Referenced in: none

Automatically associated channels: Kv7.1 , Slo1

Title: [Genetic arrhythmias and gender].

Authors: Elzbieta Katarzyna Biernacka

Journal, date & volume: Prz. Lek., 2014 , 71, 139-41

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25154209

Abstract
Sex differences in the incidence and risk of cardiac arrhythmias are well known. Men have higher incidence of sudden cardiac death, ventricular fibrillation and atrial fibrillation, whereas women are more susceptible to ventricular arrhythmias due to QT prolongation. Sex is one of the most important risk factors of sudden cardiac death in several inherited arrhythmic disorders (male sex in Brugada syndrome and catecholaminergic polymorphic ventricular tachycardia, female sex in long QT syndrome) or disease expression (arrhythmogenic right ventricular cardiomyopathy). Electrophysiological parameters differences between man's and woman's heart are assumed to be a result of genomic (slow) and nongenomic (rapid) pathways.Genomic activity of sex hormones results in higher expression of potassium channels in man's cardiomyocytes. Shorter action potential in men is a substrate for arrhythmias in a mechanism of late afterdepolarization. Longer action potentials in women and higher incidence of LQTS allele transmission to daughters increase a risk of torsade de pointes both in inherited LQTS and in drug-induced QT prolongation. Nongenomic pathway of sex hormones involves transmembrane signal transduction. Antiarrhythmic effect of estrogen which is a calcium antagonist, voltage dependent L- type calcium channels and Na/Ca2+ exchanger inhibitor is the most important rapid electrophysiological hormone effect.