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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]:28683992
[Au] Autor:Ragnarsson S; Sjögren J; Stagmo M; Wierup P; Nozohoor S
[Ad] Endereço:Department of Cardiothoracic Surgery, Skane University Hospital, Lund University, Lund, Sweden. Electronic address: sigurdur.ragnarsson@med.lu.se.
[Ti] Título:Assessment of Mitral Valve Repair With Exercise Echocardiography: Artificial Chordae vs Leaflet Resection.
[So] Source:Semin Thorac Cardiovasc Surg;29(1):25-32, 2017 Spring.
[Is] ISSN:1532-9488
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitral valve (MV) repair with artificial chordae (AC) or leaflet resection (LR) is associated with good hemodynamics at rest. The aim of this study was to compare these techniques in terms of exercise capacity and echocardiographic parameters of hemodynamics at rest and peak exercise. We conducted a study in 2015 of 56 patients, who had undergone surgery for degenerative posterior mitral leaflet prolapse between 2005 and 2014 using either AC (n = 24) or LR (n = 32). Clinical data were collected, exercise capacity was measured, and resting echocardiography and peak exercise echocardiography were performed. No significant differences were detected among groups regarding exercise duration or peak exercise workload measured in Watts (W) (AC: 136 ± 43 W and LR: 131 ± 40 W; P = 0.65). The mean mitral gradient at rest was 3.0 ± 1.3 mm Hg in the AC group and 3.0 ± 1.0 mm Hg in the LR group (P = 0.90). The mean MV gradients at peak exercise did not differ significantly between groups (AC: 8.3 ± 3.4 and LR: 11.3 ± 8.7; P = 0.19). Four patients (17%) in the AC group and 1 (3%) in the LR group had systolic anterior motion, P = 0.15. We conclude that both methods of posterior MV leaflet repair were associated with good hemodynamics at rest and peak exercise. The groups had comparable exercise capacity. MV pressure gradients at rest and peak exercise were similar in both groups.
[Mh] Termos MeSH primário: Prótese Vascular
Cordas Tendinosas/cirurgia
Ecocardiografia Doppler
Ecocardiografia sob Estresse/métodos
Teste de Esforço
Tolerância ao Exercício
Implante de Prótese de Valva Cardíaca/instrumentação
Hemodinâmica
Anuloplastia da Valva Mitral
Prolapso da Valva Mitral/cirurgia
Valva Mitral/cirurgia
[Mh] Termos MeSH secundário: Idoso
Cordas Tendinosas/diagnóstico por imagem
Cordas Tendinosas/fisiopatologia
Feminino
Implante de Prótese de Valva Cardíaca/efeitos adversos
Seres Humanos
Masculino
Meia-Idade
Valva Mitral/diagnóstico por imagem
Valva Mitral/fisiopatologia
Anuloplastia da Valva Mitral/efeitos adversos
Prolapso da Valva Mitral/diagnóstico por imagem
Prolapso da Valva Mitral/fisiopatologia
Valor Preditivo dos Testes
Estudos Prospectivos
Desenho de Prótese
Recuperação de Função Fisiológica
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


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[PMID]:28633253
[Au] Autor:Disha K; Schulz S; Kuntze T; Girdauskas E
[Ad] Endereço:Department of Cardiac Surgery, Central Hospital Bad Berka, Bad Berka, Germany. Electronic address: k_disha@hotmail.com.
[Ti] Título:Transforming Growth Factor Beta-2 Mutations in Barlow's Disease and Aortic Dilatation.
[So] Source:Ann Thorac Surg;104(1):e19-e21, 2017 Jul.
[Is] ISSN:1552-6259
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We report on a patient operated on for degenerative myxomatous mitral and tricuspid valve disease (Barlow's disease) and aortic root dilatation. A valve repair operation and the postoperative course were uneventful. Multigenerational genetic analyses revealed two different mutations in the transforming growth factor beta-2 gene in the same patient. The two mutations in different exons were inherited from both parents each. None of the parents presented with either valve dysfunction or aortic root dilatation. This rare case illustrates potentially common genetic and signaling pathways of concomitant myxomatous valve disease and aortic root dilatation.
[Mh] Termos MeSH primário: Aneurisma da Aorta Torácica/genética
DNA/genética
Prolapso da Valva Mitral/genética
Mutação
Fator de Crescimento Transformador beta2/genética
[Mh] Termos MeSH secundário: Aneurisma da Aorta Torácica/diagnóstico
Aneurisma da Aorta Torácica/cirurgia
Procedimentos Cirúrgicos Cardíacos/métodos
Análise Mutacional de DNA
Ecocardiografia Transesofagiana
Feminino
Seres Humanos
Meia-Idade
Prolapso da Valva Mitral/diagnóstico
Prolapso da Valva Mitral/cirurgia
Tomografia Computadorizada Multidetectores
Fator de Crescimento Transformador beta2/metabolismo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta2); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


