Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Tipo de documento: | Tese |
Idioma: | por |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7321776 https://repositorio.unifesp.br/handle/11600/53022 |
Resumo: | Introduction: Idiopathic pulmonary arterial hypertension (IPAH) is characterized by pulmonary vascular remodeling and an associated increased pulmonary vascular resistante (PVR), which over time, can lead to right ventricular (RV) dysfunction. IPAH´s exercise tolerance, clinical evolution and survival are known to be associated with the RV adaptation to its increased afterload. However, little is known regarding the specific hemodynamic mechanisms associated with a reduced aerobic capacity in patients with severe IPAH. Objectives: To evaluate the hemodynamic mechanisms associated with peak oxygen consumption (V̇ O2) during exercise in patients with IPAH; to describe the hemodynamic patterns during exercise right heart catheterization in IPAH; and to identify the hemodynamic predictors of peak V̇ O2. Methods: Twenty patients with IPAH from the Pulmonary Hypertension Outpatient Clinic of the Federal University of São Paulo between September 2014 and March 2016 were included in the current study. All patients were submitted to contemporary pulmonary functional test, a sixminute walk test, transthoracic echocardiography, cardiopulmonary exercise testing (CPET) and resting supine right heart catheterization (RHC) followed by exercise hemodynamic assessment. Results: 85% of the patients were female, with a median age of 34[2942] and 95% were New York Heart Association functional class (NYHAFC) II or III. During exercise right heart catheterization, peak work was 30[2030] W, peak mean pulmonary arterial pressure was 76 ± 17 mmHg, peak pulmonary arterial wedge pressure was 14 ± 5 mmHg, peak PVR was 959 ± 401 dynes.s.cm5. Peak cardiac output (CO) and the peak cardiac index (CI) were 5,7 ± 1,9 L/min and 3,5 ± 1,2 L/min/m2, respectively. Peak stroke volume index (SVI) was 29 ± 12 mL/m², peak right ventricular stroke work index (RVSWI) was 29 ± 14 g/m2/bat and peak pulmonary vascular compliance (PVC) was 0,9[0,61,2] ml/mmHg. There was a positive correlation between peak V̇ O2 and peak CO (r=0,528; p=0,017), peak CI (r=0,599; p=0,005), peak SVI (r=0,494; p=0,027), peak RVSWI (r=0,543; p=0,013) and peak peripheral oxygen saturation (peak SpO2) (r=0,408; p=0,074). There was a negative correlation between peak V̇ O2 and ΔPVC (r=0,409; p=0,073). By univariate analysis, peak CO, peak CI, peak SVI, peak RVSWI, ΔPVC and peak SpO2 were predictors of peak V̇ O2. By multivariate analysis adjusted for age, only peak RVSWI (Coefficient= 0,145, CI 95% [0,0720,2219], p=0,001) and ΔPVC (Coefficient=2,510, CI 95% [4,344( 0,677)], p=0,01) remained independent predictors of peak V̇ O2. Conclusions: In IPAH, increased peak RVSWI and decreased ΔPVC during exercise are associated with a reduced peak V̇ O2. Given that RVSWI and ΔPVC represent the RV contractility and its afterload, respectively, the study findings suggest that RVpulmonary arterial coupling determine maximal aerobic capacity in IPAH. |
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Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênioExercise heart catheterization in idiopathic pulmonary arterial hypertension: evaluation of the hemodynamic pathophysiological mechanisms associated with maximal oxygen consumptionPulmonary hypertensionHemodynamicsCardiac catheterizationMaximum oxygen consumptionHipertensão pulmonarHemodinâmicaCateterismo cardíacoExercícioConsumo máximo de oxigênioIntroduction: Idiopathic pulmonary arterial hypertension (IPAH) is characterized by pulmonary vascular remodeling and an associated increased pulmonary vascular resistante (PVR), which over time, can lead to right ventricular (RV) dysfunction. IPAH´s exercise tolerance, clinical evolution and survival are known to be associated with the RV adaptation to its increased afterload. However, little is known regarding the specific hemodynamic mechanisms associated with a reduced aerobic capacity in patients with severe