International Business Department           Liu Bojia           November 05, 2024

  The heart and the brain are both vital organs of the body and the communication between them is crucial to health, a communication that often relies on the complex action of the nervous, vascular and immune systems. For example, we all know that lack of sleep increases the risk of cardiovascular disease, and the specific mechanism behind this is that the brain regulates immune cell signalling in the blood vessels through the nervous system when sleep is lacking, thereby influencing the development of atherosclerosis.

  But conversely, does it also affect the brain's behaviour when the heart is damaged by diseases such as myocardial infarction? The answer to this question is still unclear to scientists. However, many studies are revealing that this mechanism exists, such as the fact that tachycardia in humans is often accompanied by anxiety-like behaviour in the brain, and data from clinical studies of myocardial infarction patients show that many of them are particularly ‘sleepy’ during the recovery period.

  In a recent issue of Nature, researchers from the Icahn School of Medicine at Mount Sinai revealed for the first time that the heart sends signals to the brain through the immune system to regulate sleep behaviour after damage. This regulatory mechanism could prolong sleep for heart attack patients and help the heart repair. The new study suggests that after a heart attack, getting enough sleep will be an important aid in helping patients heal.

  In the mouse experiments, the authors tried to induce heart attacks in a group of mice and then detected changes in various types of cells in their blood, as well as recording their sleep status. When healthy, the mice slept rhythmically with light and dark shifts, 70 per cent of the time in light conditions and 20 per cent of the time in dark conditions.

  However, when the heart attack occurred, everything changed and the mice's sleep rhythms were completely disrupted; they chose to sleep more than 85% of the time in all conditions, with a decrease in the overall activity of the mice and a lowering of their body temperature, all of which were associated with an increase in sleep behaviour. Based on the EEG signal data during sleep, the mice also experienced a significant increase in slow wave sleep time, which represents more deep sleep. Overall, the above changes occur rapidly after a heart attack and last for about a week.

  But how does this signal of heart damage get to the brain and manipulate individuals to actively choose to sleep more? The authors carried out a careful analysis of the brain's cellular composition, and they found that immune cells take on this task. After heart damage, the mouse brain develops a large number of mononuclear cells, and these immune cells progressively enter the brain as they travel through the circulatory system, becoming active especially in the thalamus and releasing tumour necrosis factor (TNF), a cytokine that acts as a signalling molecule to stimulate thalamic neurons and increase an individual's sleep behaviour. The authors found that this change can occur as soon as a few hours after a heart attack.

  In addition to mice, the study also found similar manifestations in humans, such as a significant increase in blood monocyte levels in heart attack patients. In addition, these patients had a better prognosis if they had better sleep during recovery. Poor sleep during the week following a heart attack not only resulted in a worse prognosis, but also increased the risk of other cardiovascular diseases. These results suggest that adequate sleep plays an important role in the recovery of heart attack patients, especially in the week following the attack.

  The researchers note that the new study reveals a new way of communication between the heart and the brain. In the future, improving the quality of sleep in heart attack patients should be a consideration in clinical care.