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[PMID]:28580713
[Au] Autor:Thacoor A
[Ad] Endereço:Department of Cardiac Surgery, Leeds General Infirmary, Great George Street, Leeds, United KIngdom.
[Ti] Título:Mitral valve prolapse and Marfan syndrome.
[So] Source:Congenit Heart Dis;12(4):430-434, 2017 Jul.
[Is] ISSN:1747-0803
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Marfan syndrome is a multisystemic genetic condition affecting connective tissue. It carries a reduced life expectancy, largely dependent on cardiovascular complications. More common cardiac manifestations such as aortic dissection and aortic valve incompetence have been widely documented in the literature. Mitral valve prolapse (MVP), however, has remained poorly documented. This article aims at exploring the existing literature on the pathophysiology and diagnosis of MVP in patients with Marfan syndrome, defining its current management and outlining the future developments surrounding it.
[Mh] Termos MeSH primário: Diagnóstico por Imagem/métodos
Síndrome de Marfan/complicações
Prolapso da Valva Mitral/etiologia
[Mh] Termos MeSH secundário: Seres Humanos
Síndrome de Marfan/diagnóstico
Prolapso da Valva Mitral/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1111/chd.12467


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[PMID]:28332088
[Au] Autor:Kamiya H; Akhyari P; Minol JP; Ites AC; Weinreich T; Sixt S; Rellecke P; Boeken U; Albert A; Lichtenberg A
[Ad] Endereço:Department of Cardiovascular Surgery, Medical Faculty, Heinrich Heine University Duesseldorf, Moorenstrasse 5, 40225, Duesseldorf, Germany.
[Ti] Título:Simple technique of repair for Barlow syndrome with posterior resection and chordal transfer via minimally invasive approach: primary experience in a consecutive series of 22 patients.
[So] Source:Gen Thorac Cardiovasc Surg;65(7):374-380, 2017 Jul.
[Is] ISSN:1863-6713
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Current techniques for mitral valve repair (MVR) in Barlow's disease require high level of surgical expertise due to a complex anatomy. A novel and simple standardized technique that particularly considers the pathological changes of the mitral valve in Barlow's disease has been developed. METHODS: Between 2009 and 2013, 22 patients underwent minimally invasive MVR for Barlow's disease and severe mitral regurgitation (MR). A simple, standardized technique was applied, including resection of P2 segment of posterior mitral leaflet (PML) with preservation of the shortest chordae, transfer of the preserved chordae to A2, and implantation of a semi-rigid open ring. In 2015, all patients were contacted for follow-up by transthoracic echocardiography (TTE) and interviewed for their clinical status. RESULTS: During follow-up (mean 2.8 ± 1.1 years; 100% complete), one patient died due to abdominal bleeding 4 months after the initial MVR and one patient with severe calcification of PML underwent valve replacement due to recurrence of MR. Among the remaining cohort (mean follow-up 3.0 ± 1.0 years), NYHA class I, II and III was present in 13, 6, and 1, respectively. TTE demonstrated MR grade 0, 1+, or 2+ in 40, 55, and 5%, respectively, with mean and maximum transvalvular gradients ranging at 1.9 ± 1.7 and 4.7 ± 3.3 mmHg, respectively. CONCLUSIONS: A simple and standardized technique facilitates the repair of MR in the presence of Barlow's, simultaneously addressing the height of PML and the position of the anterior leaflet. This technique has proven durable in the mid-term follow-up in our small series and warrants further validation in larger cohorts.
[Mh] Termos MeSH primário: Procedimentos Cirúrgicos Cardíacos/métodos
Cordas Tendinosas/cirurgia
Procedimentos Cirúrgicos Minimamente Invasivos/métodos
Prolapso da Valva Mitral/cirurgia
Valva Mitral/cirurgia
[Mh] Termos MeSH secundário: Ecocardiografia Transesofagiana
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Valva Mitral/diagnóstico por imagem
Prolapso da Valva Mitral/diagnóstico
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1007/s11748-017-0767-z


