocárdio/patologia
Feminino
Rejeição de Enxerto/diagnóstico por imagem
Rejeição de Enxerto/etiologia
Seres Humanos
Masculino
Contração Miocárdica/fisiologia
Miocárdio/patologia
Sístole
Disfunção Ventricular Esquerda/diagnóstico por imagem
Disfunção Ventricular Esquerda/etiologia
Função Ventricular Esquerda/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1007/s00246-017-1642-5


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[PMID]:28539564
[Au] Autor:Mitsutake Y; Pyun WB; Rouy D; Foo CWP; Stertzer SH; Altman P; Ikeno F
[Ad] Endereço:Division of Cardiovascular Medicine, Stanford University.
[Ti] Título:Improvement of Local Cell Delivery Using Helix Transendocardial Delivery Catheter in a Porcine Heart.
[So] Source:Int Heart J;58(3):435-440, 2017 May 31.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Cardiac regeneration strategies using stem cells have shown variable and inconsistent results with respect to patient cardiac function and clinical outcomes. There has been increasing consensus that improving the efficiency of delivery may improve results. The Helix transendocardial delivery system (BioCardia Inc.) has been developed to enable percutaneous transendocardial biotherapeutic delivery. Therefore, we evaluated cell retention using this unique system compared with direct transepicardial injection and intracoronary infusion in an animal model.Twelve healthy swine were used in this study. Fluorodeoxyglucose (FDG)-labeled bone marrow mononuclear cells were delivered via percutaneous transendocardial route using the Helix system (TE group, n = 5), via direct transepicardial injection using a straight 27-gauge needle in an open chest procedure (TP group, n = 4), or via percutaneous intracoronary (IC) infusion (IC group, n = 3). One hour after cell delivery, the distribution of injected cells within the myocardium was assessed by PET-CT. Regions of interest were defined and their signals were compared in each group. Retention rates were calculated as a percentage of the comparing signal.The distribution of injected cells in the myocardium was higher in the TE group (17.9%) than in the TP group (6.0%, versus TE, P < 0.001) and the IC group (1.0%, versus TE, P < 0.001). Consistent with previous reports, there were signal distributions in the lungs, liver, and kidneys in qualitative whole body PET assessment.TE cell delivery using a helical infusion catheter is more efficient in cell retention than either TP delivery or IC delivery using PET-CT analysis.
[Mh] Termos MeSH primário: Cateteres Cardíacos
Terapia Baseada em Transplante de Células e Tecidos/instrumentação
Sistemas de Liberação de Medicamentos/instrumentação
Isquemia Miocárdica/terapia
Transplante de Células-Tronco/métodos
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Endocárdio
Desenho de Equipamento
Feminino
Isquemia Miocárdica/diagnóstico
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-179



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