Good quality sleep has numerous benefits for health and emotional well-being, but it can also have restorative properties, since a new study has proven that, after suffering a heart attack, the heart can cause an increase in desire in the brain. of sleeping to facilitate recovery and reduce inflammation.
This finding is the result of research carried out by scientists at Mount Sinai Hospital in New York and shows for the first time how the heart and brain communicate through the immune system to promote sleep and facilitate recovery after a serious cardiovascular event.
The results have been published in the journal Nature and highlight the importance of adequate rest after a heart attack, suggesting that sleep should be considered an essential part of post-heart attack care, even in intensive care units, where sleep is often interrupted , and cardiac rehabilitation.
The lead author of the study, Cameron McAlpine, Assistant Professor of Medicine and Neuroscience at the Icahn School of Medicine at Mount Sinai, said in a note published by the center: “This study is the first to demonstrate that the heart regulates sleep during a cardiovascular injury by using the immune system to send signals to the brain. “Our data show that after a heart attack, the brain undergoes profound changes that increase sleep, and that in the weeks following a heart attack the abundance and drive of sleep increases.”
“We found that neuroinflammation and the recruitment of immune cells called monocytes in the brain after a myocardial infarction is a beneficial and adaptive response that increases sleep to allow healing of the heart and reduction of harmful cardiac inflammation,” he adds.
Stress and inflammation decrease during sleep
Researchers at the Mount Sinai Cardiovascular Research Institute conducted their first experiments with mouse models, in which a heart attack was induced. They monitored the brain’s electrical signals and analyzed their sleep patterns with electroencephalography devices. After the heart attack, they detected a threefold increase in slow-wave sleep, a deep phase of sleep characterized by slow brain waves and low muscle activity. This increase in sleep appeared quickly after the heart attack and lasted a week.
By analyzing the brains of stroked mice, they observed that immune cells called monocytes traveled to the brain through the bloodstream and activated a protein called tumor necrosis factor (TNF) in the thalamus, causing increased sleep. None of this occurred in the mice without infarction.
“This study is the first to demonstrate that the heart regulates sleep during cardiovascular injury by using the immune system to send signals to the brain.”
By manipulating TNF neural signals in the thalamus, they discovered that the sleeping brain uses the nervous system to send signals to the heart, reducing stress and promoting recovery and decreased inflammation. By interrupting the sleep of some mice after a heart attack, they noticed that the stress response in the heart and inflammation increased, making recovery more difficult.
In additional human studies, researchers observed an increase in monocytes in the brains of patients one to two days after a heart attack. They also analyzed the sleep of more than 80 patients in the weeks after the event. Patients who slept poorly had twice the risk of another cardiovascular event and showed less improvement in cardiac function compared to those who slept well.
Finally, in a five-week study with healthy adults, half of the participants slept the recommended hours, while the other half had restricted sleep. Those with restricted sleep showed stress and inflammation responses similar to those seen in mice. This suggests that sleep could be key in cardiac recovery after a heart attack, and doctors should advise their patients to prioritize rest during cardiac rehabilitation to promote heart healing.
