Study Finds Heart Signals Brain to Increase Sleep for Recovery Post-Heart Attack

Microscopy images of monocytes in the brain of a mouse after a heart attack. Schematic of hypothesized mechanism: after a heart attack, monocytes are released from the bone marrow and recruited to the brain where they produce TNF to increase sleep which limits stress signaling to the heart and promotes heart healing and recovery. Credit: Mount Sinai Health System

In groundbreaking research, scientists at Mount Sinai have discovered that after a heart attack, the heart communicates with the brain to increase sleep, aiding in heart healing and reducing inflammation. This study, published on October 30 in Nature, is the first to show how the heart and brain interact through the immune system to promote recovery following a major cardiovascular event.

As reported by medicalxpress, the findings highlight the importance of sufficient sleep for heart attack patients, suggesting that restful sleep should be a key focus in post-heart-attack care, especially in intensive care and during cardiac rehabilitation.

“This study shows that the heart regulates sleep following cardiovascular injury, using immune signals to communicate with the brain,” said Dr. Cameron McAlpine, senior author and assistant professor at Icahn School of Medicine at Mount Sinai. “We observed that after a myocardial infarction, or heart attack, the brain undergoes profound changes to increase sleep, which supports heart healing and reduces inflammation.”

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Mount Sinai researchers first studied mouse models and found that heart attacks prompted a three-fold increase in deep, slow-wave sleep within hours of the event, lasting about a week. The team observed immune cells called monocytes moving from the blood into the brain, activating neurons in the thalamus via a protein called tumor necrosis factor (TNF), which increased sleep in the mice with heart attacks. This response did not occur in healthy mice.

Further experiments showed that disrupted sleep after a heart attack led to higher heart stress and inflammation, slowing recovery. The study also included human trials, where researchers noted an increase in monocytes in the brains of patients shortly after a heart attack, mirroring the mouse models. Monitoring 80 heart attack patients over two years, the team found that those who slept poorly had twice the risk of another cardiovascular event compared to good sleepers.

Additional trials with 20 healthy adults found that restricted sleep led to increased inflammation and stress responses, similar to those seen in heart attack patients with poor sleep.

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Dr. McAlpine emphasized that restful sleep should be prioritized during cardiac rehabilitation, saying, “Our study reveals new pathways for heart-brain communication and supports the inclusion of sleep as part of post-heart-attack care.”

Michelle Olive, Ph.D., of the National Heart, Lung, and Blood Institute, noted, “This research suggests that more sleep could accelerate healing after a heart attack, potentially opening new avenues in cardiac care.” The study’s authors call for additional clinical studies to confirm these findings.