IPAH. Objectives: To evaluate the hemodynamic mechanisms associated with peak oxygen consumption (V̇ O2) during exercise in patients with IPAH; to describe the hemodynamic patterns during exercise right heart catheterization in IPAH; and to identify the hemodynamic predictors of peak V̇ O2. Methods: Twenty patients with IPAH from the Pulmonary Hypertension Outpatient Clinic of the Federal University of São Paulo between September 2014 and March 2016 were included in the current study. All patients were submitted to contemporary pulmonary functional test, a sixminute walk test, transthoracic echocardiography, cardiopulmonary exercise testing (CPET) and resting supine right heart catheterization (RHC) followed by exercise hemodynamic assessment. Results: 85% of the patients were female, with a median age of 34[2942] and 95% were New York Heart Association functional class (NYHAFC) II or III. During exercise right heart catheterization, peak work was 30[2030] W, peak mean pulmonary arterial pressure was 76 ± 17 mmHg, peak pulmonary arterial wedge pressure was 14 ± 5 mmHg, peak PVR was 959 ± 401 dynes.s.cm5. Peak cardiac output (CO) and the peak cardiac index (CI) were 5,7 ± 1,9 L/min and 3,5 ± 1,2 L/min/m2, respectively. Peak stroke volume index (SVI) was 29 ± 12 mL/m², peak right ventricular stroke work index (RVSWI) was 29 ± 14 g/m2/bat and peak pulmonary vascular compliance (PVC) was 0,9[0,61,2] ml/mmHg. There was a positive correlation between peak V̇ O2 and peak CO (r=0,528; p=0,017), peak CI (r=0,599; p=0,005), peak SVI (r=0,494; p=0,027), peak RVSWI (r=0,543; p=0,013) and peak peripheral oxygen saturation (peak SpO2) (r=0,408; p=0,074). There was a negative correlation between peak V̇ O2 and ΔPVC (r=0,409; p=0,073). By univariate analysis, peak CO, peak CI, peak SVI, peak RVSWI, ΔPVC and peak SpO2 were predictors of peak V̇ O2. By multivariate analysis adjusted for age, only peak RVSWI (Coefficient= 0,145, CI 95% [0,0720,2219], p=0,001) and ΔPVC (Coefficient=2,510, CI 95% [4,344( 0,677)], p=0,01) remained independent predictors of peak V̇ O2. Conclusions: In IPAH, increased peak RVSWI and decreased ΔPVC during exercise are associated with a reduced peak V̇ O2. Given that RVSWI and ΔPVC represent the RV contractility and its afterload, respectively, the study findings suggest that RVpulmonary arterial coupling determine maximal aerobic capacity in IPAH.Introdução: A hipertensão arterial pulmonar idiopática (HAPI) é caracterizada pelo comprometimento das artérias pulmonares de pequeno calibre, com consequente aumento da resistência vascular pulmonar (RVP) e potencial evolução para disfunção ventricular direita. Entendese, atualmente, que a capacidade de exercício, a evolução clínica e a sobrevida dos pacientes com HAP está diretamente associada à função do ventrículo direito (VD) à habilidade de adaptação do VD frente ao incremento da póscarga. Entretanto, os mecanismos hemodinâmicos fisiopatológicos ao exercício relacionados à capacidade aeróbica na HAP não estão completamente estabelecidos. Objetivos: Avaliação dos mecanismos fisiopatológicos hemodinâmicos durante o esforço associados ao consumo de oxigênio no pico do exercício (V̇ O2PICO) em uma amostra de indivíduos com HAP idiopática (HAPI); descrever o comportamento hemodinâmico durante o exercício avaliado de forma invasiva em indivíduos com HAPI; e identificar os parâmetros hemodinâmicos invasivos associados ao V̇ O2PICO. Métodos: Foram incluídos 20 pacientes com HAPI do Ambulatório de Circulação Pulmonar da Universidade Federal de São Paulo no período de setembro de 2014 até março de 2016. Eles realizaram prospectivamente os seguintes exames: prova de função pulmonar completa, teste de caminhada de 6 minutos, ecodopplercardiograma transtorácico, teste de exercício cardiopulmonar (TECP) incremental, cateterismo cardíaco direito no repouso e de exercício e coleta de gasometria arterial e venosa mista. Resultados: 85% da amostra era do sexo feminino, com mediana de idade de 34[2942] e 95% encontravase em classe funcional New York Heart Association II e III. No cateterismo cardíaco direito de exercício