Sleep Disturbance Possible Adverse Effect of Cardiac Disease, New Study Finds


The lowering melatonin levels in patients with heart disease is one example of how heart conditions can influence systems throughout the body.

In a recent paper, a team of researchers at the Technical University of Munich (TUM) found that heart diseases affect the production of melatonin in the pineal gland, with the link between the 2 organs being a ganglion in the neck. An estimated 1 in 3 people with heart disease struggle with sleep problems according to the study authors.

Woman having difficulty falling asleep | Prostock-studio |

Woman having difficulty falling asleep | Prostock-studio |

Previous knowledge indicates that melatonin levels can lower in patients with heart diseases (e.g., heart attack), providing an example of how heart conditions influence different systems throughout entire body. Melatonin—which is produced in the pineal gland—can be found inside the brain and, like the heart, is controlled through the automatic nervous system in order to regulate the body’s involuntary processes.

“In our work, we show that the problems with the heart muscle affect an organ that would seem at first glance to have no direct link to it,” said Stefan Engelhardt, professor of pharmacology and toxicology at TUM in a press release. “To get a clear sense of our results, imagine the ganglion as an electrical switchbox. In a patient suffering from sleep disturbances following a heart disease, you can think of a problem with 1 wire causing a fire to break out in the switchbox and then spreading to another wire.”

While observing mice with heart disease, it was discovered that macrophages—cells that eat dead cells—collect in the cervical ganglion. The macrophages generate inflammation and scarring in the ganglion, resulting in the destruction of nerve cells. Similar to humans, mice have long fibers that extend to the nerve cells—called axons—that lead to the pineal gland. As the disease progresses, the decrease in the number of axons that connect the gland to the nervous system grows. As a result, less melatonin is found in the bodies of mice, interrupting their day and night rhythm.

The researchers found similar results during an examination of the pineal glands in 9 heart patients. Like the mice, the 9 patients had shown scarring and an enlargement in the superior cervical ganglion. A noticeable decrease in axons was found in comparison to the control group.

“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 study author Karin Ziegler, MD, in the press release. “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.”

Previously, the researchers assumed that the negative effects caused by the dead axons were permanent if the stage was advanced; however, the study presents an opportunity to observe ganglia with a new approach, creating hope for many heart patients seeking treatment for their sleep issues.

“New methods such as spatial single cell sequencing make it possible to investigate individual nerve cells much more closely,” Engelhardt said in the release.

When the heart patients were examined, their cervical ganglia were enlarged and from a diagnostic standpoint, this can be significant due to the potential indicator of heart failure. Further, the size of ganglion can easily be checked with ultrasound devices.

Engelhardt advised that more extensive checks should be ordered if the ganglion appears enlarged. “Our study could prompt researchers to start systematically searching for connections between other diseases in organs linked via ganglia acting as switchboxes and to look at ganglia as starting points in the search for new drugs,” he said.


Technical University of Munich. Cause of sleep disturbance in cardiac disease identified: Ganglia play previously unrecognized role. News release. July 20, 2023. Accessed July 25, 2023.

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