Bone hormone could provide new treatment for heart rhythm disorder
A hormone which helps regulate bone mass is also produced by the heart and could help treat people with a dangerous heart rhythm disorder, according to new research published in the journal Nature. Queen’s Old Member Professor Svetlana Reilly (DPhil in Cardiovascular Medicine, 2006), who is British Heart Foundation Intermediate Fellow at the Radcliffe Department of Medicine, led the research team which also included Dr David Menassa, Stipendiary Lecturer in Neurophysiology and Neuroscience at Queen’s. The work was an international collaboration with the University of Montreal, Baylor College of Medicine in USA and the University of Melbourne.
Until now, the hormone calcitonin was only thought to be produced by the thyroid gland, with no known effects on the heart. The new research has revealed that cells in the upper chambers of the heart, known as the atria, produce approximately 16 times more calcitonin than cells in the thyroid.
The researchers also found that the hormone plays a vital role in reducing atrial scarring. Such scarring makes it harder for electrical impulses to travel smoothly through the atria and can cause them to beat in a chaotic manner, known as atrial fibrillation (AF).
The team studied muscle cells from atrial biopsies taken from people undergoing heart surgery and found that they released calcitonin. Interestingly, cells from biopsies of patients with severe AF produced six times less calcitonin.
Looking further, they saw that the calcitonin receptor was present in atrial cells responsible for producing collagen, a major component of scar tissue. When the team treated these cells – called fibroblasts – with calcitonin the cells produced 46 per cent less collagen.
Reducing scar tissue
Further experiments showed that mice which were unable to produce calcitonin in their hearts developed 2.5 times more atrial scar tissue, compared to mice with normal levels of calcitonin. They also developed AF at a younger age and had approximately 16 times longer episodes of AF. Strikingly, atrial scarring and AF were completely prevented in mice whose hearts produced greater amounts of calcitonin.
Around 1.4 million people in the UK have been diagnosed with atrial fibrillation, which can significantly increase a person’s risk of stroke by promoting the formation of blood clots in the heart that may then travel to the brain and block blood vessels there.
Researchers now hope that this new heart hormone and its receptor may hold the key to treating this potentially devastating condition.
Adding a new heart hormone to the list
Professor Svetlana Reilly said: ‘For a long time we’ve known the heart only produces a small number of hormones, and we can now add a new one to the list. Discovering that calcitonin is released by the heart should open new doors for developing heart treatments. We now need to explore how we can best restore the actions of this hormone to treat people with this type of AF, and to understand when the best time to treat someone would be.’
Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said: ‘Many of the treatments available for AF focus on restoring a normal atrial rhythm, controlling the rate at which the heart beats or thinning the blood to reduce the risk of stroke – but they do not tackle the atrial scarring seen in people with severe AF. These discoveries could be game-changing for the management of AF. Developing a new treatment to prevent or reverse atrial scarring could provide a lifeline to many people at risk of or living with AF.’
Read the full paper: ‘Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia’.
Below: a summary figure of the main findings shown in the paper, by Dr Jenny Dewing