Reduced melatonin levels in the body and associated sleep disturbances are common side effects of heart disease. However, the underlying mechanism of the problem has remained elusive. A team led by Professor Stefan Engelhardt, head of the Department of Pharmacology and Toxicology at the Technical University of Munich (TUM), and first author Karin A. Ziegler has now identified a direct consequence of sleep disorders in patients with cardiovascular disease. Both the pineal gland as part of the epithalamus, which produces the sleep hormone melatonin, and the heart are controlled by the autonomic nervous system. The upper cervical ganglion plays an essential role in transmitting electrical impulses to both organs. In an animal model, the researchers found pathological changes in the cervical ganglia of mice with heart failure. An accumulation of macrophages led to progressive inflammation and scarring within the ganglia, which in advanced disease caused permanent damage to the nervous system. This led to a reduced level of melatonin in the animals' bodies and circadian disruption.
Similar effects have been observed in humans: The cervical ganglion was also scarred and enlarged in people with the disease. Early medical intervention with drugs that restore melatonin production by destroying macrophages in the mouse model offers hope for future human treatment. Focusing on ganglia in general may also be useful in diagnosing heart patients, as they can be easily and non-invasively measured using ultrasound.