a carga pico foi de 30[2030] W, a pressão média da artéria pulmonar pico foi 76 ± 17 mmHg, a pressão de oclusão da artéria pulmonar pico foi 14 ± 5 mmHg, a RVPPICO foi 959 ± 401 dinas.s/cm5. O débito cardíaco pico (DCPICO) e o índice cardíaco pico (ICPICO) foram de 5,7 ± 1,9 L/min e 3,5 ± 1,2 L/min/m2, respectivamente, o volume sistólico indexado pico foi de (VSiPICO) foi 29 ± 12 ml/m², o índice de trabalho sistólico do VD (ITSVDPICO) foi de 29 ± 14 g/m2/bat e a complacência vascular pulmonar (CVPPICO) foi 0,9[0,61,2] ml/mmHg. Houve correlação positiva entre o V̇ O2PICO com o DCPICO (r:0,528; p:0,017), ICPICO (r:0,599; p:0,005), VSiPICO (r:0,494; p:0,027), o ITSVDPICO (r:0,543; p:0,013) e a saturação da hemoglobina pelo oxigênio por oximetria de pulso (SpO2PICO) (r:0,408; p:0,074). Houve correlação negativa com o ΔCVP (r:0,409; p:0,073). Na análise univariada o DCPICO, ICPICO, o ITSVDPICO, o ΔCVP e a SpO2PICO foram preditores do V̇ O2PICO. Na análise multivariada ajustada por idade, apenas o ITSVDPICO (Coeficiente: 0,145, IC 95% [0,0720,2219], p:0,001) e o ΔCVP (Coeficiente:2,510, IC 95% [4,344( 0,677)], p:0,01) permaneceram como preditores independentes do V̇ O2PICO. Conclusão: o aumento do ITSVD e a redução do ΔCVP durante o cateterismo cardíaco direito de exercício estão associados à redução do V̇ O2PICO. Essas variáveis representam, respectivamente, a póscarga e, indiretamente, à contratilidade do VD e quando analisadas em conjunto, refletem o papel do acoplamento ventrículoarterial na determinação da capacidade aeróbica máxima na HAP.Dados abertos - Sucupira - Teses e dissertações (2018)Universidade Federal de São Paulo (UNIFESP)Arakaki, Jaquelina Sonoe Ota [UNIFESP]Ferreira, Eloara Vieira Machado [UNIFESP]Oliveira, Rudolf Krawczenko Feitoza de [UNIFESP]http://lattes.cnpq.br/6639042770205771http://lattes.cnpq.br/7475520878817375http://lattes.cnpq.br/4282849546206947http://lattes.cnpq.br/7415297086270978Universidade Federal de São Paulo (UNIFESP)Messina, Carolina Montemor Soares [UNIFESP]2020-03-25T12:10:51Z2020-03-25T12:10:51Z2018-05-24info:eu-repo/semantics/doctoralThesisinfo:eu-repo/semantics/publishedVersion129 f.application/pdfhttps://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=73217762018-0967.pdfhttps://repositorio.unifesp.br/handle/11600/53022porSão Pauloinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-10T16:31:30Zoai:repositorio.unifesp.br/:11600/53022Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-10T16:31:30Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio Exercise heart catheterization in idiopathic pulmonary arterial hypertension: evaluation of the hemodynamic pathophysiological mechanisms associated with maximal oxygen consumption |
title |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
spellingShingle |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio Messina, Carolina Montemor Soares [UNIFESP] Pulmonary hypertension Hemodynamics Cardiac catheterization Maximum oxygen consumption Hipertensão pulmonar Hemodinâmica Cateterismo cardíaco Exercício Consumo máximo de oxigênio |
title_short |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
title_full |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
title_fullStr |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
title_full_unstemmed |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
title_sort |
Cateterismo cardíaco de exercício na hipertensão arterial pulmonar idiopática: avaliação dos mecanismos hemodinâmicos fisiopatológicos associados ao consumo máximo de oxigênio |
author |
Messina, Carolina Montemor Soares [UNIFESP] |
author_facet |
Messina, Carolina Montemor Soares [UNIFESP] |
author_role |
author |
dc.contributor.none.fl_str_mv |
Arakaki, Jaquelina Sonoe Ota [UNIFESP] Ferreira, Eloara Vieira Machado [UNIFESP] Oliveira, Rudolf Krawczenko Feitoza de [UNIFESP] http://lattes.cnpq.br/6639042770205771 http://lattes.cnpq.br/7475520878817375 http://lattes.cnpq.br/4282849546206947 http://lattes.cnpq.br/7415297086270978 Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Messina, Carolina Montemor Soares [UNIFESP] |