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[PMID]:28286166
[Au] Autor:Kumar B; Lenert P
[Ad] Endereço:Division of Immunology, University of Iowa, Iowa City. Electronic address: Bharat-Kumar@UIowa.edu.
[Ti] Título:Joint Hypermobility Syndrome: Recognizing a Commonly Overlooked Cause of Chronic Pain.
[So] Source:Am J Med;130(6):640-647, 2017 Jun.
[Is] ISSN:1555-7162
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Joint hypermobility syndrome, also known as benign hypermobility syndrome, is a connective tissue disease characterized by joint instability, chronic pain, and minor skin changes. It shares many clinical features of Ehlers-Danlos syndrome, Hypermobility Type; enough so that many authorities consider them as one disease process. Approximately 3% of the general population is believed to have joint hypermobility syndrome, but despite this high prevalence, due to lack of awareness, heterogeneity of clinical presentation, and reliance on physical examination for diagnosis, it is largely overlooked by primary care physicians as well as by specialists. This leads to delayed or missed opportunities for diagnosis, and inappropriate interventions that frustrate both providers and patients. We review the literature regarding the pathophysiology, diagnosis, treatment options, and prognosis of joint hypermobility syndrome, and advocate for primary care physicians to consider it in the differential diagnosis of patients with chronic pain.
[Mh] Termos MeSH primário: Dor Crônica/etiologia
Síndrome de Ehlers-Danlos/diagnóstico
[Mh] Termos MeSH secundário: Dor Abdominal/etiologia
Síndrome de Ehlers-Danlos/epidemiologia
Síndrome de Ehlers-Danlos/fisiopatologia
Síndrome de Ehlers-Danlos/terapia
Fadiga/etiologia
Cefaleia/etiologia
Seres Humanos
Prolapso da Valva Mitral/etiologia
Dor Musculoesquelética/etiologia
Dor Pélvica/etiologia
Prevalência
Disautonomias Primárias/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


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[PMID]:28261377
[Au] Autor:Songia P; Porro B; Chiesa M; Myasoedova V; Alamanni F; Tremoli E; Poggio P
[Ad] Endereço:Centro Cardiologico Monzino IRCCS, Milan, Italy; Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
[Ti] Título:Identification of Patients Affected by Mitral Valve Prolapse with Severe Regurgitation: A Multivariable Regression Model.
[So] Source:Oxid Med Cell Longev;2017:6838921, 2017.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:. Mitral valve prolapse (MVP) is the most common cause of severe mitral regurgitation. Besides echocardiography, up to now there are no reliable biomarkers available for the identification of this pathology. We aim to generate a predictive model, based on circulating biomarkers, able to identify MVP patients with the highest accuracy. . We analysed 43 patients who underwent mitral valve repair due to MVP and compared to 29 matched controls. We assessed the oxidative stress status measuring the oxidized and the reduced form of glutathione by liquid chromatography-tandem mass spectrometry method. Osteoprotegerin (OPG) plasma levels were measured by an enzyme-linked immunosorbent assay. The combination of these biochemical variables was used to implement several logistic regression models. . Oxidative stress levels and OPG concentrations were significantly higher in patients compared to control subjects (0.116 ± 0.007 versus 0.053 ± 0.013 and 1748 ± 100.2 versus 1109 ± 45.3 pg/mL, respectively; < 0.0001). The best regression model was able to correctly classify 62 samples out of 72 with accuracy in terms of area under the curve of 0.92. . To the best of our knowledge, this is the first study to show a strong association between OPG and oxidative stress status in patients affected by MVP with severe regurgitation.
[Mh] Termos MeSH primário: Biomarcadores/análise
Insuficiência da Valva Mitral/etiologia
Prolapso da Valva Mitral/complicações
Prolapso da Valva Mitral/diagnóstico
[Mh] Termos MeSH secundário: Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
Prolapso da Valva Mitral/sangue
Análise Multivariada
Osteoprotegerina/sangue
Estresse Oxidativo
Análise de Regressão
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Osteoprotegerin); 0 (TNFRSF11B protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE
[do] DOI:10.1155/2017/6838921


