The impact of sleeping duration on atherosclerosis in the community: insights from the Corinthia study

Sleep is an essential physiologic process whose disturbances have been regarded as a risk factor in various pathophysiologic processes, including atherosclerosis and cardiovascular disease. Although the negative influence of short sleep duration has been well-established, recent data suggest a possible harmful effect of prolonged sleeping pattern.

In the setting of the Corinthia cross-sectional study, self-reported night sleep duration was recorded in 1752 apparently healthy individuals and was classified as normal sleep duration (NSD, 7-8 h), short sleep duration (SSD, 6-7 h), very short sleep duration (VSSD, < 6 h), and long sleep duration (LSD, > 8 h). Carotid duplex ultrasonography was performed in order to measure the mean and maximum carotid intima-media thickness (cIMT) as a non-invasive marker of atherosclerosis.

Subjects with LSD and VSSD had significantly higher mean cIMT (VSSD: 1.02 ± 0.45 mm, SSD: 0.95 ± 0.35, NSD: 0.96 ± 0.38 mm, LSD: 1.07 ± 0.52 mm; p < 0.001) and maximum cIMT (VSSD: 1.39 ± 0.9 mm, SSD: 1.25 ± 0.71 mm, NSD: 1.23 ± 0.76 mm, LSD: 1.41 ± 0.93 mm). Following a regression analysis adjusting for known cardiovascular risk factors, individuals with LSD and VSSD had higher mean cIMT by 0.054 mm and 0.067 mm respectively compared to those with NSD.

A balanced sleeping duration of 6-8 h is associated with decreased mean and maximum IMT while both very short sleep duration and long sleep duration are associated with increased carotid intima-media thickness, a marker of subclinical atherosclerosis.