Accelerometer-Measured Sedentary Behavior and Risk of Future Cardiovascular Disease
- PMID: 39545903
- PMCID: PMC11851520
- DOI: 10.1016/j.jacc.2024.10.065
Accelerometer-Measured Sedentary Behavior and Risk of Future Cardiovascular Disease
Abstract
Background: Beyond serving as a marker for insufficient physical activity, sedentary behavior may directly affect future cardiovascular (CV) disease risk.
Objectives: This study sought to examine associations between accelerometer-measured sedentary behavior with risk of specific CV outcomes, including potential relations with moderate to vigorous physical activity (MVPA).
Methods: Among participants of the UK Biobank prospective cohort study, we fit Cox models adjusted for demographic and lifestyle factors to assess associations between accelerometer-measured daily sedentary time with incident atrial fibrillation (AF), myocardial infarction (MI), heart failure (HF), and CV mortality. We assessed the potential effect of MVPA on associations between sedentary time and CV disease by including MVPA as an adjustment variable, as well as performing subgroup analyses stratified at the guideline-recommended MVPA threshold (ie, ≥150 min/wk). We then performed compositional analyses to estimate the effects of reallocating sedentary time to other activities.
Results: Among 89,530 individuals (age 62 ± 8 years, 56.4% women) undergoing 1 week of accelerometry, median sedentary time was 9.4 h/d (Q1-Q3: 8.2-10.6). In multivariable models, using the second quartile (8.2-9.4 h/d) as a referent, sedentary time in the top quartile (>10.6 h/d) was associated with greater risks of HF (HR: 1.45; 95% CI: 1.28-1.65) and CV mortality (HR: 1.62; 95% CI: 1.34-1.96), with an inflection of risk at 10.6 h/d. Higher sedentary time was also associated with greater risks of incident AF (HR: 1.11; 95% CI: 1.01-1.21) and MI (HR: 1.15; 95% CI: 1.00-1.32), with an approximately linear relation. Associations with HF and CV mortality persisted among individuals meeting guideline-recommended MVPA levels. Among individuals with >10.6 h/d of sedentary time, reallocating sedentary behavior to other activities substantially reduced the excess CV risk conferred by sedentary behavior (eg, 30-minute decrease in sedentary time for HF: HR: 0.93; 95% CI: 0.90-0.96), even among individuals meeting guideline-recommended MVPA (HR: 0.93; 95% CI: 0.87-0.99).
Conclusions: Sedentary behavior is broadly associated with future adverse CV outcomes, with particularly prominent effects on HF and CV mortality, where risk inflected at approximately 10.6 h/d. Although guideline-adherent MVPA partially mitigates excess risk, optimizing sedentary behavior appears to be important even among physically active individuals.
Keywords: accelerometer; atrial fibrillation; cardiovascular; heart failure; mortality; myocardial infarction; sedentary; sitting.
Copyright © 2025 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Funding Support and Author Disclosures Dr Ajufo is supported by the John S. LaDue Memorial Fellowship in Cardiovascular Medicine or Vascular Biology grant. Dr Kany is supported by the Walter Benjamin Fellowship from the Deutsche Forschungsgemeinschaft (521832260). Dr Rämö is supported by a research fellowship from the Sigrid Jusélius Foundation. Dr Churchill is supported by the National Institutes of Health (K23HL159262-01A1). Dr Guseh is supported by the American Heart Association (19AMFDP34990046) and the President and Fellows of Harvard College (5KL2TR002542-04). Dr Aragam is supported by grants from the National Institutes of Health (1K08HL153937) and the American Heart Association (862032); receives sponsored research support from Sarepta Therapeutics and Bayer AG; and receives a research collaboration with the Novartis Institutes for Biomedical Research. Dr Ellinor is supported by grants from the National Institutes of Health (RO1HL092577, R01HL157635), from the American Heart Association (18SFRN34230127, 961045), and from the European Union (MAESTRIA 965286); receives sponsored research support from Bayer AG, IBM Research, Bristol Myers Squibb, Pfizer and Novo Nordisk; and has served on Advisory Boards and/or consulted for Bayer AG. Dr Khurshid is supported by the NIH (K23HL169839-01) and the American Heart Association (2023CDA1050571).
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