Understanding the link between heart disease and sleep problems
The team found that mice with heart disease experience an accumulation of macrophages, cells responsible for engulfing dead cells, in their cervical ganglion.
London: Heart diseases, which affect the production of the sleep hormone melatonin in the brain, is the major reason why people with cardiac problems find it hard to sleep, according to a research.
Around one third of people with heart disease suffer from sleep problems such as sleep apnea, insomnia, waking up throughout the night, and restless legs syndrome. The study led by a team from University of Munich (TUM) in Germany showed that heart diseases affect the production of the sleep hormone melatonin in the pineal gland, located inside the brain. The link between the two organs is a ganglion in the neck region.
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Melatonin is produced in the pineal gland. Like the heart, it is controlled through the autonomic nervous system, which regulates involuntary processes in the body. The related nerves originate in the ganglia, among other places. Particularly important for the heart and pineal gland is the superior cervical ganglion.
“To get a clear sense of our results, imagine the ganglion as an electrical switch box. In a patient suffering from sleep disturbances following a heart disease, you can think of a problem with one wire causing a fire to break out in the switchbox and then spreading to another wire,” said Stefan Engelhardt, Professor of Pharmacology and Toxicology at TUM.
The team discovered that macrophages — cells that eat dead cells — accumulate in the cervical ganglion of mice with heart disease. These cause inflammation and scarring in the ganglion and the destruction of nerve cells. In mice, as in humans, long fibres extending from these nerve cells, called axons, lead to the pineal gland. At advanced stages of disease, there was a substantial decrease in the number of axons connecting the gland to the nervous system.
There was less melatonin in the bodies of the animals and their day/night rhythm was disrupted. Comparable organic effects were seen in humans. The team investigated the pineal glands in nine heart patients. Compared to the control group, significantly fewer axons were found. As with the mice, the superior cervical ganglion in the humans with heart disease showed scarring and was noticeably enlarged. The researchers assume that the negative effects of the dead axons become permanent at an advanced stage.
“In an early stage we were able to return melatonin production in mice to the original level by using drugs to destroy the macrophages in the superior cervical ganglion,” said first author Dr Karin Ziegler,. “First, this demonstrates the role of the ganglion in this phenomenon.
And second, it inspires hope that we can develop drugs to prevent irreparable sleep disturbances in heart disease.” The researchers believe the study shows new hope for a large number of heart patients that a treatment will be found for sleep disturbances and that ganglia could become important from a diagnostic standpoint.
