Irregular sleep duration and timing associated with increased risk of CVD

Introduction and methods

Circadian mechanisms might play a role in the pathogenesis of CVD [1-3]. Certain forms of disrupted circadian rhythms are linked to increased CVD risk, such as shift work and transition to daylight savings time [4-6]. In addition, circadian disruption may be a ubiquitous phenomenon not only restricted to specific settings such as in shift workers, and may accumulate over time. For example, it has been demonstrated that disrupted circadian rhythms due to frequently altering sleep duration or timing may result in higher cardiometabolic risk and CVD [7-15]. However, such exposure to chronic circadian disruption on CV health has not been addressed at the population level.

The present study examined the association between sleep regularity (sleep duration and sleep-onset timing) and CVD risk using data from the MESA (Multi-Ethnic Study of Atherosclerosis) cohort, a prospective study of clinical risk factors of atherosclerosis [16]. Included for analysis in the present study were CVD-free participants (n=1992 after implementing exclusion criteria) from 6 field centres across the United States. Participants completed sleep examination in the MESA Sleep Ancillary Study at MESA Exam 5 (2010 to 2013), including 7-day wrist actigraphy, 1 night of at-home polysomnography, and questionnaire-based sleep assessment [17]. The primary sleep regularity measure was 7-day SD of sleep duration or sleep-onset timing. Participants were divided into 4 groups in 30-min increments of 7-day SD sleep duration and timing to allow sufficient numbers of CVD cases in each group. Due to the different data distributions, the categories were ≤60, 61 to 90, 91 to 120, and >120 min for sleep duration SD and ≤30, 31 to 60, 61 to 90, and >90 min for sleep-onset timing SD. Primary endpoint of the present study was defined as incident total CVD events, including CHD death, myocardial infarction, angina followed by revascularization, resuscitated cardiac arrest, stroke, death from stroke, and other atherosclerotic or CVD deaths. Median follow-up was 4.9 years.

Main results

• Participants with higher (≥90 min, n=786) versus lower (<90 min, n=1206) sleep duration SD and higher sleep-onset timing SD (≥90 min, n=510) vs lower (<90 min, n=1482) in general had worse metabolic parameters, including higher levels of body mass index, higher systolic BP, higher diastolic BP, higher diabetes prevalence, higher heart rate during sleep, and were more likely to be current smoker.
• Compared with sleep duration SD ≤60 min, the HRs (95% CIs) of incident CVD risk, after adjustment for CVD risk factors and sleep-related factors, were 1.09 (0.62-1.92) for sleep duration SD 61 to 90 min, 1.59 (0.91-2.76) for 91 to 120 min, and 2.14 (1.24-3.68) for >120 min, with 39% higher risk (95% CI: 1.08-1.78; P-trend=0.002) for every 1-h increase in sleep duration SD.
• Compared with sleep-onset timing SD ≤30 min, the HRs (95% CIs) of incident CVD risk, after adjusting for CVD risk factors and sleep-related factors, were 1.16 (0.64-2.13) for 31 to 60 min, 1.52 (0.81-2.88) for 61 to 90 min, and 2.11 (1.13-3.91) for >90 min, with 18% higher risk (95% CI: 1.06-1.31; P-trend=0.002) for every 1-h increase in sleep-onset timing SD.

Conclusion

References

Find this article online at J Am Coll Cardiol.