Sleep disorders contribute to increased hypertension risk
Patients with sleep disorders may be at a greater risk of developing hypertension, with the risk particularly pronounced among those who are younger and those with insomnia, according to a cohort study.
“Compared with well-accepted hypertension risk factors such as family history, sedentary lifestyle, diet and ageing, sleep problems are an unconventional and often overlooked risk factor,” the authors said. “Our study results have provided further evidence that [sleep disorder] is a risk factor for developing hypertension.”
Using data from Taiwan’s National Health Insurance Research Database (NHIRD), the authors retrospectively examined the risk of hypertension in a cohort of 1,739 patients with sleep disorders (insomnia, sleep disturbance, sleep apnoea syndrome and the others) and 2,117 individuals without sleep problems (controls). In both groups, majority were in the 41-to-65 age group and more than half were females.
Compared with the control group, the sleep disorder group had a significantly higher incidence of hypertension (120.7 vs 76.4 per 1,000 person-years). The difference in hypertension incidence between the two groups rose significantly from 1.3 percent in the first year to 18.2 percent in the fifth year (log-rank test; p<0.001). [J Hum Hypertens 2017;31:220–224]
Cox analysis found patients with sleep disorders to be 1.58 (95 percent CI, 1.26 to 1.79) times as likely as controls to develop hypertension (p<0.001). The risk was particularly evident among patients aged ≤40 years (adjusted HR, 2.90; 2.46 to 3.14; p<0.05) and those with insomnia (adjusted HR, 1.21; 1.01 to 1.76; p=0.04). Although patients with sleep apnoea syndrome showed a higher risk for hypertension compared with patients without the condition, the difference lacked significance (adjusted HR, 1.09; 0.47 to 1.58; p=0.61).
The authors pointed out that the pronounced finding for young adults in the present study indicates that with advanced ageing, sleep disorders present a decreasing trend for the risk of hypertension. “The effects of SDs on the risk of hypertension seen in different age groups could be attributed by other factors including lifestyle factors, habits and health status.”
Consistent with the findings of multiple previous studies, the present data lend support to the need for cautious assessment for hypertension risk in patients with sleep problems, they said. [Hypertension 2012;60:929–935; J Occup Health 2003;45:344–350; Am J Epidemiol 2011;173:300–309]
Potential mechanisms underlying the relationship between sleep disorders and hypertension include the activation of hypothalamic–pituitary axis, excessive secretion of cortisol and increased cardiovascular load associated with short sleep duration, the authors said. [Chest 2010;138:434–443]
In addition, long-term sleep disorders have been also shown to lead to excessive activation of sympathetic nerves, gradual hypertrophic cardiomyopathy, augmented salt appetite, suppressed secretion of renal salt fluid and increased hemodynamic load, they continued. [Scand Cardiovasc J 2001;35:163–172]
The study was limited by potential residual confounding due to the lack of information on patient factors (eg, blood pressure, body mass index, physical activity, smoking, alcohol use), as well as a relatively short follow-up period. “As hypertension usually has a long and insidious onset, it [is] possible that a longer follow-up period may have yielded even better results,” the authors said.
In an accompanying editorial, Dr David Calhoun from the University of Alabama in Birmingham, US, commented that the findings of the present study are important in confirming the increased risk of hypertension attributable to sleep disorders in a large Asian cohort.” [J Hum Hypertens 2017;31:371–372]
He noted that the divergent risk observed with insomnia vs obstructive sleep apnoea (OSA) is perplexing, explaining that “[a] positive relation between cardiovascular [CV] risk, including hypertension, and sleep-related disorders is likely more firmly established for OSA compared with insomnia, so for [the authors] to report the opposite is intriguing, but unexplained by the current study design.”
“One can speculate that perhaps the lack of a significant relation with sleep apnoea and incident hypertension in the current analysis is related to how sleep apnoea or even hypertension is diagnosed and/or coded in Taiwan versus other countries; differences in severity of OSA compared with other study cohorts; or use of continuous positive airway pressure for treatment of OSA, which was not accounted for in the current results,” he said.
Finally, he emphasized that “while observational studies [such as the present study] clearly implicate sleep disorders as important mediators of CV risk, the limited benefit of treating those disorders, as suggested by recent interventional trials, highlights our need to better understand the mechanisms of CV disease progression associated with sleep disturbances in order to better prevent and/or reverse that associated risk.” [N Engl J Med 2016;375:919–931; JAMA 2012;307:2161–2168; Eur Respir J 2011;37:1128–1136; Am J Respir Crit Care Med 2016;194:613–620]