Epicardial Connections as Intra-Atrial Conduction Routes in a Patient With Advanced Atrial Remodeling
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ABSTRACT:
SUBMITTER: Tsumagari Y
PROVIDER: S-EPMC8603051 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectivesThis study sought to characterize direction-dependent and coupling interval-dependent changes in left atrial conduction and electrogram morphology in uniformly classified patients with paroxysmal atrial fibrillation (AF) and normal bipolar voltage mapping.BackgroundAlthough AF classifications are based on arrhythmia duration, the clinical course, and treatment response vary between patients within these groups. Electrophysiological mechanisms responsible for this variability are incompletely described.MethodsIntracardiac contact mapping during incremental atrial pacing was used to characterize atrial conduction, activation dispersion, and electrogram morphology in 15 consecutive paroxysmal AF patients undergoing first-time pulmonary vein isolation. Outcome measures were vulnerability to AF induction at electrophysiology study and 2-year follow-up for arrhythmia recurrence.ResultsConduction delay showed a bimodal distribution, occurring at either long (high right atrium pacing: 326 ± 13 ms; coronary sinus pacing: 319 ± 16 ms) or short (high right atrium pacing: 275 ± 11 ms; coronary sinus pacing: 271 ± 11 ms) extrastimulus coupling intervals. Arrhythmia recurrence was found only in patients with conduction delay at long extrastimulus coupling intervals, and patients with inducible AF were characterized by increased activation dispersion (activation dispersion time: 168 ± 29 ms vs. 136 ± 11 ms). Electrogram voltage and duration varied throughout the left atrium, between patients, and with pacing site but were not correlated with AF vulnerability or arrhythmia recurrence.ConclusionsWithin the single clinical entity of paroxysmal AF, incremental atrial pacing identified a spectrum of activation patterns correlating with AF vulnerability and arrhythmia recurrence. In contrast, electrogram morphology (characterized by electrogram voltage and duration) was highly variable and not associated with AF vulnerability or recurrence. An improved understanding of the electrical phenotype in AF could lead to improved mechanistic classifications.
| S-EPMC5612260 | biostudies-literature
Project description:ObjectiveIt is unknown whether epicardial and endocardial validation of bidirectional block after thoracoscopic surgical ablation for atrial fibrillation is comparable. Epicardial validation may lead to false-positive results due to epicardial tissue edema, and thus could leave gaps with subsequent arrhythmia recurrence. It is the aim of the present study to answer this question in patients who underwent hybrid atrial fibrillation ablation (combined thoracoscopic epicardial and endocardial catheter ablation).MethodsAfter epicardial ablation of the pulmonary veins (PVs) and connecting inferior and roof lines (box lesion), exit and entrance block were epicardially and endocardially evaluated using an endocardial His Bundle catheter and electrophysiological workstation. If incomplete lesions were found, endocardial touch-up ablation was performed. Validation results were also compared to predictions about conduction block based on tissue conductance measurements of the epicardial ablation device.ResultsTwenty-five patients were included. Epicardial validation results were 100% equal to the endocardial results for the left superior, left inferior, and right inferior PVs and box lesion. For the right superior PV, 85% similarity was found. Based on tissue conductance measurements, 139 lesions were expected to be complete; however, in 5 (3.6%) a gap was present.ConclusionsEpicardial bidirectional conduction block in the PVs and the box lesion corresponded well with endocardial bidirectional conduction block. Conduction block predictions by changes in tissue conductance failed in few cases compared to block confirmation. This emphasizes that tissue conduction measurements can provide a rough indication of lesion effectiveness but needs endpoint confirmation by either epicardial or endocardial block testing.
| S-EPMC7715993 | biostudies-literature
Project description:A 73-year-old woman was admitted for atrial tachycardia (AT) ablation. The activation map and pacing study indicated that the AT propagated around the left pulmonary vein and that the Marshall bundle (MB) bypassed the scar area of the left pulmonary vein ridge and mitral isthmus. The Rhythmia Mapping System revealed double potentials propagated along the assumed position of the MB. The mapping system includes a confidence mask that can be used to visually identify low-confidence areas of the map based upon extremely low-voltage signals. Given the low-voltage area in the endocardial side, the epicardial conduction was emphasized.
| S-EPMC6009767 | biostudies-literature
Project description:A 66-year-old male had an atrial tachycardia (AT) during a first extensive pulmonary vein (PV) isolation (PVI) of persistent atrial fibrillation. Activation mapping during the AT using Rhythmia (Boston Scientific, Marlborough, MA, USA) exhibited a centrifugal pattern with the earliest activation at the left-sided carina, and conduction towards the inferior left atrium (LA) over the left PVI line. The post-pacing interval was similar to the tachycardia cycle length (TCL) upon entrainment from the LA roof, left-sided carina, and anterior, inferior, and septal LA, but was longer than the TCL upon entrainment from the left superior PV and lateral and posterior LA. These findings suggested the presence of a macroreentrant AT circuit with epicardial conduction from the roof toward the inferior LA via the left-sided carina over the PVI line and propagation to the anterior LA through the septum. A radiofrequency application at the left-sided carina terminated the AT. This case suggested a rare type of PV-gap reentrant AT with multiple epicardial conduction gaps by high-resolution activation mapping and entrainment pacing, which may have been associated with non-transmural radiofrequency lesions along the PVI line. Further, the origin of the residual epicardial gaps may have been subepicardial myocardial strands or the Marshall ligament. <Learning objective: Pulmonary vein (PV)-gap reentrant atrial tachycardias (ATs) generally have conduction gaps on the previous PV isolation lines. However, this case had a variant of PV-gap reentrant AT with multiple epicardial conduction gaps, without any endocardial gaps on the PV isolation line. High-resolution activation mapping during PV pacing and the AT in combination with entrainment pacing may facilitate an identification of residual epicardial connections associated with the PV-gap reentrant AT circuits.>.
