Short night-time sleep raises risk of peripheral artery disease

People who sleep less than 5 hours a night are at heightened risk of incident peripheral artery disease (PAD), as shown in a study.

In a cohort analysis involving 53,416 Swedish adults, wherein 1,202 incident cases of PAD were recorded over a median follow-up of 10.4 years, “a U-shaped association [was seen] between sleep duration and PAD risk,” according to the investigators led by Dr Shuai Yuan of the Karolinska Institute, Stockholm, Sweden.

The risk of incident PAD was 74-percent higher among people with short sleep (<5 hours; hazard ratio [HR], 1.74, 95 percent confidence interval [CI], 1.31–2.31) and 24-percent higher among people with long sleep (≥8 hours; HR, 1.24, 9 percent CI, 1.08–1.43) than among those who slept 7 to <8 hours a night. [Eur Heart J Open 2023;doi:10.1093/ehjopen/oead008]

These findings were replicated in the Million Veteran Program cohort (n=156,582; <5 hours: odds ratio [OR], 1.38, 95 percent CI, 1.14–1.67; ≥8 hours: OR, 1.48, 95 percent CI, 1.38–1.59) and the UK Biobank cohort (n=452,028; <5 hours: HR, 1.87, 95 percent CI, 1.50–2.34; ≥8 hours: HR, 1.14, 95 percent CI, 1.07–1.22). 

Another interesting observation, according to Yuan, was that daytime napping also correlated with increased PAD risk (HR, 1.32, 95 percent CI, 1.18–1.49).

Are links causal?

“Observational analyses are limited by reverse causality‒meaning that if an association between sleep habits and PAD is found, we cannot be certain if sleep habits caused PAD or having PAD caused the sleep habits,” Yuan said.

To examine the causal relationship between sleep habits and PAD, the investigators conducted a Mendelian randomization (MR) analysis involving 31,307 individuals with PAD and 211,753 of those without PAD. This could provide more certainty about the results of the study, Yuan pointed out.

Results showed that sleep duration had a causal effect on PAD, such that for every hour that a person sleeps longer, the chance of developing PAD decreases by 30 percent (OR, 0.70, 95 percent CI, 0.55–0.89). Moreover, the relationship was bidirectional, with people who had genetic variants that increased their risk of PAD being more likely to have short sleep duration (OR, 1.20, 95 percent CI, 1.04–1.38). No association was observed for long sleep duration.

“Our MR analysis did not support our observational finding that longer sleep duration might be detrimental. Reverse causality, whereby PAD-related pain leads to poor sleep quality but increased time in bed, might explain the discordant results of the observational and MR analyses,” Yuan explained.

The takeaway is that “brief night-time sleep can raise the chance of developing PAD, and that having PAD increases the risk of getting insufficient sleep,” he said. “These results provide consistent support for short sleep duration as a harmful risk factor for PAD.”

Clinical implications

The present data, according to Yuan, may aid in the diagnosis and management of both PAD and sleep disorders.

“[I]nterventions to improve sleep may have downstream effects on PAD, and likewise interventions to treat PAD may improve sleep. Although the optimal interventions for interrupting the sleep–PAD link is not yet known, the American Heart Association has identified sleep research as an important priority for improving cardiometabolic health,” he said. [Circulation 2016;134:e367-e386]

Yuan acknowledged that their work bears limitations that could be improved in further studies. He called for additional research to assess the associations between sleep and PAD risk in other populations to expand the generalizability, given that the current findings were mainly based on European populations. Future studies should also use objective measurements of sleep traits (eg, polysomnography techniques), ascertain whether a shorter sleep duration is associated with the severity of PAD, and identify potential pathways explaining the association between short sleep duration and high PAD risk.