The pulmonary vein myocardium exhibits unique electrophysiological properties, such as intracellular Ca(2+) oscillations and low repolarizing potency, which may underlie atrial fibrillation.
Understanding the electrophysiological mechanisms of pulmonary vein automaticity, particularly intracellular Ca2+ handling and repolarization, may guide novel pharmacological therapies for atrial fibrillation.
The pulmonary vein contains a myocardial layer extending from the left atrium, which is receiving attention as the source of ectopic electrical activity underlying atrial fibrillation. Electrophysiological and pharmacological analysis of the pulmonary vein myocardium performed in various experimental animal species have revealed characteristics such as presence of intracellular Ca(2+) oscillations and low repolarizing potency. The automaticity of the pulmonary vein myocardium is affected by various neurotransmitters, hormones and pharmacological agents. Clarification of the mechanisms and regulation of pulmonary vein automaticity would lead to the development of novel therapeutic strategies and pharmacological agents for atrial fibrillation.
Namekata et al. (Tue,) conducted a review in Atrial fibrillation. The pulmonary vein myocardium exhibits unique electrophysiological properties, such as intracellular Ca(2+) oscillations and low repolarizing potency, which may underlie atrial fibrillation.
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