Wearable device-measured moderate to vigorous physical activity and risk of degenerative aortic valve stenosis.

Aortic regurgitation Aortic stenosis Aortic valve replacement Exercise Mitral regurgitation

Journal

European heart journal
ISSN: 1522-9645
Titre abrégé: Eur Heart J
Pays: England
ID NLM: 8006263

Informations de publication

Date de publication:
02 Jul 2024
Historique:
received: 27 08 2023
revised: 04 04 2024
accepted: 17 06 2024
medline: 2 7 2024
pubmed: 2 7 2024
entrez: 2 7 2024
Statut: aheadofprint

Résumé

Physical activity has proven effective in preventing atherosclerotic cardiovascular disease, but its role in preventing degenerative valvular heart disease (VHD) remains uncertain. This study aimed to explore the dose-response association between moderate to vigorous physical activity (MVPA) volume and the risk of degenerative VHD among middle-aged adults. A full week of accelerometer-derived MVPA data from 87 248 UK Biobank participants (median age 63.3, female: 56.9%) between 2013 and 2015 were used for primary analysis. Questionnaire-derived MVPA data from 361 681 UK Biobank participants (median age 57.7, female: 52.7%) between 2006 and 2010 were used for secondary analysis. The primary outcome was the diagnosis of incident degenerative VHD, including aortic valve stenosis (AS), aortic valve regurgitation (AR), and mitral valve regurgitation (MR). The secondary outcome was VHD-related intervention or mortality. In the accelerometer-derived MVPA cohort, 555 incident AS, 201 incident AR, and 655 incident MR occurred during a median follow-up of 8.11 years. Increased MVPA volume showed a steady decline in AS risk and subsequent AS-related intervention or mortality risk, levelling off beyond approximately 300 min/week. In contrast, its association with AR or MR incidence was less apparent. The adjusted rates of AS incidence (95% confidence interval) across MVPA quartiles (Q1-Q4) were 11.60 (10.20, 13.20), 7.82 (6.63, 9.23), 5.74 (4.67, 7.08), and 5.91 (4.73, 7.39) per 10 000 person-years. The corresponding adjusted rates of AS-related intervention or mortality were 4.37 (3.52, 5.43), 2.81 (2.13, 3.71), 1.93 (1.36, 2.75), and 2.14 (1.50, 3.06) per 10 000 person-years, respectively. Aortic valve stenosis risk reduction was also observed with questionnaire-based MVPA data [adjusted absolute difference Q4 vs. Q1: AS incidence, -1.41 (-.67, -2.14) per 10 000 person-years; AS-related intervention or mortality, -.38 (-.04, -.88) per 10 000 person-years]. The beneficial association remained consistent in high-risk populations for AS, including patients with hypertension, obesity, dyslipidaemia, and chronic kidney disease. Higher MVPA volume was associated with a lower risk of developing AS and subsequent AS-related intervention or mortality. Future research needs to validate these findings in diverse populations with longer durations and repeated periods of activity monitoring.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Physical activity has proven effective in preventing atherosclerotic cardiovascular disease, but its role in preventing degenerative valvular heart disease (VHD) remains uncertain. This study aimed to explore the dose-response association between moderate to vigorous physical activity (MVPA) volume and the risk of degenerative VHD among middle-aged adults.
METHODS METHODS
A full week of accelerometer-derived MVPA data from 87 248 UK Biobank participants (median age 63.3, female: 56.9%) between 2013 and 2015 were used for primary analysis. Questionnaire-derived MVPA data from 361 681 UK Biobank participants (median age 57.7, female: 52.7%) between 2006 and 2010 were used for secondary analysis. The primary outcome was the diagnosis of incident degenerative VHD, including aortic valve stenosis (AS), aortic valve regurgitation (AR), and mitral valve regurgitation (MR). The secondary outcome was VHD-related intervention or mortality.
RESULTS RESULTS
In the accelerometer-derived MVPA cohort, 555 incident AS, 201 incident AR, and 655 incident MR occurred during a median follow-up of 8.11 years. Increased MVPA volume showed a steady decline in AS risk and subsequent AS-related intervention or mortality risk, levelling off beyond approximately 300 min/week. In contrast, its association with AR or MR incidence was less apparent. The adjusted rates of AS incidence (95% confidence interval) across MVPA quartiles (Q1-Q4) were 11.60 (10.20, 13.20), 7.82 (6.63, 9.23), 5.74 (4.67, 7.08), and 5.91 (4.73, 7.39) per 10 000 person-years. The corresponding adjusted rates of AS-related intervention or mortality were 4.37 (3.52, 5.43), 2.81 (2.13, 3.71), 1.93 (1.36, 2.75), and 2.14 (1.50, 3.06) per 10 000 person-years, respectively. Aortic valve stenosis risk reduction was also observed with questionnaire-based MVPA data [adjusted absolute difference Q4 vs. Q1: AS incidence, -1.41 (-.67, -2.14) per 10 000 person-years; AS-related intervention or mortality, -.38 (-.04, -.88) per 10 000 person-years]. The beneficial association remained consistent in high-risk populations for AS, including patients with hypertension, obesity, dyslipidaemia, and chronic kidney disease.
CONCLUSIONS CONCLUSIONS
Higher MVPA volume was associated with a lower risk of developing AS and subsequent AS-related intervention or mortality. Future research needs to validate these findings in diverse populations with longer durations and repeated periods of activity monitoring.