dc.subject.por.fl_str_mv |
Pulmonary hypertension Hemodynamics Cardiac catheterization Maximum oxygen consumption Hipertensão pulmonar Hemodinâmica Cateterismo cardíaco Exercício Consumo máximo de oxigênio |
topic |
Pulmonary hypertension Hemodynamics Cardiac catheterization Maximum oxygen consumption Hipertensão pulmonar Hemodinâmica Cateterismo cardíaco Exercício Consumo máximo de oxigênio |
description |
Introduction: Idiopathic pulmonary arterial hypertension (IPAH) is characterized by pulmonary vascular remodeling and an associated increased pulmonary vascular resistante (PVR), which over time, can lead to right ventricular (RV) dysfunction. IPAH´s exercise tolerance, clinical evolution and survival are known to be associated with the RV adaptation to its increased afterload. However, little is known regarding the specific hemodynamic mechanisms associated with a reduced aerobic capacity in patients with severe IPAH. Objectives: To evaluate the hemodynamic mechanisms associated with peak oxygen consumption (V̇ O2) during exercise in patients with IPAH; to describe the hemodynamic patterns during exercise right heart catheterization in IPAH; and to identify the hemodynamic predictors of peak V̇ O2. Methods: Twenty patients with IPAH from the Pulmonary Hypertension Outpatient Clinic of the Federal University of São Paulo between September 2014 and March 2016 were included in the current study. All patients were submitted to contemporary pulmonary functional test, a sixminute walk test, transthoracic echocardiography, cardiopulmonary exercise testing (CPET) and resting supine right heart catheterization (RHC) followed by exercise hemodynamic assessment. Results: 85% of the patients were female, with a median age of 34[2942] and 95% were New York Heart Association functional class (NYHAFC) II or III. During exercise right heart catheterization, peak work was 30[2030] W, peak mean pulmonary arterial pressure was 76 ± 17 mmHg, peak pulmonary arterial wedge pressure was 14 ± 5 mmHg, peak PVR was 959 ± 401 dynes.s.cm5. Peak cardiac output (CO) and the peak cardiac index (CI) were 5,7 ± 1,9 L/min and 3,5 ± 1,2 L/min/m2, respectively. Peak stroke volume index (SVI) was 29 ± 12 mL/m², peak right ventricular stroke work index (RVSWI) was 29 ± 14 g/m2/bat and peak pulmonary vascular compliance (PVC) was 0,9[0,61,2] ml/mmHg. There was a positive correlation between peak V̇ O2 and peak CO (r=0,528; p=0,017), peak CI (r=0,599; p=0,005), peak SVI (r=0,494; p=0,027), peak RVSWI (r=0,543; p=0,013) and peak peripheral oxygen saturation (peak SpO2) (r=0,408; p=0,074). There was a negative correlation between peak V̇ O2 and ΔPVC (r=0,409; p=0,073). By univariate analysis, peak CO, peak CI, peak SVI, peak RVSWI, ΔPVC and peak SpO2 were predictors of peak V̇ O2. By multivariate analysis adjusted for age, only peak RVSWI (Coefficient= 0,145, CI 95% [0,0720,2219], p=0,001) and ΔPVC (Coefficient=2,510, CI 95% [4,344( 0,677)], p=0,01) remained independent predictors of peak V̇ O2. Conclusions: In IPAH, increased peak RVSWI and decreased ΔPVC during exercise are associated with a reduced peak V̇ O2. Given that RVSWI and ΔPVC represent the RV contractility and its afterload, respectively, the study findings suggest that RVpulmonary arterial coupling determine maximal aerobic capacity in IPAH. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-05-24 2020-03-25T12:10:51Z 2020-03-25T12:10:51Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/doctoralThesis |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
doctoralThesis |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7321776 2018-0967.pdf https://repositorio.unifesp.br/handle/11600/53022 |
url |
https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7321776 https://repositorio.unifesp.br/handle/11600/53022 |
identifier_str_mv |
2018-0967.pdf |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
129 f. application/pdf |
dc.coverage.none.fl_str_mv |
São Paulo |
dc.publisher.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
publisher.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
_version_ |
1814268461524713472 |