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Sleep can repair the heart

 

After a heart attack, getting enough sleep and rest is crucial for the long - term recovery of the heart!

This is the conclusion drawn from a new study involving mice and humans. The study shows that after a heart attack, immune cells rush to the brain to promote deep sleep. This deep sleep can alleviate heart inflammation and help repair the damaged heart.

These research results have been published in the recent issue of the journal "Nature".

Sleep and heart disease in mice

In recent years, there has been a growing awareness that sleep is an important factor in maintaining heart health. Scientists have long known that there is a connection between sleep and cardiovascular health. For example, some studies have shown that sleep can improve blood pressure and reduce cholesterol. People with poor sleep are at a higher risk of high blood pressure than those with good sleep.

However, for a long time, it has not been fully clear whether insufficient sleep increases the risk of heart disease, and there has been little research on how cardiovascular diseases affect sleep.

In the new study, researchers conducted experiments on mice. They induced heart attacks in the mice and then examined their brainwaves. They found that compared with mice that did not experience a heart attack, these mice spent much more time in slow - wave sleep (a deep sleep stage associated with recovery).

The researchers tried to understand what caused this effect. After a heart attack, immune cells trigger large - scale inflammation in the heart. The researchers wondered if these immune changes also occurred in the brain. They found that after a mouse had a heart attack, a type of immune cell called monocytes flooded its brain. These cells produce a large amount of a protein called tumor necrosis factor (TNF), which is an important regulator of inflammation and can promote sleep.

To confirm that these cells were indeed related to the increase in sleep, the researchers prevented monocytes from accumulating in the brains of these mice. They found that when they did this, the mice that had experienced a heart attack no longer showed an increase in slow - wave sleep. This means that the influx of monocytes into the brain does contribute to the increase in sleep after a heart attack. Similar experiments confirmed the role of tumor necrosis factor as a messenger for sleep - inducing brain cells.

To understand the role of this increased sleep, the researchers repeatedly interrupted the slow - wave sleep of mice with heart disease. They found that doing so led to more inflammation in both the brains and hearts of the mice. Compared with mice that could sleep undisturbed after a heart attack, the mice that were disturbed had a much worse prognosis. In other words, sufficient sleep is crucial for the recovery of mice that have experienced a heart attack.

Similar situations may occur in humans

The researchers also analyzed human data samples collected from another sleep restriction study and found that sleep may play the same role in humans. In this sleep restriction study, to determine whether insufficient sleep is a cause of heart disease development, the researchers asked the participating volunteers to reduce their sleep time by 90 minutes each night for a continuous 6 - week period. All the participants were healthy and had never had a heart attack. They wanted to measure the impact of long - term insufficient sleep on human health by doing so.

The results of the previous study showed that insufficient sleep can cause changes in the body and increase the risk of heart disease. In the new study, when the researchers began to analyze the blood samples of the participants in the sleep restriction study, they found similar mobile inflammatory cells. This indicates that what happens to sleep - deprived mice after a heart attack also happens to sleep - deprived humans.

The researchers also investigated the situation of people with acute coronary syndrome. Acute coronary syndrome is a condition that includes heart attacks and is caused by a sudden reduction in blood flow to the heart muscle. Compared with people with good sleep, those who had poor sleep quality within a few weeks after such an event were at a higher risk of heart disease and other serious cardiovascular diseases in the next two years.

These findings highlight the importance of getting a good sleep after a heart attack and emphasize the bidirectional relationship between sleep and the immune system. After a heart attack, the focus of treatment is usually on changing diet, increasing exercise, and losing weight. But from these new findings, it seems necessary to recommend that cardiovascular disease patients improve their heart conditions by improving their sleep.

 

 

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