Experimental therapy shows promise in easing heart scarring linked to irregular rhythms

Scientists have identified a method that may reverse some existing heart scarring and lessen abnormal heart rhythms in experimental studies. The strategy focuses on a small genetic signal that disrupts the heart’s ability to regulate scar-forming cells.

The research could open the door to a new way of treating atrial fibrillation, a common disorder in which the upper chambers of the heart beat irregularly. Rather than targeting only the electrical problem, the researchers examined the tissue changes that help keep the condition going.

Researchers at Baylor College of Medicine and the University of Oxford tested the method in mice and in heart cells taken from people with atrial fibrillation. The findings represent an early step toward a possible human therapy and do not show that the treatment already works in patients.

Published in Nature Cardiovascular Research, the study focused on fibroblasts. These cells help support the heart’s structure, but when they become too active, they can create excess scar tissue.

That scarring can interfere with the passage of electrical signals through the upper chambers of the heart. As a result, abnormal rhythm and tissue changes can reinforce each other, creating a cycle that is difficult to break.

The team traced a key part of this process to a molecule called microRNA-31-5p. MicroRNAs are small genetic regulators that influence how cells use instructions for making proteins.

In this case, the molecule reduced production of a receptor that responds to calcitonin, a hormone. Without that receptor, the fibroblasts lost an important restraint, became more active, and produced more scar tissue.

The researchers created a blocker that shields the precise site where the microRNA interferes with the receptor’s genetic instructions. The aim is to preserve that helpful signal without shutting down all of the microRNA’s other functions.

In cells from people with atrial fibrillation, the blocker restored production of the receptor. Tests in mice then showed that the therapy could both prevent additional scarring and reduce scar tissue that had already formed.

In mice with established disease, scar tissue dropped by roughly 30% from its starting level, while untreated animals continued to worsen. The treated mice also showed a lower burden of abnormal atrial rhythms.

Although the results are encouraging, reversing scarring in mice is not the same as proving a treatment is safe and effective in people. Human trials would still need to determine how to deliver the blocker, what dose to use, and whether the benefits last.

The discovery points to a possible way to address part of the tissue damage that helps sustain irregular heartbeats. If future research succeeds, treatment could target the scar-forming process as well as the rhythm disturbance it helps create.

If you are interested in this topic, please read articles about Exploring the best diet for people with heart rhythm disorders, and Drinking more coffee linked to heart rhythm disease.

For more information, please see articles about Why coffee may affect your heartbeat, and Omega-3 fatty acids and heart health: What you need to know.

Source: Baylor College of Medicine and University of Oxford.