Author + information
- Jacquelyn P. Kulinski, MD∗ (, )
- Julia Kozlitina, PhD,
- Jarett D. Berry, MD, MS,
- James A. de Lemos, MD and
- Amit Khera, MD, MSc
- ↵∗Department of Internal Medicine, Division of Cardiovascular Medicine, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Suite 5100, Milwaukee, Wisconsin 53226
Habitual sedentary behavior has been associated with incident cardiovascular disease, regardless of physical activity (1). However, there are currently no published data on the relationship between objectively measured sedentary behavior and coronary artery calcium (CAC), and increased subclinical atherosclerosis may represent an additional mechanism through which sedentary behavior influences cardiovascular (CVD) risk. We sought to investigate the association between accelerometer measured sedentary behavior and CAC using data from the Dallas Heart Study (DHS).
The DHS is a longitudinal, multiethnic population-based probability sample of Dallas County residents, with oversampling of black individuals to ensure approximately 50% of black and nonblack participants. Details of the study design and recruitment procedures have been previously described (2). Briefly, 2,201 participants from DHS-2 had available measures of both physical activity and CAC. After exclusions (<4 days of accelerometer wear, missing medical history), 2,031 participants were included in this analysis.
Measurements of CAC were performed with multidetector computed tomography (Toshiba Aquilion 64-slice), reported in Agatston units. Participants wore an Actical (Philips Respironics, Bend, Oregon) activity monitor on their nondominant wrist for 7 days. Detailed accelerometer data processing and quality control procedures have been previously published (3). Moderate-to-vigorous physical activity (MVPA) was quantified using established thresholds (>1,500 counts/min). Sedentary time was defined as <100 counts/min (4). The associations of sedentary time with CAC prevalence (CAC >10) and continuous CAC score were assessed using logistic and Tobit regression analyses, respectively.
The mean age of the study population was 50 ± 10 years (62% women). Participants spent an average of 5.1 h between 8 AM and 8 PM (range 1.1 to 11.6 h) in sedentary time and an average of 29 min (range 0 to 200 min) in MVPA per day. Higher sedentary time burden was associated with older age, higher body mass index, diabetes and hypertension, and a higher prevalence of CAC (p < 0.001).
After multivariable adjustment, each additional hour of daily sedentary time was associated with a 12% higher odds of having any CAC (model 4, Table 1). This association was maintained in a sensitivity analysis with sedentary time defined as ≤200 counts/min (OR: 1.15; 95% confidence interval: 1.04 to 1.28; p = 0.006). In Tobit regression analyses, each hour of sedentary time was associated with a 16% increase in CAC score (Table 1). In the fully adjusted model, the association between MVPA and CAC was not significant (p = 0.16) (Table 1).
In this study, we observed a significant association between increasing sedentary time and CAC in participants without known CVD. These associations were independent of exercise activity, traditional CVD risk factors, and socioeconomic factors. This suggests that increased subclinical atherosclerosis may be one of the mechanisms through which sedentary behavior increases cardiovascular risk and differs from the cardioprotective mechanisms of exercise activity. From a prevention standpoint, strategies designed to decrease the burden of sedentary behavior may represent a novel companion strategy (in addition to exercise) to reduce cardiovascular risk, particularly in an increasingly sedentary society in which people spend more time sitting and many do not meet physical activity guideline recommendations.
The strengths of our study include quantification of physical activity and sedentary behavior using accelerometer data rather than self-report. We used a large, multiethnic, population-based sample, which is free from selection bias inherent in some study designs and is more generalizable to the population at large.
Notable limitations are that a single week of physical activity monitoring may not be representative of one’s lifetime exercise habits, but with a large population, these tendencies should be randomly distributed. Additionally, this is a cross-sectional study design that limits our ability to assess for causality.
Increasing sedentary time was associated with subclinical atherosclerosis in a large, representative sample. Reducing daily “sitting time” by even 1 to 2 h per day could have a significant and positive impact on future cardiovascular health, and this hypothesis should be investigated in future studies targeting novel interventions to reduce the burden of sedentary behaviors.
Please note: Dr. Berry has received consultant fees/honoraria from Nihon; and is a member of the Speakers Bureau for Merck. Dr. de Lemos has received consultant fees/honoraria from Amgen, DiaDexus, Data and Safety Monitoring Board for Novo Nordisk, St. Jude Medical, and Siemen’s Diagnostics; and research grants from Abbott Diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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