Abstract
The definition of atrial fibrillation (AF) as a functional electrical disorder does not reflect the significant underlying structural abnormalities. Atrial and Pulmonary Vein (PV) muscle sleeve microstructural remodeling is present, and establishes a vulnerable substrate for AF maintenance. In spite of an incomplete understanding of the anatomo-functional basis for AF, current evidence demonstrates that this arrhythmia usually requires a trigger for initiation and a vulnerable electrophysiological and/or anatomical substrate for maintenance. It is still unclear whether the trigger mechanisms include focal enhanced automaticity, triggered activity and/or micro re-entry from myocardial tissue. Initiation of AF can be favored by both parasympathetic and sympathetic stimulation, which also seem to play a role in maintaining AF. Finally, evolving clinical evidence demonstrates that inflammation is associated with new-onset and recurrent AF through a mechanism that possibly involves cellular degeneration, apoptosis, and subsequent atrial fibrosis.
Highlights
There continues to be a lack of understanding of the pathogenesis of atrial fibrillation (AF)
Current evidence suggests that the pathogenesis of AF is multifactorial, because this arrhythmia may accompany a variety of pathological conditions and may occur in the normal heart, a condition known as ‘lone AF’ [1]
We have demonstrated the variable anatomy of the Pulmonary Vein (PV) myocardium [18,19]; the ostia of the veins were ellipsoid with a similar diameter
Summary
There continues to be a lack of understanding of the pathogenesis of atrial fibrillation (AF). The presence of a susceptible atrial anatomical substrate with areas of conduction block, causing spatial dissociation of the wavelets and promoting re-entry, has been implicated in the perpetuation of the arrhythmia [6] (Fig. 1), the so called chronic AF (persistent or permanent). In chronic AF, atrial remodeling increases the complexity of wave propagation, leads to a multiplication of sites with maximal dominant frequency (known as rotors) and shifts their location away from the PV region into the left atrium. It remains unclear whether this structural remodeling, with features of interstitial fibrosis and myolysis, or an increase in autonomic tone are pro-fibrillatory factors; or whether AF can be induced or produced as a feature of older age or underlying heart disease [7]
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