Although arrhythmia improved, the animals still had heart scarring, a symptom from a different underlying condition. Palatinus noted that was actually an encouraging result. It suggests arrhythmia and heart scarring can occur independently and that it could be possible to treat abnormal heart rhythms even when the heart is severely scarred. “This is a new paradigm,” he says.
The treatment success in mice suggests that raising levels of GJA1-20k might restore normal heart rhythms in patients with arrhythmogenic cardiomyopathy, too. For patients, Palatinus says, it might be possible to deliver the therapeutic protein directly to the heart. Further research will be needed to develop the treatment for clinical use.
Disruptions in protein trafficking are thought to contribute to arrhythmias beyond those caused by arrhythmogenic cardiomyopathy, and Palatinus is optimistic that a similar treatment strategy might be useful for those conditions, too. If so, that could one day give patients and their doctors an alternative to the ion channel-blocking drugs currently used to treat many arrhythmias, which can slow the heart and even lead to new rhythm problems for some patients.
-Written by Jennifer Michalowski
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The research was supported by the National Institutes of Health, The Harold Geneen Charitable Trust, and the Nora Eccles Treadwell Foundation and published as “GJA1-20k Rescues Cx43 Localization and Arrhythmias in Arrhythmogenic Cardiomyopathy.”