Cardiac gap junction and pacemaker cells in alcoholic sudden cardiac death

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The influences of myocardial fibrosis and gap junction remodeling on the alcoholic life-threatening ventricular arrhythmias were evaluated in rats, particularly in acute ethanol withdrawal rats. Acute ethanol withdrawal followed 49-day continuous ethanol treatment induced a high risk of myocardial fibrosis formation; down-regulation of gap junction protein connexin (Cx) 43 protein and mRNA expressions; down-regulation of phosphorylated Cx43 protein expression; however, all of them were normalized by carvedilol (can block the sympathetic nervous system completely via β1, β2, and - adrenergic receptors) pretreatment. Acute ethanol withdrawal followed 49-day continuous ethanol treatment is sufficient to increase the risk of myocardial fibrosis formation and gap junction remodeling via the shift of cardiac sympathovagal balance toward sympathetic predominance, and then leads to the onset of the life-threatening ventricular arrhythmias in alcoholic subjects.