Mice pushed to the brink of heart attacks have unveiled the healing mechanism of sleep.

Researchers have repeatedly pointed out that poor sleep increases the risk of developing cardiovascular diseases. Experiments have shown that the harm to heart health from regular sleep deprivation during the workweek cannot be compensated by additional hours of sleep on weekends.

In a recent study, specialists in cardiology and other fields from the USA and Germany demonstrated that in the case of cardiovascular injury, the heart engages in sleep regulation, utilizing the immune system to send appropriate signals to the brain.

In experiments with laboratory mice, medical researchers found that after a heart attack, immune cells called monocytes circulating in the blood actively migrated to the brain, where they produced a protein known as tumor necrosis factor (TNF). This protein is involved in inflammatory processes of various origins.

This compound activated neurons in the thalamus—a part of the brain that plays a crucial role in regulating consciousness, sleep, and wakefulness, which increased the urge to sleep and its duration. This adaptive response facilitated the healing of damaged heart tissue and reduced inflammation within it.

To further validate this, the scientists interrupted the sleep of some test rodents that had suffered a heart attack. As a result, the mice post-infarction, who were deprived of sleep, exhibited an increase in sympathetic stress responses in the heart and inflammation, which slowed their recovery compared to the group that was allowed to sleep undisturbed.

The findings were further supported by several studies involving humans. Patients who had recently suffered a heart attack also showed an increase in monocytes in their blood. Sleep analyses of dozens of post-infarction patients and two years of monitoring confirmed the importance of quality sleep for heart health recovery and reducing the risk of recurrent attacks.

In a separate experiment, medical professionals tracked the consequences of sleep restrictions in healthy subjects. It turned out that individuals who regularly slept an hour and a half less than those in the control group developed stress and inflammatory responses similar to those previously identified in mice.

The scientific work, which was published in the journal Nature, emphasizes the critical importance of longer sleep after a heart attack. According to the authors, ensuring that patients have the opportunity to get adequate sleep should be a focal point in the care of post-infarction patients, alongside measures for cardiac rehabilitation.