Atrial fibrillation (AF) is a rapid irregular electrical activity in the upper chamber and the most common sustained cardiac arrhythmia. Many patients require radiofrequency ablation (RFA) therapy to restore sinus rhythm. Pulmonary vein isolation requires distinguishing normal atrial wall from the pulmonary vein tissue, and atrial substrate ablation requires differentiating scar tissue, fibrosis, and adipose tissue. However, current anatomical mapping methods for strategically locating ablation sites by identifying structural substrates in real-time are limited. An intraoperative tool that accurately provides detailed structural information and classifies endocardial substrates could help improve RF guidance during RF ablation therapy. In this work, we propose a 7F NIRS integrated ablation catheter and demonstrate endocardial mapping on
- NSF-PAR ID:
- 10273170
- Date Published:
- Journal Name:
- Frontiers in Physiology
- Volume:
- 12
- ISSN:
- 1664-042X
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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ex vivo swine (n = 12) and human (n = 5) left atrium (LA). First, pulmonary vein (PV) sleeve, fibrosis and ablation lesions were identified with NIRS-derived contrast indices. Based on these key spectral features, classification algorithms identified endocardial substrates with high accuracy (<11% error). Then, a predictive model for lesion depth was evaluated on classified lesions. Model predictions correlated well with histological measurements of lesion dimensions (R = 0.984). Classified endocardial substrates and lesion depth were represented in 2D spatial maps. These results suggest NIRS integrated mapping catheters can serve as a complementary tool to the current electroanatomical mapping system to improve treatment efficacy. -
Abstract Background Optical coherence tomography (OCT) has the potential to provide real‐time imaging guidance for atrial fibrillation ablation, with promising results for lesion monitoring. OCT can also offer high‐resolution imaging of tissue composition, but there is insufficient cardiac OCT data to inform the use of OCT to reveal important tissue architecture of the human left atrium. Thus, the objective of this study was to define OCT imaging data throughout the human left atrium, focusing on the distribution of adipose tissue and fiber orientation as seen from the endocardium.
Methods and Results Human hearts (n = 7) were acquired for imaging the left atrium with OCT. A spectral‐domain OCT system with 1325 nm center wavelength, 6.5 μm axial resolution, 15 μm lateral resolution, and a maximum imaging depth of 2.51 mm in the air was used. Large‐scale OCT image maps of human left atrial tissue were developed, with adipose thickness and fiber orientation extracted from the imaging data. OCT imaging showed scattered distributions of adipose tissue around the septal and pulmonary vein regions, up to a depth of about 0.43 mm from the endocardial surface. The total volume of adipose tissue detected by OCT over one left atrium ranged from 1.42 to 28.74 mm3. Limited fiber orientation information primarily around the pulmonary veins and the septum could be identified.
Conclusion OCT imaging could provide adjunctive information on the distribution of subendocardial adipose tissue, particularly around thin areas around the pulmonary veins and septal regions. Variations in OCT‐detected tissue composition could potentially assist ablation guidance.
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Atrial fibrillation (AF) is the most common arrhythmia encountered clinically, and as the population ages, its prevalence is increasing. Although the CHA 2 DS 2 − VASc score is the most used risk-stratification system for stroke risk in AF, it lacks personalization. Patient-specific computer models of the atria can facilitate personalized risk assessment and treatment planning. However, a challenge faced in creating such models is the complexity of the atrial muscle arrangement and its influence on the atrial fiber architecture. This work proposes a semi-automated rule-based algorithm to generate the local fiber orientation in the left atrium (LA). We use the solutions of several harmonic equations to decompose the LA anatomy into subregions. Solution gradients define a two-layer fiber field in each subregion. The robustness of our approach is demonstrated by recreating the fiber orientation on nine models of the LA obtained from AF patients who underwent WATCHMAN device implantation. This cohort of patients encompasses a variety of morphology variants of the left atrium, both in terms of the left atrial appendages (LAAs) and the number of pulmonary veins (PVs). We test the fiber construction algorithm by performing electrophysiology (EP) simulations. Furthermore, this study is the first to compare its results with other rule-based algorithms for the LA fiber architecture definition available in the literature. This analysis suggests that a multi-layer fiber architecture is important to capture complex electrical activation patterns. A notable advantage of our approach is the ability to reconstruct the main LA fiber bundles in a variety of morphologies while solving for a small number of harmonic fields, leading to a comparatively straightforward and reproducible approach.more » « less
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Abstract Atrial fibrillation (AF) is the most common arrhythmia and is associated with inflammation. AF patients have elevated levels of inflammatory cytokines known to promote vascular leak, such as vascular endothelial growth factor A (VEGF). However, the contribution of vascular leak and consequent cardiac edema to the genesis of atrial arrhythmias remains unknown. Previous work suggests that interstitial edema in the heart can acutely promote ventricular arrhythmias by disrupting ventricular myocyte intercalated disk (ID) nanodomains rich in cardiac sodium channels (NaV1.5) and slowing cardiac conduction. Interestingly, similar disruption of ID nanodomains has been identified in atrial samples from AF patients. Therefore, we tested the hypothesis that VEGF-induced vascular leak can acutely increase atrial arrhythmia susceptibility by disrupting ID nanodomains and slowing atrial conduction. Treatment of murine hearts with VEGF (30–60 min, at clinically relevant levels) prolonged the electrocardiographic P wave and increased susceptibility to burst pacing-induced atrial arrhythmias. Optical voltage mapping revealed slower atrial conduction following VEGF treatment (10 ± 0.4 cm/s vs. 21 ± 1 cm/s at baseline,
p < 0.05). Transmission electron microscopy revealed increased intermembrane spacing at ID sites adjacent to gap junctions (GJs; 64 ± 9 nm versus 17 ± 1 nm in controls,p < 0.05), as well as sites next to mechanical junctions (MJs; 63 ± 4 nm versus 27 ± 2 nm in controls,p < 0.05) in VEGF–treated hearts relative to controls. Importantly, super-resolution microscopy and quantitative image analysis revealed reorganization of NaV1.5 away from dense clusters localized near GJs and MJs to a more diffuse distribution throughout the ID. Taken together, these data suggest that VEGF can acutely predispose otherwise normal hearts to atrial arrhythmias by dynamically disrupting NaV1.5-rich ID nanodomains and slowing atrial conduction. These data highlight inflammation-induced vascular leak as a potential factor in the development and progression of AF. -
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