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The key role of sleep in cardiac recovery
Last reviewed: 02.07.2025
Research shows how sleep reduces heart inflammation and speeds recovery after a heart attack by regulating immune and neural pathways.
In a recent study published in the journal Nature, researchers examined the effects of sleep on inflammation and recovery after a heart attack. In mice and humans, sleep was found to reduce inflammation in the heart by recruiting monocytes to the brain and limiting sympathetic nerve activity to the heart.
The connection between the brain and the heart
The brain and heart are closely connected and interact through immune signals and neural pathways to maintain health. Sleep is especially important for cardiovascular health, as poor sleep quality and lack of sleep can increase the risk of heart attacks.
Current research suggests that the brain regulates heart health during sleep through complex neural and immune pathways. For example, signals from the hypothalamus influence immune cell activity and the progression of cardiovascular disease.
Blood vessels that carry oxygen from the heart are also essential for communicating the physiological state of the heart to the brain. Despite a significant amount of research on sleep disturbances in patients with heart disease, the effects of cardiac injury on sleep, as well as the reciprocal effects of altered sleep on cardiac recovery, remain largely unexplored.
For the human study, the researchers analyzed brain tissue from donors who had suffered a myocardial infarction within two weeks of death. Individuals with a history of neurodegenerative diseases, brain injury, cancer, or stroke were excluded from the analysis. The human tissue samples were stained for CCR-2 (CC chemokine receptor) and CD68 (cluster of differentiation 68).
To assess sleep, the researchers looked at 78 patients who were part of a German study of people with acute coronary syndrome. Patients who were prescribed sleep medications or had sleep disorders were excluded from the analysis.
The group underwent coronary angiography and ejection fraction measurements using echocardiography. The patients' sleep quality was also assessed using the Pittsburgh Mini-Sleep Scale, which measures sleep duration, latency, disturbances, and overall quality.
A randomized controlled crossover trial was also conducted to examine how chronic sleep deprivation impacts immune cell programming. Participants were exposed to adequate and restricted sleep conditions for six weeks, after which blood samples were collected for analysis.
Myocardial infarction was induced in mice by ligating the anterior descending coronary artery under anesthesia. After the mice recovered from myocardial infarction, they were placed in a sleep fragmentation chamber. The mice were also implanted with an electroencephalogram (EEG) and electromyography (EMG) for monitoring.
Bone marrow, blood, heart, and brain samples were obtained from mice for flow cytometry and immunostaining analysis. Plasma biomarkers and tissue proteins associated with cardiac and brain function were measured using immunoassays and RNA analysis, including quantitative polymerase chain reaction (qPCR) and single-cell RNA sequencing (scRNAseq).
Cardiovascular injury such as myocardial infarction increases the duration of slow wave sleep in mice, which disrupts their natural sleep patterns, suggesting a link between sleep regulation and immune responses after cardiac events.
Mice with cardiovascular injury had longer slow-wave sleep periods and reduced rapid eye movement (REM) sleep. In the case of myocardial infarction, the increased sleep duration lasted for more than one week, along with decreased activity levels and lower body temperature.
Immune signals in the blood activated microglia in the brain after myocardial infarction. Elevated levels of interleukin-1β (IL-1β) activate microglia activity and cause an enhanced chemokine response, thereby increasing the recruitment of immune cells to the brain.
Flow cytometry analysis also showed an influx of monocytes into various brain regions, such as the choroid plexus, third ventricle, and thalamus, within 24 hours of myocardial infarction. These monocytes can release signals that increase slow-wave sleep, which has been shown to support the healing process.
Inhibiting monocyte entry into the brain using CCR2 antagonists prevented sleep changes in mice. Thus, CCR2 plays a critical role in the immune response that influences how the brain and body regulate sleep after a cardiac event.
Myocardial infarction-associated monocytes expressed a tumor necrosis factor (TNF) signature that was not present in normal monocytes in the blood. Moreover, blocking TNF activity in the brain restored normal sleep patterns.
The results of the study show that after myocardial infarction, immune signals via monocyte-produced TNF activate specific neurons in the thalamus, which increases the duration of slow-wave sleep. These observations provide new evidence for how immune responses following cardiac events may influence sleep patterns that impede healing and recovery.