WASHINGTON, May 21, 2018 /PRNewswire/ — An article published in Experimental Biology and Medicine (Volume 243, Issue 8, May, 2018) identifies a new approach for treating cardiac arrythmias (http://journals.sagepub.com/doi/full/10.1177/1535370218769420). The study, led by Dr. Congxin Huang, in the Cardiovascular Research Institute at Wuhan University in China, reports that treatment with a β-receptor antagonist abolishes cardiac arrythmias in a mouse model without AMPKa2, an important energy sensing enzyme in the heart.
Cardiac arrhythmias account for over 600,000 sudden cardiac deaths each year. Arrhythmias occur when the electrical impulses that coordinate the beating of the heart do not function properly. Improper electrical activity results in a heartbeat that is too fast, too slow or irregular. Sudden death occurs when the heart quivers rather than beating, resulting in an insufficient blood supply to vital organs. Over half of the unexplained sudden deaths are due to genetic mutations that alter the heart’s electrical activity. Identifying these mutations and their impact on heart function may decrease the incidence of sudden death and lead to new treatments for patients.
The present study by Dr. Huang and colleagues explored the role of an important energy sensing enzyme, AMPKα2, in cardiac electrophysiology. Although AMPKa2 deficiency has been reported to alter the function of the sympathetic nervous system, which is essential for normal heart function, its role in cardiac arrythmias has not been explored. Mice without AMPKα2 were more vulnerable to induced cardiac arrythmias than mice with normal levels of AMPKα2. Furthermore, treatment with a β-receptor antagonist abolished the effects of AMPKα2 deficiency on cardiac physiology. Dr. Huang said that “the incidence of arrhythmia is very high in the world. Though there are several methods used to treat arrhythmias, some are ineffective and others have limitations. So, identifying new targets for the treatment of arrhythmias has great significance.”
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology & Medicine, said, “Huang and colleagues have demonstrated that AMP-activated protein kinase-a2 knockout (AMPKa2-/-) mice had shortened repolarization of the monophasic action potential of the heart and facilitated the incidence of ventricular arrhythmias. They further showed that β-adrenoceptor activation, resulting from catecholamine release, was primarily responsible for the changes observed in cardiac electrophysiology.”
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SOURCE Society of Experimental Biology and Medicine
