PCSK9 inhibitor pre‐treatment was shown, relative to control, to result in the following: (a) improved mitochondrial function as indicated by a decrease in mitochondrial ROS, mitochondrial depolarization and mitochondrial swelling; (b) inhibition of mitochondrial fission; (c) attenuated cardiac arrhythmia via increased phosphorylation of Cx43; (d) decreased apoptosis related protein expression as indicated by decreased Bax, cytochrome c and cleaved‐caspase 3; (e) infarct size reduction; and (f) improved left ventricular function. This evidence concerns the gene GJA1 and cardiac rhythm disease.