Arterial Stiffness: A Long Sleeper Issue?

It is well known that the large arteries constitute crucial components of the cardiovascular system in performing two main functions: 1) conduit for blood to reach peripheral tissues; 2) vascular buffering to each ventricular contraction through arterial-ventricular coupling.¹ The proximal aorta is rich in elastin that allows the support of each systolic impulse and accommodates the stroke volume. Thus, the thoracic aorta shows greater elasticity, whereas more distal vessels become progressively stiffer, given the predominance of collagen fibers. Increased arterial stiffness (easily measured noninvasively by pulse wave velocity) is one of the earliest detectable manifestations of adverse structural and functional changes within the arterial wall. Arterial stiffening causes the incident (generated by the heart) and reflected waves (generated by the arteries) to travel faster, leading to early return of the reflected wave to the heart resulting in boost of aortic and left ventricular pressure in systole. The resulting increased left ventricular load contributes to heart remodeling, consisting in the development of left ventricular hypertrophy, progressing to left ventricular dysfunction and cardiac failure. Several conditions, including aging, hypertension, diabetes, and renal disease are well established factors that can increase arterial stiffness. Recent studies have shown that increased arterial stiffness in various populations was an independent predictor of cardiovascular morbidity and all-cause mortality.² There is also evidence that sleep disordered breathing can increase arterial stiffness^3–5 that is probably independent of circadian variations.⁶

In this issue of SLEEP, Yoshioka and colleagues⁷ provide intriguing evidence that sleep duration may be a novel factor influencing arterial stiffness. The authors studied the association between self-reported sleep duration and arterial stiffness (evaluated by brachial-ankle pulse wave velocity) in a large cohort of over 4,000 middle-age Japanese civil servants. The crude analysis showed a dose-response pattern between sleep duration and arterial stiffness. Compared with subjects sleeping 7 hours, those sleeping 8 hours and 9 hours or more had significantly elevated pulse wave velocity, while those sleeping 6 hours or 5 hours or less and had significantly lower pulse wave velocity. Multiple linear regression analyses (using six different models) showed that sleep duration of 9 hours or more was independently associated with higher arterial stiffness compared with the reference group (7 hours of sleep). The association between long sleep duration and worse arterial stiffness was only positive in male subjects. The absence of a positive relationship in females may be explained by the fact that few women were long sleepers.

Sleep curtailment is a hallmark of our society, and well-controlled studies have shown that partial sleep deprivation may trigger a cascade of deleterious effects to the metabolic and cardiovascular systems, including systemic inflammation,⁸ metabolic alterations, and endothelial dysfunction.⁹ Most epidemiological studies, however, have shown a U-shaped relationship—not only short sleep but also long sleep was associated with poor coronary heart disease, stroke, total cardiovascular disease¹⁰ and total mortality.¹¹ Interestingly enough, a recent systematic review of the association between sleep duration with either all-causes of or cause-specific mortality indicated that long sleepers were at increased risk of cardiovascular-related mortality, but short sleepers were not.¹² Therefore, the study of Yoshioka and colleagues⁷ is to some extent in line with the literature coming from large cohort studies and is the first to show the association of long sleep duration and increased arterial stiffness. Their main results may provide a link to explain the poor cardiovascular outcome in long sleepers.

The study of Yoshioka and colleagues is novel and provocative. However, many questions remain unanswered. It is difficult to explain the selective impairment of arterial stiffness only in long sleepers and ignore the potential harmful effects of short sleep duration. Several possibilities may help explain the findings. Firstly, information on sleep duration was obtained through self-reporting rather than objectively measured by actigraphy and can therefore be subject to error. Secondly, the group of longer sleepers in Yoshioka study was also older, presented higher systolic blood pressure, used more medications for hypertension, presented higher alcohol consumption, shorter working hours, larger numbers of days off, lower scores of job strain, and less education. Although the authors were very careful, using several models that adjusted for the multiple confounding variables, it is possible that the model was not able to fully control for all these confounding factors. More importantly, other factors not fully evaluated in the study may have exerted profound effects and thus may help explain the association (e.g., several drugs not monitored in the study may have affected arterial stiffness). Finally, long sleep duration could be associated with confounding diseases, such as depression and obstructive sleep apnea (OSA). Despite similar body mass index among groups, OSA is associated with several factors presented in the long sleepers (see Table 1 in the original paper), including higher proportion of male gender, higher age, and higher alcohol consumption. It is also possible that OSA is directly associated with increased sleep duration due to nonrestorative sleep. There is good evidence indicating that OSA promotes accelerated atherosclerosis and increased pulse wave velocity.^3,4,13 Therefore, a higher proportion of OSA in the long sleepers could help explain the main results.

In conclusion, the study of Yoshioka and colleagues⁷ points to an intriguing association between long sleep duration and increased arterial stiffness in a large cohort study. Epidemiological studies show associations rather than a cause and effect relationships. Future studies will be necessary to fully elucidate the findings.

DISCLOSURE STATEMENT

The authors have indicated no financial conflicts of interest.

CITATION

Drager LF; Lorenzi-Filho G. Arterial stiffness: a long sleeper issue? SLEEP 2011;34(12):1623-1624.