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[PMID]:28167462
[Au] Autor:Tarantini G; Masiero G; Cucchini U; Nai Fovino L
[Ad] Endereço:Department of Cardiac, Thoracic and Vascular Sciences, University Hospital of Padua, Padua, Italy.
[Ti] Título:A2-P3 oblique clipping for the treatment of severe mitral regurgitation in the presence of mitral valve cleft and flail.
[So] Source:EuroIntervention;12(15):e1858, 2017 Feb 03.
[Is] ISSN:1969-6213
[Cp] País de publicação:France
[La] Idioma:eng
[Mh] Termos MeSH primário: Anormalidades Cardiovasculares/cirurgia
Insuficiência da Valva Mitral/cirurgia
Prolapso da Valva Mitral/cirurgia
Valva Mitral/cirurgia
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Anormalidades Cardiovasculares/diagnóstico
Doenças das Valvas Cardíacas/diagnóstico
Doenças das Valvas Cardíacas/cirurgia
Seres Humanos
Masculino
Insuficiência da Valva Mitral/diagnóstico
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


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[PMID]:28124513
[Au] Autor:Mihos CG; Yucel E; Santana O
[Ad] Endereço:Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA - cmihos@mgh.harvard.edu.
[Ti] Título:A systematic review and meta-analysis of chordal replacement versus leaflet resection for isolated posterior mitral valve prolapse.
[So] Source:J Cardiovasc Surg (Torino);58(5):779-786, 2017 Oct.
[Is] ISSN:1827-191X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chordal replacement (Chord MVr) for isolated posterior mitral valve prolapse allows for preservation of the native mitral valve apparatus. The potential benefits of this approach, as compared with leaflet resection (Resection), are not clearly defined. EVIDENCE ACQUISITION: A systematic review and meta-analysis was conducted on operative, clinical, and echocardiographic outcomes. Risk ratios (RR) were calculated by the Mantel-Haenszel method under a fixed or random effects model, as appropriate. EVIDENCE SYNTHESIS: Eight studies were included, with a total of 1922 patients (Chord MVr, N.=835; Resection, N.=1087). Baseline characteristics were similar, except for a higher incidence of atrial fibrillation in the Chord MVr group (15.5% versus 9.9%, P=0.03), and a slightly greater mitral regurgitation grade in the Resection group (3.5 versus 3.4, P=0.008). P2 segment prolapse was the most common pathology, however, patients undergoing Chord MVr had a higher incidence of multi-segment prolapse (32.1% versus 13.9%, P=0.0006). There was no difference in operative mortality (1.1% for both) or perioperative complications. At a mean follow-up of 2.9±2.8 years (median=2.8 years, IQR 1.6-4.4), Chord MVr was associated with a lower risk of reoperation (1.1% versus 4.3%; RR 0.26, 95% CI 0.12-0.56, P=0.0007), and similar survival and recurrence of moderate mitral regurgitation, when compared with Resection. Finally, a lower transmitral gradient (2.5 versus 2.8 mmHg, P=0.0004) and larger orifice area (3.2 versus 3.0 cm2, P=0.002) were observed with Chord MVr. CONCLUSIONS: At 2.9-year follow-up, Chord MVr for isolated posterior mitral valve prolapse was associated with a lower reoperation rate and favorable valve hemodynamics, when compared with leaflet resection.
[Mh] Termos MeSH primário: Cordas Tendinosas/transplante
Implante de Prótese de Valva Cardíaca/instrumentação
Próteses Valvulares Cardíacas
Anuloplastia da Valva Mitral/instrumentação
Insuficiência da Valva Mitral/cirurgia
Prolapso da Valva Mitral/cirurgia
Valva Mitral/transplante
[Mh] Termos MeSH secundário: Adulto
Idoso
Distribuição de Qui-Quadrado
Cordas Tendinosas/diagnóstico por imagem
Cordas Tendinosas/fisiopatologia
Ecocardiografia
Feminino
Implante de Prótese de Valva Cardíaca/efeitos adversos
Implante de Prótese de Valva Cardíaca/mortalidade
Hemodinâmica
Seres Humanos
Masculino
Meia-Idade
Valva Mitral/diagnóstico por imagem
Valva Mitral/fisiopatologia
Anuloplastia da Valva Mitral/efeitos adversos
Anuloplastia da Valva Mitral/mortalidade
Insuficiência da Valva Mitral/diagnóstico por imagem
Insuficiência da Valva Mitral/mortalidade
Insuficiência da Valva Mitral/fisiopatologia
Prolapso da Valva Mitral/diagnóstico por imagem
Prolapso da Valva Mitral/mortalidade
Prolapso da Valva Mitral/fisiopatologia
Desenho de Prótese
Recuperação de Função Fisiológica
Recidiva
Reoperação
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE
[do] DOI:10.23736/S0021-9509.17.09634-3


