What is poor sleep doing to the cardiovascular health of your older patients? It may be setting them up for stroke. Researchers affiliated with Rush University in Chicago found a strong correlation between sleep fragmentation, arteriolosclerosis, and subcortical infarcts in older adults.1
Sleep disruption and stroke are known to be associated, but the Rush study delved into the relationship between sleep and the histopathology of cerebrovascular disease. Its aim was to show that the more severe the sleep fragmentation, the higher the burden of cerebrovascular damage and infarct pathology at autopsy. The study authors hope that their findings and the research that ensues from it can ultimately provide greater insight into not only the pathology of stroke but also that of progressive cognitive and motor diseases.
The researchers sourced autopsy data from 315 participants from the Rush Memory and Aging Project, a community-based cohort study of aging in which participants permit the donation of their brain upon death. All participants underwent at least 1 actigraphic recording, with the protocol in the Rush Memory and Aging Project being biennial capture of 10 days of ambulatory actigraphy. Actigraphic data were analyzed using the metric kRA, which strongly correlates (P <.0001) with polysomnographic measures of sleep fragmentation (ie, arousal index and sleep efficiency). The number of macroscopic and microscopic infarcts present at brain autopsy also was assessed. Ordinal logistic regression models were used to correlate sleep fragmentation to the severity of arteriolosclerosis, atherosclerosis, and cerebral amyloid angiopathy.
The average age of the participants at death was 90.4 years. Twenty-nine percent had had clinical stroke and 61% had had at least 1 moderate to severe vascular disease. Whereas no correlation was seen between the severity of sleep fragmentation and atherosclerosis, amyloid angiopathy, or cortical macroscopic infarcts, the researchers found that for every 1 standard deviation higher of sleep fragmentation, the odds of having more severe arteriolosclerosis were nearly 30% higher (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.02-1.59; P =.03), and the odds of having more subcortical macroscopic infarcts were more than 30% higher (OR, 1.31; 95% CI, 1.01-1.68; P =.04). After adjusting for potential confounders—such as cardiovascular risk factors, Alzheimer disease, pain syndromes, depression, and heart failure—and nuances related to actigraphy measures, time of autopsy, and total daily rest and activity, these associations remained significant.
The researchers noted that further study is needed to clarify whether the cardiovascular effects seen are consequences or causes of sleep fragmentation. Underlying biological mechanisms and the role of various contributors to sleep fragmentation, such as sleep apnea, also need to be explored, they said. Study limitations included an observational design that compromised determination of causality. Also, use of kRA does not allow for direct measurement of neurocerebral electrical activity, and actigraphy itself does not identify sleep fragmentation cause, creating a scenario where conditions such as sleep apnea could have confounded study results despite precautions taken regarding confounding factors. Also, although factors such as physical activity, body mass index, blood pressure, and pulmonary and renal functions were objectively quantified, self-reported information related to heart disease, smoking, and diabetes mellitus were not. Nevertheless, the findings highlight the impact of sleep fragmentation on cardiovascular integrity and pave the way for further research into sleep pathology and the histopathology of stroke.
- Lim AS, Yu L, Schneider JA, Bennett DA, Buchman AS. Sleep fragmentation, cerebral arteriolosclerosis, and brain infarct pathology in community-dwelling older people. Stroke. 2016 Jan 14. [Epub ahead of print]