A new study from Mount Sinai researchers reveals that after a heart attack, the heart sends signals to the brain to encourage increased sleep, promoting healing and reducing inflammation. This research, published in Nature, is the first to explore how the heart and brain communicate through the immune system to facilitate recovery following a major cardiovascular event.
“This study is the first to demonstrate that the heart regulates sleep during cardiovascular injury by using the immune system to signal to the brain,” said Cameron McAlpine, PhD, the study’s senior author and an assistant professor of medicine and neuroscience at the Icahn School of Medicine at Mount Sinai. “Our data show that after a myocardial infarction (heart attack), the brain undergoes profound changes that augment sleep, and that in the weeks following a myocardial infarction, sleep abundance and drive is increased.”
The investigators, from the Cardiovascular Research Institute at Icahn Mount Sinai, first used mouse models to discover this increased sleep pattern. The team induced heart attacks in the mouse model and then used high-resolution imaging and cell analysis, as well as implantable wireless electroencephalogram devices, to monitor electrical brain activity and sleep patterns after a myocardial infarction. This analysis showed that the mice had a three-fold increase after a myocardial infarction of a deep stage of sleep characterized by slow brain waves and reduced muscle activity called slow-wave sleep.
Examination of the brains of the mice that had induced heart attacks, the researchers found that immune cells called monocytes were recruited from the blood to the brain, using a protein known as tumor necrosis factor (TNF) to activate neurons in the thalamus, which led to increased sleep. This response occurred rapidly after the cardiac event and none of the mice in the control group that did not have heart attacks showed this activity.
The researchers then manipulated neuron TNF signaling and found that the sleeping brain uses the nervous system to return signals to the heart to reduces stress, decrease inflammation, and promote health following a heart attack. To understand the impact of increased sleep post cardiac event, the investigators interrupted the sleep for a subset of the mice and found it created an increase in sympathetic stress responses and inflammation, resulting in slower recovery compared to mice that had not had sleep disruptions.
Moving to studying this effect in humans, the researchers assessed the brains of patients one to two days post-heart attack and similar to the mouse study, found an increase in monocytes, compared to people who had not experienced a heart attack or had other cardiovascular diseases. They also followed 80 heart attack patients over four weeks, dividing them into two groups, either good sleepers or poor sleepers. The patients in the poor sleeper group showed poor prognosis and double the risk of having a second heart attack than the good sleepers. Good sleepers also showed large improvements in heart function, while poor sleepers showed little improvement.
Additionally, the researchers conducted a study with 20 healthy adults, monitoring their sleep over five weeks. Half of the participants adhered to the recommended seven to eight hours of uninterrupted sleep, while the other half restricted their sleep by 1.5 hours nightly. Blood analyses revealed sympathetic stress signaling and inflammatory responses like those seen in the sleep-restricted mice.
“Our study uncovers new ways in which the heart and brain communicate to regulate sleep and supports including sleep as part of the clinical care of patients after a heart attack,” McAlpine concluded. “Physicians should inform their patients to prioritize restful sleep during cardiac rehabilitation to help the heart heal and recover after a heart attack.”