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[PMID]:28121998
[Au] Autor:Martins CO; Demarchi L; Ferreira FM; Pomerantzeff PM; Brandao C; Sampaio RO; Spina GS; Kalil J; Cunha-Neto E; Guilherme L
[Ad] Endereço:Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.
[Ti] Título:Rheumatic Heart Disease and Myxomatous Degeneration: Differences and Similarities of Valve Damage Resulting from Autoimmune Reactions and Matrix Disorganization.
[So] Source:PLoS One;12(1):e0170191, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoimmune inflammatory reactions leading to rheumatic fever (RF) and rheumatic heart disease (RHD) result from untreated Streptococcus pyogenes throat infections in individuals who exhibit genetic susceptibility. Immune effector mechanisms have been described that lead to heart tissue damage culminating in mitral and aortic valve dysfunctions. In myxomatous valve degeneration (MXD), the mitral valve is also damaged due to non-inflammatory mechanisms. Both diseases are characterized by structural valve disarray and a previous proteomic analysis of them has disclosed a distinct profile of matrix/structural proteins differentially expressed. Given their relevance in organizing valve tissue, we quantitatively evaluated the expression of vimentin, collagen VI, lumican, and vitronectin as well as performed immunohistochemical analysis of their distribution in valve tissue lesions of patients in both diseases. We identified abundant expression of two isoforms of vimentin (45 kDa, 42 kDa) with reduced expression of the full-size protein (54 kDa) in RHD valves. We also found increased vitronectin expression, reduced collagen VI expression and similar lumican expression between RHD and MXD valves. Immunohistochemical analysis indicated disrupted patterns of these proteins in myxomatous degeneration valves and disorganized distribution in rheumatic heart disease valves that correlated with clinical manifestations such as valve regurgitation or stenosis. Confocal microscopy analysis revealed a diverse pattern of distribution of collagen VI and lumican into RHD and MXD valves. Altogether, these results demonstrated distinct patterns of altered valve expression and tissue distribution/organization of structural/matrix proteins that play important pathophysiological roles in both valve diseases.
[Mh] Termos MeSH primário: Doenças Autoimunes/patologia
Prolapso da Valva Mitral/patologia
Cardiopatia Reumática/patologia
[Mh] Termos MeSH secundário: Adulto
Doenças Autoimunes/imunologia
Doenças Autoimunes/metabolismo
Colágeno Tipo VI/análise
Matriz Extracelular/química
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Lumicana/análise
Masculino
Meia-Idade
Valva Mitral/química
Prolapso da Valva Mitral/etiologia
Prolapso da Valva Mitral/imunologia
Prolapso da Valva Mitral/metabolismo
Domínios Proteicos
Proteômica
Cardiopatia Reumática/imunologia
Cardiopatia Reumática/metabolismo
Vimentina/análise
Vitronectina/análise
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type VI); 0 (LUM protein, human); 0 (Lumican); 0 (Vimentin); 0 (Vitronectin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0170191



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