Study reveals the interaction between the heart and brain that affects sleep patterns and aids in recovery after heart attack.
Research from Mount Sinai suggests that a heart attack can lead to an increased need for sleep, helping the heart to recuperate and decreasing inflammation. The study uncovers that this happens due to the heart sending specific signals to the brain. This groundbreaking research highlights how the heart and brain communicate through the immune system to enhance sleep and recovery following a significant cardiovascular incident.
Published on October 30 in Nature, this study underscores the necessity of ample sleep after a heart attack. It implies that ensuring proper sleep should be a vital aspect of treatment and care in the aftermath of a heart attack, especially in intensive care units where sleep patterns are often disrupted, in addition to during cardiac rehabilitation.
According to Cameron McAlpine, PhD, an Assistant Professor of Medicine (Cardiology) and Neuroscience at the Icahn School of Medicine at Mount Sinai, “This study is the first to show that the heart influences sleep during cardiovascular injuries by signaling to the brain via the immune system. Our findings indicate that the brain undergoes significant adaptations after a myocardial infarction (heart attack) that enhance sleep, with increased sleep drive observed in the weeks following the event.” He adds, “We found that neuro-inflammation and the migration of immune cells, known as monocytes, to the brain post-heart attack is a positive response that fosters sleep, facilitating heart recovery while reducing harmful cardiac inflammation.”
The Icahn Mount Sinai researchers initially employed mouse models to explore this phenomenon. They induced heart attacks in 50% of the mice and utilized advanced imaging and cell analysis, coupled with implantable wireless electroencephalogram devices, to capture electrical activity in their brains and assess sleep patterns. They discovered a threefold rise in slow-wave sleep—a deeper sleep phase identified by slower brain waves and less muscle activity—occurring shortly after heart attacks and lasting for a week.
Upon examining the brains of the heart-attack-afflicted mice, the researchers noted that monocytes were drawn from the bloodstream to the brain, using a protein called tumor necrosis factor (TNF) to activate neurons in the thalamus. This process triggered the increase in sleep, occurring within hours of the heart event, unlike in the mice that did not experience heart attacks.
The team then employed innovative techniques to adjust TNF signaling among the thalamic neurons and discovered that the sleeping brain communicates back to the heart via the nervous system to alleviate heart stress, encourage healing, and lower heart inflammation post-heart attack. They also manipulated the sleep of some mice, which revealed that those experiencing sleep disruptions after a heart attack exhibited heightened sympathetic stress responses and inflammation, leading to a prolonged recovery process compared to those with uninterrupted sleep.
The researchers extended their investigation to human subjects as well. They analyzed the brains of patients one to two days following a heart attack and found elevated monocytes compared to individuals without heart issues, mirroring the mouse study results. Furthermore, they monitored the sleep of over 80 heart attack patients over four weeks, tracking their progress for two years. The patients were categorized into good and poor sleepers based on their rest quality in the month post-incident. Poor sleepers displayed a significantly worse prognosis, with twice the risk of experiencing another cardiovascular event compared to their well-rested counterparts. Good sleepers showed noteworthy improvement in heart function, while poor sleepers showed minimal or no benefitting changes.
In another segment of their research, the team studied the effects of five weeks of limited sleep among 20 healthy adults. Participants maintained sleep diaries and used electronic devices for monitoring. During this period, half of the subjects achieved the recommended seven to eight hours of uninterrupted sleep, while the other half reduced their sleep by 1.5 hours nightly—either by going to bed later or waking up earlier. Post-study, blood monocytes were analyzed, and similar sympathetic stress and inflammatory responses were observed in the sleep-restricted group as seen in the earlier mouse tests.
“Our research uncovers new dimensions of how the heart and brain collaborate to regulate sleep, emphasizing the importance of sleep in the clinical care of heart attack patients. Physicians should encourage their patients to focus on restful sleep during cardiac rehabilitation to aid in heart recovery,” explains Dr. McAlpine.
Michelle Olive, PhD, Associate Director of the Basic and Early Translational Research Program in the National Heart, Lung, and Blood Institute, which helped fund this study, stated, “This research provides fresh perspectives on the relationship between heart health and sleep. It suggests that additional sleep could accelerate recovery following a heart attack and highlights possible avenues for enhancing cardiac care. Further clinical studies are necessary to validate these findings.”
This study was supported by various National Institutes of Health grants including: R01HL158534, R00HL151750, R01AG082185, 5T32HL007824-25, P01-HL142494, DP2-CA281401, R01HL128226, R35HL155670, T32HL007343, and UL1TR001873.
Disclaimer: The views expressed here are solely those of the authors and do not necessarily reflect the official perspective of the National Institutes of Health.
