Mapeamento com Software Coherent para Ablacao de Flutter Atrial Atipico – Um Passo a Frente na Compreensao do Mecanismo da Arritmia
Ontology highlight
ABSTRACT:
SUBMITTER: Sousa P
PROVIDER: S-EPMC8757155 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava-tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases.
| S-EPMC5522718 | biostudies-other
Project description: Not available
| S-EPMC7498508 | biostudies-literature
Project description:BackgroundStandard therapy of atypical atrial flutter (AFL) aims at deploying ablation lines between two non-conducting anatomical structures, thereby creating a line of block within the re-entry circuit. We have developed an ablation strategy, where we incorporate voltage information as a surrogate for atrial fibrosis from the electro-anatomical map (EAM) during AFL ablation procedures to create individualized, substrate-based ablation lines along the area of most pronounced low-voltage within the reentry-circuit.ObjectiveThe aim of this study was to evaluate acute procedural success and long-term outcome of a substrate-based ablation (SBA) strategy in comparison to a standard anatomically based ablation (ABA) strategy for the ablation of atypical AFL.MethodsPatients that underwent ablation for AFL at our institution were included. SBA procedures were compared to ABA procedures. Endpoints were acute termination of AFL and recurrence of the index AFL or any other AFL during follow-up.ResultsWe included 47 patients, 24 individuals (51.1%) in the SBA group and 23 patients (48.9%) in the ABA group. Most patients had signs of atrial cardiomyopathy, namely enlarged left atrial diameter (LAD) and extended amount of left atrial low-voltage areas (LVA). Termination of AFL occurred in 27 of 29 (93.1%) AFL in the SBA group and in 28 of 31 (90.3%) AFL in the ABA group (p = 0.99). Freedom from recurrence of any atypical AFL after 2.5 years was 21.5% in the ABA group compared to 48.8% in the SBA group (p = 0.047).ConclusionSubstrate-based ablation is as effective as an anatomically-based ablation in the acute termination of AFL but yields better rhythm outcome with less recurrence of AFL in patients with atrial cardiomyopathy.
| S-EPMC9043977 | biostudies-literature
Project description:Atrial flutter (AFL) is a common atrial arrhythmia typically characterized by electrical activity propagating around specific anatomical regions. It is usually treated with catheter ablation. However, the identification of rotational activities is not straightforward, and requires an intense effort during the first phase of the electrophysiological (EP) study, i.e., the mapping phase, in which an anatomical 3D model is built and electrograms (EGMs) are recorded. In this study, we modeled the electrical propagation pattern of AFL (measured during mapping) using network theory (NT), a well-known field of research from the computer science domain. The main advantage of NT is the large number of available algorithms that can efficiently analyze the network. Using directed network mapping, we employed a cycle-finding algorithm to detect all cycles in the network, resembling the main propagation pattern of AFL. The method was tested on two subjects in sinus rhythm, six in an experimental model of in-silico simulations, and 10 subjects diagnosed with AFL who underwent a catheter ablation. The algorithm correctly detected the electrical propagation of both sinus rhythm cases and in-silico simulations. Regarding the AFL cases, arrhythmia mechanisms were either totally or partially identified in most of the cases (8 out of 10), i.e., cycles around the mitral valve, tricuspid valve and figure-of-eight reentries. The other two cases presented a poor mapping quality or a major complexity related to previous ablations, large areas of fibrotic tissue, etc. Directed network mapping represents an innovative tool that showed promising results in identifying AFL mechanisms in an automatic fashion. Further investigations are needed to assess the reliability of the method in different clinical scenarios.
| S-EPMC8577834 | biostudies-literature
Project description: Not available
| S-EPMC5509953 | biostudies-literature
Project description: Not available
| S-EPMC9877210 | biostudies-literature
Project description: Not available
| S-EPMC11319868 | biostudies-literature
Project description:IntroductionIdentifying the critical isthmus region (CIR) of atrial re-entry tachycardias (AT) is challenging. The Lumipoint® (LP) software, developed for the Rhythmia® mapping system, aims to facilitate the successful ablation of ATs by identifying the CIR.ObjectiveThe objective of this study was to evaluate the quality of LP regarding the percentage of arrhythmia-relevant CIR in patients with atypical atrial flutter (AAF).MethodsIn this retrospective study, we analyzed 57 AAF forms. Electrical activity (EA) was mapped over tachycardia cycle length resulting in a two-dimensional EA pattern. The hypothesis was that EA minima suggest potential CIRs with slow-conduction-zone.ResultsA total of n = 33 patients were included, with the majority of patients being already preablated (69.7%). LP algorithm identified a mean of 2.4 EA minima and 4.4 suggested CIRs per AAF form. Overall, we observed a low probability of identifying only the relevant CIR (POR) at 12.3% but a high probability that at least one CIR is detected (PALO) at 98.2%. Detailed analysis revealed EA minima depth (≤20%) and width (>50 ms) as the best predictors of relevant CIRs. Wide minima occurred rarely (17.5%), while low minima were more frequently present (75.4%). Minima depth of EA ≤ 20% showed the best PALO/POR overall (95% and 60%, respectively). Analysis in recurrent AAF ablations (five patients) revealed that CIR in de novo AAF was already detected by LP during the index procedure.ConclusionThe LP algorithm provides an excellent PALO (98.2%), but poor POR (12.3%) to detect the CIR in AAF. POR improved by preselection of the lowest and widest EA minima. In addition, there might be the role of initial bystander CIRs becoming relevant for future AAFs.
| S-EPMC10189070 | biostudies-literature
Project description:Transient ischemic attacks (TIAs) typically present with easily recognizable neurological focal deficits. Symptoms such as paroxysmal involuntary movements are not usually considered to be a manifestation of TIA. We report a case with video documentation of TIA due to permanent atrial flutter presenting as acute left hemichorea. To our knowledge, such a case has not yet been reported. The present case constitutes a crucial diagnostic challenge in neurological practice in order to prevent a high risk of subsequent ischemic stroke.
| S-EPMC6380122 | biostudies-literature
Project description:Cerebral ischemia and excitotoxic injury induce transient or permanent bioenergetic failure, and may result in neuronal apoptosis or necrosis. We have previously shown that ATP depletion and activation of AMP-activated protein kinase (AMPK) during excitotoxic injury induces neuronal apoptosis by transcription of the pro-apoptotic BH3-only protein, Bim. AMPK, however, also exerts pro-survival functions in neurons. The molecular switches that determine these differential outcomes are not well understood. Using an approach combining biochemistry, single-cell imaging and computational modeling, we here demonstrate that excitotoxic injury activated the bim promoter in a FOXO3-dependent manner. The activation of AMPK reduced AKT activation, and led to dephosphorylation and nuclear translocation of FOXO3. Subsequent mutation studies indicated that bim gene activation during excitotoxic injury required direct FOXO3 phosphorylation by AMPK in the nucleus as a second activation step. Inhibition of this phosphorylation prevented Bim expression and protected neurons against excitotoxic and oxygen/glucose deprivation-induced injury. Systems analysis and computational modeling revealed that these two activation steps defined a coherent feed-forward loop; a network motif capable of filtering any effects of short-term AMPK activation on bim gene induction. This may prevent unwanted AMPK-mediated Bim expression and apoptosis during transient or physiological bioenergetic stress.
| S-EPMC3438498 | biostudies-literature