Hypertension increased with decrease in slow-wave sleep

Fung M. Hypertension. 2011;doi:10.1161/HYPERTENSIONAHA.111.174409.

Issue: October 2011

A low percentage of slow-wave sleep can increase hypertension in older community-dwelling men, according to a study.

Researchers contacted participants from the Outcomes in Sleep Disorders in Older Men Study. Seven hundred eighty-four participants from the previous sleep study met criteria for the current sleep study. The mean age of participants was 75 years. Self-administered questionnaires, focusing on participant demographics, including race, lifestyle factors and classification of medication, were given to participants. Participant height, weight, BMI, and waist, hip and neck circumferences were all recorded by researchers. At the time of the initial study, participants had two seated resting BP measurements taken. In a follow-up visit, participant BP was taken again.

According to the study, “in-home, single-night sleep studies using unattended polysomnography were performed” to record rapid eye movement sleep and nonrapid eye movement sleep stages N1, N2 and slow-wave sleep (SWS).

Increased hypoxemia, sleep stages N1 and N2, and decreased SWS were all associated with incident hypertension. When researchers adjusted for age, nonwhite race, study site and BMI, SWS percentage was still significantly associated with incident hypertension. The mean respiratory disturbance index for participants at baseline was 10; 54% of participants had an indication of mild sleep-disordered breathing with a respiratory disturbance index of more than 5. According to the study, average percentage of time in rapid eye movement was 20.2%; stage N1 was 6.5%; stage N2 was 62%; SWS was 11.2%; and the average total sleep duration was 6.1 hours.

Researchers found that “sleep time in SWS was associated with increasing age, BMI, and neck circumference but not baseline systolic BP and diastolic BP.” Participants were more likely to have sleep-disordered breathing or moderate-severe sleep-disordered breathing if they were in the lowest quartile of sleep time in SWS. Incident hypertension had a positive correlation with poor sleep architecture. Poor sleep architecture caused less SWS, which corresponded with more stage N1 and N2 sleep. In a 3.4-year follow-up, 243 participants developed incident hypertension. Participants who were diagnosed with incident hypertension were diagnosed by BP (24.3%), self-report of hypertension (3.7%), BP and self-report (2.1%), and taking antihypertensive medication (70%). Incident hypertension was found in participants who were older and had CVD.

Disclosure: Dr. Fung, owns stock and is an employee at Amgen. The study received grant support from Forest Laboratories.

Franz Messerli

The paper by Fung and colleagues, reporting that time in SWS to be adversely associated with incident hypertension in a population of older men, is provocative and throws some light on the complex relationship between sleep pattern and CV health. As provocative as the data are, however, we should not forget that this is a chicken and egg situation. Any correlation between A and B means that either A causes B, B causes A or both are caused by a third factor. Conceivably, therefore, incident hypertension in the elderly man may cause a shortening of time in SWS in older men or both shortening of SWS, as well as hypertension, may be caused by a common denominator such as, for instance, obesity and the metabolic syndrome. Neither of these possibilities is considered by the authors, who seem to be convinced that the abnormal sleep pattern leads to hypertension. Obviously, the chicken and egg puzzle can only be resolved by further research.

– Franz Messerli, MD
Cardiology Today Editorial Board member

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