Atrial fibrillation and atrial flutter are the most common sustained arrhythmias, however their underlying mechanisms are yet to be fully characterised. This thesis evaluates the electrophysiological and electroanatomical substrate of the atria in patients with these arrhythmias. Experimental studies of atrial fibrillation have demonstrated effective refractory period shortening and conduction slowing as a result of atrial fibrillation giving rise to the concept that "atrial fibrillation begets atrial fibrillation". However, cardioversion to prevent electrical remodelling does not prevent progression of disease, suggesting a "second factor" drives this process. Chapters 2 and 3 evaluate the atrial substrate in patients with "lone" atrial fibrillation. These studies demonstrate such patients, remote from an arrhythmic event, have prolongation of atrial refractoriness, conduction slowing, impairment of sinus node function, site-specific conduction delay, lower voltage and a greater proportion of complex electrograms compared to reference patients. These abnormalities constitute the "second factor" critical to the development and progression of atrial fibrillation. Atrial flutter has a close inter-relationship with atrial fibrillation and these rhythms frequently co-exist. Atrial fibrillation often occurs in patients with heart disease known to demonstrate abnormal atrial substrate; whether similar substrate exists in patients with atrial flutter to account for the co-existence of both arrhythmias is unknown. Chapters 4 and 5 evaluate the atrial substrate in patients with atrial flutter, remote from arrhythmia, demonstrating structural abnormalities characterised by loss of myocardial voltage, conduction slowing and impaired sinus node function, without reduction in atrial refractoriness. These findings implicate a common substrate as the cause of the close inter-relationship between these arrhythmias. There is a frequent association between atrial arrhythmia and sinus node disease for which several mechanisms have been postulated. In addition, there is a size discrepancy between the anatomical sinus node and the much larger functional sinus node complex. little is known about normal sinus node function or the effects of remodelling due to arrhythmia. Chapter 6 characterises sinus node activation to determine the nature and extent of the functional sinus node complex in patients with and without chronic atrial flutter. The functional sinus node complex demonstrates dynamic shifts in activation with preferential pathways of conduction to atrial myocardium. Patients with atrial flutter demonstrate lesser voltage, longer conduction times along preferential pathways and a smaller functional sinus node complex. These findings provide insights into the function of the human sinus node in health and disease. Sites of complex fractionated atrial electrograms and highest dominant frequency are implicated in maintaining atrial fibrillation. Chapter 7 determines the minimum recording duration that accurately characterises electrogram complexity and activation frequency. An electrogram duration of 5 seconds is required to accurately identify these sites. Chapter 8 evaluates the relationship between sites of fractionation and high frequency activation during atrial fibrillation. Greater fractionation and higher dominant frequency are seen in persistent atrial fibrillation and left atria. Preferential areas of high dominant frequency are observed in paroxysmal but not persistent atrial fibrillation. Areas of complex fractionated atrial electrograms are found adjacent to sites of high dominant frequency. / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2009
| Identifer | oai:union.ndltd.org:ADTP/264741 |
| Date | January 2009 |
| Creators | Stiles, Martin Kingsland |
| Source Sets | Australiasian Digital Theses Program |
| Detected Language | English |
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