Lea Ann Matura, PhD, RN, on Improving Sleep in Patients With PAH
Many patients with pulmonary arterial hypertension (PAH) experience sleep disturbance and poor sleep quality.
To better understand the association, researchers recently investigated1 the relationship between actigraphy sleep variables and biomarkers among 60 women with PAH.
Over a 7-day period, the researchers assessed the following actigraphy variables: sleep onset latency, wake after sleep onset, sleep efficiency, total time in bed, total sleep time, number of awakenings, and average time awake during awakenings. Phlebotomy for biomarkers was also performed.
The results of the study showed that the participants had poor sleep quality, impaired physical function, sleep-related impairment, reduced health-related quality of life, and objective signs of insomnia.
The researchers also found that the actigraphy sleep variables were associated with the sympathetic nervous system (norepinephrine), the hypothalamic pituitary adrenal axis (copeptin), and inflammation (C-reactive protein).
Lea Ann Matura, PhD, RN, an associate professor at the University of Pennsylvania’s School of Nursing, was the study’s lead author. Pulmonology Consultant asked her about these findings and how they may aid you in selecting targeted interventions to treat your patients with PAH.
PULMONOLOGY CONSULTANT: Patients with PAH experience sleep disturbance and poor sleep quality. Can you expand on this relationship and how it affects patients’ health relative to their PAH? Why is improving sleep in PAH important?
Lea Ann Matura: We are still trying to determine the health implications of poor sleep in PAH. We have found that patients with poor sleep quality also report worsened fatigue, dyspnea, and depressive symptoms. Additionally, poor sleepers have worse physical function and functional exercise capacity (6-minute walk distance). While we do not know the temporal effects—and while more research is needed—we believe improving sleep among patients with PAH may improve other symptoms, such as fatigue and depression, and may have a positive impact on physical functioning. Although we do not know the long-term effects of poor sleep in PAH, in other populations, poor sleep contributes to morbidity.
PULM CON: What knowledge gaps were you hoping to bridge through your study?
LAM: We know some of the physiological manifestations in PAH, such as activation of the sympathetic nervous system, hypothalamic pituitary adrenal axis, and inflammatory pathways. Understanding the association of biomarkers with sleep and other symptoms can help us target those biomarkers to improve sleep. This can help with developing targeted interventions to help with sleep in PAH. Additionally, our study shows impairment in sleep from an objective measure: actigraphy.
PULM CON: According to your findings, what interventions may clinicians want to consider to improve sleep among patients with PAH?
LAM: As an example, our results showed an association between inflammation, activation of the sympathetic nervous system, and sleep variables such as sleep onset latency (how long it takes to fall asleep) and wake after sleep onset (amount of time spent awake after sleep onset). Additionally, we have found in our research that patients with PAH are profoundly inactive, with most of their daytime activity being spent sedentary. An intervention that promotes an increase in physical activity may improve sleep by decreasing inflammation and/or decreasing the sympathetic response. Physical activity may promote a physiological response that ultimately improves sleep and perhaps other symptoms such as fatigue.
PULM CON: Are there any biomarkers or actigraphy variables that you recommend clinicians should initially or especially focus on when working to improve their patients’ sleep? What do you recommend clinicians keep in mind to successfully target these or any of the other interventions?
LAM: Initially, defining the sleep problem is helpful. In our PAH study, it appears insomnia (difficulty imitating sleep and/or staying asleep) is the predominant sleep issue. Therefore, targeting those actigraphy variables, sleep onset latency and/or wake after sleep onset, are important. Determining contributing factors should be carefully assessed. For example, if patients are having trouble staying asleep (increased wake after sleep onset), it is necessary to determine what may be contributing to this. Are they having trouble staying asleep due to nocturia? Perhaps reminding patients to take their diuretics earlier in the day or not consuming liquids too late in the day could be helpful.
PULM CON: How do you hope your findings impact clinical practice?
LAM: Patients with PAH have sleep problems. It is important to be aware of and assess such problems. Currently, cognitive behavioral therapy is an evidence-based treatment for insomnia, though it has not been tested specifically among patients with PAH. Increasing physical activity may also act on those underlying mechanisms that are inherent in PAH, such as inflammation, that are associated with sleep problems.
- Matura LA, Fargo JD, Fritz JS, et al. Association of sleep (actigraphy) and biomarkers in pulmonary arterial hypertension. Am J Respir Crit Care Med. 2020; 201:A4639. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm-conference.2020.201.1_MeetingAbstracts.A4639
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