| S-EPMC7718528 | biostudies-literature
Project description:BackgroundEpicardial adipose tissue (EAT) accumulation is associated with cardiac arrhythmias. The effect of EAT secretome (EATs) on cardiac electrophysiology remains largely unknown.ObjectiveThe purpose of this study was to investigate the arrhythmogenicity of EATs and its underlying molecular and electrophysiological mechanisms.MethodsWe collected atrial EAT and subcutaneous adipose tissue (SAT) from 30 patients with atrial fibrillation (AF), and EAT from 3 donors without AF. The secretome was collected after a 24-hour incubation of the adipose tissue explants. We cultured neonatal rat ventricular myocytes (NRVMs) with EATs, subcutaneous adipose tissue secretome (SATs), and cardiomyocytes conditioned medium (CCM) for 72 hours. We implemented the electrophysiological changes observed after EATs incubation into a model of human left atrium and tested arrhythmia inducibility.ResultsIncubation of NRVMs with EATs decreased expression of the potassium channel subunit Kcnj2 by 26% and correspondingly reduced the inward rectifier K+ current IK1 by 35% compared to incubation with CCM, resulting in a depolarized resting membrane of cardiomyocytes. EATs decreased expression of connexin43 (29% mRNA, 46% protein) in comparison to CCM. Cells incubated with SATs showed no significant differences in Kcnj2 or Gja1 expression in comparison to CCM, and their resting potential was not depolarized. Cardiomyocytes incubated with EATs showed reduced conduction velocity and increased conduction heterogeneity compared to SATs and CCM. Computer modeling of human left atrium revealed that the electrophysiological changes induced by EATs promote sustained reentrant arrhythmias if EAT partially covers the myocardium.ConclusionEAT slows conduction, depolarizes the resting potential, alters electrical cell-cell coupling, and facilitates reentrant arrhythmias.
| S-EPMC9558493 | biostudies-literature
Project description:PurposePR interval prolongation > 200 ms resulting in the diagnosis of first-degree atrioventricular block (AVB1) is caused by a delay in the AV nodal/His conduction and/or the right intra-atrial conduction (RIAC). The aim of the study was to assess the prevalence of AVB1 due to RIAC delay (AVB1 with normal AH and HV) in patients with atrial fibrillation (AF) and atrial flutter (AFlu).MethodsWe included 1067 consecutive patients (33% female, age 63 ± 13 years) referred for catheter ablation of AF (AF-group) (453 patients), AF and AFlu (136 patients), AFlu (292 patients), and AVNRT/AVRT (186 patients). AH-, HV-, PR-interval, and P-wave duration were measured on the 12-lead ECG and the intracardiac electrograms in sinus rhythm. RIAC delay was defined as a prolonged PR interval > 200 ms with normal AH and HV intervals.ResultsThe prevalence of AVB1 is higher in patients with AFlu (41%) and AF (21%) and patients with both arrhythmias (30%) as compared with a reference group (8%) of patients with AVNRT/AVRT. AVB1 was due to RIAC delay in 42 of 67 patients (63%) in the AF-group, in 37 of 96 patients (39%) in the AFlu-group, and in 17 of 36 patients (47%) in the AF/AFlu group, respectively. AV nodal conduction delay was more common in AFlu patients compared with AF patients.ConclusionRIAC delay is a common underlying cause of AVB1 in patients with AF and AFlu. These findings may impact the prescription of antiarrhythmic and AV-nodal blocking drugs.
| S-EPMC8324594 | biostudies-literature
Project description:BackgroundImproved understanding of the interconnectedness of structural remodeling processes in atrial fibrillation (AF) in patients could identify targets for future therapies.MethodsWe present transcriptome sequencing of atrial tissues of patients without AF, with paroxysmal AF, and persistent AF (total n = 64). RNA expression levels were validated in the same and an independent cohort with qPCR. Biological processes were assessed with histological and immunohistochemical analyses.ResultsIn AF patients, epicardial cell gene expression decreased, contrasting with an upregulation of epithelial-to-mesenchymal transition (EMT) and mesenchymal cell gene expression. Immunohistochemistry demonstrated thickening of the epicardium and an increased proportion of (myo)fibroblast-like cells in the myocardium, supporting enhanced EMT in AF. We furthermore report an upregulation of endothelial cell proliferation, angiogenesis, and endothelial signaling. EMT and endothelial cell proliferation concurred with increased interstitial (myo)fibroblast-like cells and extracellular matrix gene expression including enhanced tenascin-C, thrombospondins, biglycan, and versican. Morphological analyses discovered increased and redistributed glycosaminoglycans and collagens in the atria of AF patients. Signaling pathways, including cell-matrix interactions, PI3K-AKT, and Notch signaling that could regulate mesenchymal cell activation, were upregulated.ConclusionOur results suggest that EMT and endothelial cell proliferation work in concert and characterize the (myo)fibroblast recruitment and ECM remodeling of AF. These processes could guide future research toward the discovery of targets for AF therapy.
