Scientists have made a significant discovery, potentially unraveling the mystery behind sleep problems frequently experienced by individuals with heart disease. The research indicates that damage to a specific group of nerves, known as the superior cervical ganglion (SCG), which regulates both heart and brain function, may be the missing link.

Heart disease patients often suffer from sleep disturbances, with up to 73% of those with heart failure reporting symptoms of insomnia. Past studies have indicated reduced levels of the sleep hormone melatonin in people with heart disease, but the underlying cause remained elusive.

The study, conducted on mice and human tissues, demonstrated that heart disease could interfere with the production of melatonin in the brain due to damage to nerves connecting the heart and the pineal gland, responsible for melatonin production. The SCG, located in the neck, is part of the autonomic nervous system, controlling involuntary processes like heart rate and breathing.

To investigate this potential connection, the researchers analyzed brain tissue samples from deceased heart disease patients and individuals without heart disease. The postmortem analysis revealed a reduced number of nerve fibers in the SCG of heart disease patients compared to the control group, and these nerves exhibited signs of inflammation and scarring.

In mouse experiments, the team observed that mice with heart disease had fewer axons in their pineal glands and lower melatonin levels in their blood. Furthermore, their circadian rhythms, responsible for regulating day-night responses, were disrupted. However, when the mice were given melatonin, the disruption was completely reversed. Additionally, the researchers found that immune cells called macrophages were present in the cervical ganglia of the mice with heart disease, suggesting an immune response may contribute to the nerve damage.

These findings, published in the journal Science, are considered “important and timely” by Brooke Aggarwal, an assistant professor of medical sciences at Columbia University, who was not involved in the study. However, she emphasized the need for further prospective studies and clinical trials before potential treatments based on this mechanism can be developed.

The researchers hope that this study will lead to the development of new drugs to address sleep disturbances caused by heart disease. A randomized clinical trial will be essential to determine the efficacy of therapeutic melatonin in treating sleep disorders in patients with chronic heart disease. If successful, this treatment approach could spare many patients from the side effects associated with conventional sleeping pills.

As scientists delve deeper into this newfound connection between heart disease and sleep problems, the potential impact on improving the quality of life for individuals with heart conditions is promising. However, further research will be required to fully understand the mechanisms driving immune cells to the SCG and to explore the role of nerve cells and cytokines in this process.

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