Identifiants

pubmed: 38953786
pii: 7702752
doi: 10.1093/eurheartj/ehae406
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences
ID : 2021-I2M-C&T-A-010
Organisme : Capital's Funds for Health Improvement and Research
ID : 2022-4-4037

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.

Auteurs

Ziang Li (Z)

State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.
Research Center, Institut Universitaire de Cardiologie et de Pneumologie de Québec (Quebec Heart & Lung Institute), Université Laval, 2725 Chemin Sainte-Foy, Québec City, Québec, Canada G1V-4G5.

Sijing Cheng (S)

State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.

Bo Guo (B)

Department of Medicine for Sports and Performing Arts, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.

Lu Ding (L)

Institute for Molecular Bioscience, The University of Queensland, St Lucia, QLD, Australia.
Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.

Yu Liang (Y)

Department of Mathematical Sciences, University of Copenhagen, Copenhagen, Denmark.

Yinghan Shen (Y)

Institute of Computing Technology, Chinese Academy of Sciences, Beijing, China.

Jinyue Li (J)

Key Laboratory of Cardiovascular Epidemiology, Department of Epidemiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.

Yiqing Hu (Y)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Tianxin Long (T)

State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.

Xinli Guo (X)

State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.

Junbo Ge (J)

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.

Runlin Gao (R)

Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, No.167 Beilishi Road, Beijing 100037, China.

Philippe Pibarot (P)

Research Center, Institut Universitaire de Cardiologie et de Pneumologie de Québec (Quebec Heart & Lung Institute), Université Laval, 2725 Chemin Sainte-Foy, Québec City, Québec, Canada G1V-4G5.

Bin Zhang (B)

State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China.
Research Center, Institut Universitaire de Cardiologie et de Pneumologie de Québec (Quebec Heart & Lung Institute), Université Laval, 2725 Chemin Sainte-Foy, Québec City, Québec, Canada G1V-4G5.

Haiyan Xu (H)

Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, No.167 Beilishi Road, Beijing 100037, China.

Marie-Annick Clavel (MA)

Research Center, Institut Universitaire de Cardiologie et de Pneumologie de Québec (Quebec Heart & Lung Institute), Université Laval, 2725 Chemin Sainte-Foy, Québec City, Québec, Canada G1V-4G5.

Yongjian Wu (Y)

Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Science, Peking Union Medical College, No.167 Beilishi Road, Beijing 100037, China.

Classifications MeSH