Ectopic and reentrant activation patterns in the posterior left atrium during stretch-related atrial fibrillation
Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, 2800 Plymouth Road, Ann Arbor, MI 48109, USAProgress in Biophysics and Molecular Biology (Impact Factor: 2.27). 08/2012; 110(2-3). DOI: 10.1016/j.pbiomolbio.2012.08.004
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in humans and is predicted to dramatically increase its prevalence in the future. There is experimental evidence that increasing stretch increases the dominance of the pulmonary veins (PVs) during AF in isolated hearts and ectopic activity in the isolated PVs, but the ionic mechanisms underlying such effects are not clear and the ability of the PVs to favorably host functional reentry during stretch cannot be excluded. We used a combination of endocardial-epicardial optical mapping with phase and spectral analysis to study stretch-related AF (SRAF) in normal isolated sheep hearts. We have found rapid AF sources in the posterior left atrium (PLA) and PV region and their activation frequency and level of organization correlated with intra-atrial pressure. Analysis of the surfaces' optical mapping data in the phase domain reveals that activation of the PLA consisted of alternating patterns of breakthroughs, reentries and relatively simple waves swiping across the mapped field. The patterns on the endocardial and epicardial PLA surface at any given moment of time of the SRAF could be either identical or not identical, and the activity in the thickness of the PLA wall is hypothesized to conform to either ectopic discharge or scroll waves, but a definite evidence for the presence of such mechanisms is currently lacking. Thus the understanding of the manner by which the mechano-electric feedback effects in the PLA, including the PVs, become important in the initiation and maintenance of AF requires further detailed investigation.
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ABSTRACT: Introduction: Left ventricular hypertrophy (LVH) predisposes patients to arrhythmias, but the mechanism of these arrhythmias is unclear. Here we show that hearts from spontaneously hypertensive rats (SHR) have a lower threshold for induction mechanically induced arrhythmias compared to age matched Wistar-Kyoto (WKY). Methods: Recordings were made from isolated hearts from nine month old SHR (n = 18) and WKY (n = 17) rats. A water filled balloon in the left ventricle had its volume controlled by a servo-driven syringe. LVEDP was abruptly increased in increments until an ectopic beat was detected by an epicardial MAP electrode. Alternatively, LVEDP was abruptly reduced back to 5 mm Hg from an elevated pressure. Results: SHR hearts had a lower threshold for stretch induced ectopics (29.87 ± 2.79 mm Hg vs. 42.23 ± 2.33 mm Hg, p < 0.01) and for release induced ectopics (24.09 ± 1.40 vs. 37.23 ± 3.22, p < 0.01). Perfusion with 100 μM streptomycin increased threshold for stretch induced ectopics in both strains (from 49.4 ± 4.7 to 69.5 ± 6.9 mm Hg in WKY; p < 0.05 and from 21.2 ± 3.5 to 39.7 ± 9.0 mm Hg in SHR; p = 0.07). 100 μM streptomycin also increased threshold for release induced ectopics in SHR (from 23.5 ± 3.6 to 32.6 ± 4.9 mm Hg; p < 0.05) but not in WKY. Perfusion with 0.01 μM isoprenaline decreased the threshold for stretch induced ectopics in both strains (from 40.6 ± 5.0 to 22.6 ± 2.5 mm Hg in WKY; not significant at p < 0.05; p = 0.07 and from 31.0 ± 5.5 to 14.3 ± 2.5 mm Hg in SHR; p < 0.05). Conclusions: Hearts from SHR are more susceptible to both stretch-induced and release-induced arrhythmia.
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ABSTRACT: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in human beating hearts. AF initiates self-perpetuating changes in electrophysiology, structure and functional properties of the atria, a phenomenon known as atrial remodeling. Hypertension, heart failure, valvular heart disease, sleep apnea, congenital heart disease are well known risk factors for AF that contribute to the development of atrial substrate. There is some evidence that reversal of atrial remodeling is possible with correction of antecedent conditions, however the timing of the intervention or upstream therapy may be critical. This review will describe the pathophysiology of atrial remodeling as it pertains to AF. We will describe components of remodeling including changes in atrial refractoriness, conduction and atrial structure, in addition to autonomic changes and anatomic factors that predispose to remodeling. We will discuss our current understanding of the electrophysiological changes that contribute to AF persistence. We will describe nature of atrial and pulmonary vein remodeling in the context of different forms of AF, with and without predisposing risk factors. We will describe the nature of remodeling over time following therapeutic interventions such as AF ablation in order to show that it does not necessarily improve and may worsen.
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