The Role of Impaired Interatrial Conduction in Paroxysmal Atrial Fibrillation
Abstract: The aim of this thesis was to evaluate the role of interatrial conduction defects in the genesis of lone paroxysmal atrial fibrillation (AF) using combined approach of non-invasive signal-averaged P-wave ECG, invasive electrophysiological (EP) studies, anatomical studies and animal experiments. Non-filtered signal-averaged P-wave ECG revealed irregularities in orthogonal P-wave morphology and the presence of double-peaked configurations of P-wave spatial magnitude in patients with lone paroxysmal AF compared with healthy individuals (I), suggesting the presence of interatrial conduction delays localised in the posterior-inferior interatrial route. The interpretation of human P-wave ECG was supported by the experimental study (V), in which similar configurations of P-wave spatial magnitudes were reproduced by the interruption of conduction over the posterior interatrial route in pigs. In a series of endocardial EP studies (II), predominant conduction disturbances within the right atrium causing localised inferior-posterior interatrial conduction delays were found in a group of patients with lone paroxysmal AF during sinus rhythm and atrial stimulation. In AF patients, induction of the arrhythmia paroxysms was associated with conduction disturbances in the posterior septal region (III), suggesting that the initial re-entry occurs there. In the pathology study (IV), we showed that in addition to the anteriorly located Bachmann's bundle, numbers of muscle bundles connect the right and the left atria across the posterior interatrial groove. These posterior interatrial routes are non-uniform structures subjected to substantial variability, which may be an anatomical prerequisite for interatrial conduction defects and explain why some patients are more prone to developing interatrial conduction blocks and atrial fibrillation than others.
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