| S-EPMC8567047 | biostudies-literature
Project description:BackgroundEpicardial mapping has shown that atrial substrate may play a role in the characteristics of the resulting atrial fibrillation (AF). However, it is not known whether these differences also occur in 3 dimensions.ObjectiveThis study sought to examine the 3-dimensional characteristics of AF by simultaneously analyzing AF on the epicardial and endocardial surfaces.MethodsDogs were divided into 5 groups: congestive heart failure (CHF), rapid atrial pacing (RAP), mitral regurgitation (MR), control, and methylcholine. A noncontact mapping catheter (Ensite 3000 [Endocardial Solutions, Inc., St. Paul, Minnesota]) was placed in the left atrium (LA), and electrode plaques (240 unipoles) were placed over the epicardial surface. Several AF episodes of at least 30 s were recorded, and isopotential videos of activation and isochronal maps were constructed. In addition, each pair of matched electrograms were cross-correlated (XC) and analyzed with a fast Fourier transform (FFT).ResultsThe RAP model was the only one with an AF mechanism of multiple wavelets in every dog on both surfaces. In addition, when individual signals were compared, the RAP model had the least amount of similarities between the recording surfaces, whereas the CHF model had the most as it had a higher percentage of signals with XC coefficients >0.8 and a higher percentage of signals with similar dominant frequencies (30 +/- 35% vs. 12 +/- 13% and 66 +/- 30% vs. 26 +/- 10%, P < .05).ConclusionAlthough the RAP model had similar AF mechanisms in 3 dimensions, this did not correlate to transmural similarities. Focal mechanisms of AF may have a more uniform wavefront of activation, whereas models with mechanisms of multiple wavelets may have more 3-dimensional properties.
| S-EPMC2843810 | biostudies-literature
Project description:Background:Atrial fibrillation (AF) is accompanied by progressive epicardial fibrosis, dissociation of electrical activity between the epicardial layer and the endocardial bundle network, and transmural conduction (breakthroughs). However, causal relationships between these phenomena have not been demonstrated yet. Our goal was to test the hypothesis that epicardial fibrosis suffices to increase endo-epicardial dissociation (EED) and breakthroughs (BT) during AF. Methods:We simulated the effect of fibrosis in the epicardial layer on EED and BT in a detailed, high-resolution, three-dimensional model of the human atria with realistic electrophysiology. The model results were compared with simultaneous endo-epicardial mapping in human atria. The model geometry, specifically built for this study, was based on MR images and histo-anatomical studies. Clinical data were obtained in four patients with longstanding persistent AF (persAF) and three patients without a history of AF. Results:The AF cycle length (AFCL), conduction velocity (CV), and EED were comparable in the mapping studies and the simulations. EED increased from 24.1 ± 3.4 to 56.58 ± 6.2% (p < 0.05), and number of BTs per cycle from 0.89 ± 0.55 to 6.74 ± 2.11% (p < 0.05), in different degrees of fibrosis in the epicardial layer. In both mapping data and simulations, EED correlated with prevalence of BTs. Fibrosis also increased the number of fibrillation waves per cycle in the model. Conclusion:A realistic 3D computer model of AF in which epicardial fibrosis was increased, in the absence of other pathological changes, showed increases in EED and epicardial BT comparable to those in longstanding persAF. Thus, epicardial fibrosis can explain both phenomena.
| S-EPMC7047215 | biostudies-literature
Project description:Ischemic heart disease remains the leading cause of mortality and morbidity worldwide despite improved possibilities in medical care. Alongside interventional therapies, such as coronary artery bypass grafting (CABG), adjuvant tissue-engineered and cell-based treatments can provide regenerative improvement. Unfortunately, most of these advanced approaches require multiple lengthy and costly preparation stages without in turn delivering significant clinical benefit.
Here, we investigated the effect of epicardial matrix patch-encased atrial appendage micrografts (AAMs) in a mouse model of myocardial infarction. The matrix-covered AAM patches salvaged the myocardium from infarction-induced functional tissue loss. Fibrosis was attenuated, and site-targeted proteomics revealed AAM patch-activated pathways for angiogenesis and cardiogenesis. The matrix component of the graft further supports functional myocardial recovery by ventricular unloading.
The composite epicardial matrix graft encasing AAM micrografts delivers effects desirable for adjuvant cardiac therapy preserving functional cardiac tissue and restricting fibrosis after myocardial infarction.
2019-07-23 | MSV000084120 | MassIVE