According to research, heart diseases, which affect the production of the sleep hormone melatonin in the brain, is a major reason why people with heart problems find it difficult to sleep. About one-third of people with heart disease also suffer from sleep problems such as sleep apnea, insomnia, nighttime waking, and restless legs syndrome.
The study, led by a team from the University of Munich (TUM) in Germany, showed that heart disease affects 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.
Melatonin is produced in the pineal gland. Like the heart, it is controlled through the autonomic nervous system, which controls involuntary processes in the body. The associated nerves originate in the ganglia, among other places. Particularly important for the heart and pineal gland is the superior cervical ganglion.
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Stefan Engelhardt, Professor of Pharmacology and Toxicology at TUM, said, “To get a clear understanding of our results, imagine the ganglion as an electrical switch box. In a patient suffering from sleep disturbances after heart disease, you can think of the problem of one wire causing the switch box to fire and then spreading to the other wire.”
The team found that macrophages – cells that eat up dead cells – accumulated in the cervical ganglion of mice suffering from heart disease. These cause inflammation and scarring in the ganglion and lead to the destruction of nerve cells. In rats, as in humans, long fibers, called axons, extending from these nerve cells lead to the pineal gland.
In advanced stages of the disease, the number of axons connecting the gland to the nervous system was significantly reduced. The animals lost melatonin and their day/night rhythms were disrupted.
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Comparable biological effects were observed in humans. The team examined the pineal glands in nine heart patients. Compared to the control group, significantly fewer axons were found. As in rats, lesions in the superior cervical ganglion appeared and became significantly larger in humans with heart disease.
Researchers believe that the negative effects of dead axons become permanent in the advanced stage. “At an early stage we were able to bring melatonin production back to the original level in mice by using drugs to destroy macrophages in the upper cervical ganglion,” said first author Dr. Karin Ziegler. “First, it demonstrates the ganglion’s role in this phenomenon. And second, it raises hope that we can develop drugs to prevent irreversible sleep disturbances in heart disease.”
The researchers believe that the study offers new hope for a large number of heart patients that a treatment for the sleep disorder may be found and that the ganglia may be clinically important.