Korean researchers reported on work showing the role a small heat-shock protein, alpha B-crystallin, could play in suppressing arrhythmia.
A small heat-shock protein, alpha B-crystallin, could play a role in suppressing arrhythmia.
Hyelim Park, of the Division of Cardiology, Yonsei University College of Medicine, Seoul, Korea, looked at what happened to lab rats injected with porcine cardiac myosin. The animals were experimental autoimmune myocarditis rats. Another group of similar rats got injections of alpha B-crystallin with TAT protein transduction domain or GFP.
At the end of the study their hearts were perfused, mapped optically to analyze action potential durations and restitution kinetics and they were tested for VF vulnerability. The intracellular calcium dynamics were measured in rat neonatal cardiomyocyte treated with TNF.
In the first group, 4 rats died and had ventricular arrhythmia. But in the group that got Myo+CryAB none of the rats died.
“CryAB treatment suppressed ventricular arrhythmia,” Park wrote in a poster presented Saturday, March 14 at the American College of Cardiology meeting in San Diego.
It did so “by preventing spontaneous Ca2+ release, and attenuating inflammation and oxidative stress,” he said.
The study suggests that CryAB may be a new way to manage myocarditis by reversing inflammation and oxidative stress.