Wavefront Collision Time: A Novel Marker of Atrial Myopathy
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Authors
Ryckman, Nick
Date
Type
thesis
Language
eng
Keyword
electrophysiology , atrial flutter , atrial fibrillation , conduction
Alternative Title
Abstract
Atrial myopathy is a common disease among all populations and varies between patients, however it is predominantly caused by damage to cardiac tissue that ultimately affects the atria. Insults to tissue can range from oxidative stress and inflammation to the natural aging effects, any of which can contribute to myopathic tissue development. Atrial myopathy is an umbrella term for a variety of atrial conditions and promotes a tissue substrate that facilitates the induction of arrhythmias such as atrial fibrillation and flutter. The conduction velocity and propagation are influenced by various factors such as structural, functional, and anatomical barriers. In conjunction, cellular properties may be altered which contributes to changes in action potentials and gap junction remodelling. Altogether, changes in any of these elements will have an impact on conduction velocity and wavefront propagation. Furthermore, we lack a reproducible metric that can detect asymptomatic or pre-clinical atrial myopathy. Therefore, the purpose of this thesis was to investigate a novel metric, known as wavefront collision time, and its ability to characterize atrial myopathy. We explored both the left and right atrium of patients with atrial fibrillation and typical atrial flutter, respectively. During the right atrial portion of our study, we determined that patients with atrial flutter had a significantly slower wavefront propagation than the control cohort (132.6±17.3msec vs 99.1±11.6msec, p<0.001). There was also a higher proportion of hypertension, ischemic heart disease, and sleep apnea seen among patients with AFL (p=0.001, 0.006, and 0.017, respectively). In the left atrial portion of this project, we determined that patients who experience recurrence of atrial fibrillation displayed a significantly slower propagation when compared to patients who remained in sinus rhythm (134.0±35.1msec vs 116.4±25.7msec, p=0.03). Moreover, patients with persistent atrial
fibrillation displayed a significantly slower propagation in comparison to those with paroxysmal ii
(127.4±25.7msec vs 113.6±20.9msec, p=0.02). Overall, utility of wavefront propagation and collision time is an objective marker of atrial myopathy and propensity for both atrial flutter and atrial fibrillation. Assessment of collision time may identify patients at risk of atrial arrhythmia and can inform larger studies to investigate this as a tool for clinical decision making.
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ProQuest PhD and Master's Theses International Dissemination Agreement
Intellectual Property Guidelines at Queen's University
Copying and Preserving Your Thesis
This publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.