Abstract
The purpose of this communication is to introduce in the medical literature an additional factor until now hypothesized action of atrial cells depolarization as factor in intracellular flow of glycogen molecules coalescing against the gap junctions. The demonstrated effect of gap junction blockers on paired cells contractility combined with gap junction’s selectivity towards glycogen molecules; and the visualization of contrasting intracellular glycogen images during atrial fibrillation are shown. Published data supporting atrial myocytes contraction as a mechanism in intracellular glycogen molecules migration and its deleterious effects leading into atrial fibrillation (AF) is proposed.
Highlights
In a previous publication in 2014, we show that in atrial myocytes glycogen is heterogeneously distributed in both atria in the normal goat heart; in atrial fibrillation (AF) the density of glycogen deposits concentrating against the intercalated discs and side to side connections in the left atrial appendage is a critically distinct difference
MATERIALS AND METHODS A literature search was conducted relevant to changes in atrial myocytes architecture, with specific emphasis in the effect of myocytes intercellular gap junction blockage, such as from glycogen molecules which has been previously hypothesized as additional factor in the genesis of atrial fibrillation (AF)
Published data presented supports the physical force transduction by atrial intracellular depolarization as a primary factor in glycogen molecules accumulating against intercalated discs and causing deleterious effects in cell contractility
Summary
In a previous publication in 2014, we show that in atrial myocytes glycogen is heterogeneously distributed in both atria in the normal goat heart; in AF the density of glycogen deposits concentrating against the intercalated discs and side to side connections in the left atrial appendage is a critically distinct difference. Impediment of cell to cell conduction could result in a non-uniform wavefront of activation, with areas of slowed conduction, predisposing the left atrium to reentrant based atrial fibrillation” [1]
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