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Researchers Identify Calcium-Triggered Mechanism Involved in Arrhythmias

Rush University Medical Center researchers have identified the underlying mechanism of calcium-triggered cardiac arrhythmias, or irregular heartbeats. The discovery, described in the Jan. 19 issue of Nature Medicine, has major implications for the development of molecularly designed drugs specifically targeted at this form of arrhythmia.

The study was led by Wayne, Chen, PhD, professor of molecular biophysics and physiology at Rush and professor of physiology and biochemistry at the University of Calgary-Libin Institute. Michael Fill, PhD, professor of molecular biophysics and physiology at Rush, collaborated on the research.

Cardiac arrhythmias can cause dizziness and fainting, or in severe cases, sudden death. While many factors, including genetics, contribute to the development of arrhythmias, research has shown that a common cause of cardiac arrhythmias is calcium overload. Calcium overload disrupts the finely controlled electrical activity governing contraction of heart muscle.

Calcium is stored inside cardiac cells, much like skeletal muscle cells, in preparation for contraction. The protein responsible for release of calcium is known as the cardiac ryanodine receptor (RyR2), or the calcium release channel, which acts like a safety valve that prevents calcium overload.

“This is a very important protein because naturally occurring mutations in the gene have been linked to many cardiac diseases, including atrial fibrillation and sudden cardiac death,” Chen said. 

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