Abstract
Ectopic activity in the pulmonary vein cardiac muscle sleeves can both induce and maintain human atrial fibrillation. A central issue in any study of the pulmonary veins is their difference from the left atrial cardiac muscle. Here, we attempt to summarize the physiological phenomena underlying the occurrence of ectopic electrical activity in animal pulmonary veins. We emphasize that the activation of multiple signaling pathways influencing not only myocyte electrophysiology but also the means of excitation–contraction coupling may be required for the initiation of triggered or automatic activity. We also gather information regarding not only the large-scale structure of cardiac muscle sleeves but also recent studies suggesting that cellular heterogeneity may contribute to the generation of arrythmogenic phenomena and to the distinction between pulmonary vein and left atrial heart muscle.
Highlights
It has been known since the late 19th century [1], interest in the study of cardiac muscle into mammalian thoracic vein exploded with the discovery within human pulmonary veins (PV) of sites of focal ectopic electrical discharges triggering and maintaining atrial fibrillation (AF) [2].In this context, it should be emphasized that the PV retain a venous structure, including endothelium and vascular smooth muscle layers
Excitation–contraction coupling is initiated by action potential (AP) triggering the opening of L-type calcium channels (LCC) and calcium entry, which induces in return the release of calcium from the sarcoplasmic reticulum through ryanodine receptors (RyR)
This review focuses on the physiology of the PV myocardial sleeves, similar results have been observed in the rat superior vena cava (SVC) and azygos vein [31,45,72], in which myocardial sleeves extend and constitute a source of arrhythmia in humans [2]
Summary
It has been known since the late 19th century [1], interest in the study of cardiac muscle into mammalian thoracic vein exploded with the discovery within human pulmonary veins (PV) of sites of focal ectopic electrical discharges triggering and maintaining atrial fibrillation (AF) [2] In this context, it should be emphasized that the PV retain a venous structure, including endothelium and vascular smooth muscle layers. In parallel with laboratory studies intended for translation to the clinic, basic physiological research has been conducted to characterize differences in the electrophysiology, pharmacology and excitation–contraction coupling of atrial muscle and that of the PV sleeves in an attempt to understand the phenomena underlying the occurrence of PV ectopic electrical activity promoting AF.
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