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Academic literature on the topic 'ARRHYTHMOGENIC'

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Published: 1 April 2023

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Journal articles on the topic "ARRHYTHMOGENIC"

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Podgoršek, Blaž, Gregor Poglajen, Andraž Cerar, Matjaž Šinkovec, and Bojan Vrtovec. "Arrhythmogenic Cardiomyopathy." Slovenian Medical Journal 87, no. 11-12 (January 4, 2019): 599–618. http://dx.doi.org/10.6016/zdravvestn.2723.

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Arrhythmogenic cardiomyopathy (AC) is a genetic disease of the myocardium characterized by fibro-fatty replacement of the apoptotic myocardium. It primarily affects the right ventricle, however in advanced stages of the disease the left ventricle can also be significantly affected. AC is a challenging diagnosis, especially in the early stages of the disease, and should be considered in all patients presenting with palpitations, syncope or sudden cardiac death when other, more common causes of these symptoms/signs are excluded. In patients with suspected AC, evaluation according to the current Task Force Criteria should be applied to achieve optimal diagnostic yield. The main therapeutic concern in AC patients is the prevention of SCD, and thus all patients with established diagnosis have to be evaluated for potential ICD implantation, which is indicated in the majority of symptomatic patients. In this narrative review we aim to outline current knowledge on the pathophysiology, diagnosis and treatment strategies of AC.
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Priori, Silvia G., and Demetrio J. Santiago. "Arrhythmogenic Cardiomyopathy." Circulation Research 121, no. 12 (December 8, 2017): 1296–98. http://dx.doi.org/10.1161/circresaha.117.312211.

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Abraham, Terri. "Arrhythmogenic Mechanisms." AACN Advanced Critical Care 3, no. 1 (February 1, 1992): 157–65. http://dx.doi.org/10.4037/15597768-1992-1020.

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The arrhythmogenic mechanisms are the basis for the genesis of a wide variety of complex dysrhythmias that can arise in both pacemaker and nonpacemaker cells. Automaticity, or the ability to rhythmically and spontaneously depolarize cardiac cells, is normally the domain of the sinus node. Altered automaticity takes place when conduction is enhanced or abnormal. A second mechanism, reentry, refers to a phenomenon that occurs when an impulse is delayed within a pathway of slow conduction and then reenters surrounding tissue and produces another impulse. One-way conduction is necessary to produce a return route for the reentrant circuit. Lastly, late potentials are fragmented, low-amplitude electrical currents that occur at the terminal portion of the QRS complex or during the ST segment. Supraventricular and ventricular beats and tachydysrhythmias are the consequences of these mechanisms. Common contributing factors include but are not limited to hypoxia, hypercapnia, electrolyte disturbance, catecholamines, and pharmacotherapy
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Corrado, Domenico, Cristina Basso, and Daniel P. Judge. "Arrhythmogenic Cardiomyopathy." Circulation Research 121, no. 7 (September 15, 2017): 784–802. http://dx.doi.org/10.1161/circresaha.117.309345.

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Beffagna, Giorgia, Alessandro Zorzi, Kalliopi Pilichou, Martina Perazzolo Marra, Ilaria Rigato, Domenico Corrado, Federico Migliore, et al. "Arrhythmogenic Cardiomyopathy." European Heart Journal 41, no. 47 (November 9, 2020): 4457–62. http://dx.doi.org/10.1093/eurheartj/ehaa719.

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Mestroni, Luisa, and Orfeo Sbaizero. "Arrhythmogenic Cardiomyopathy." Circulation 137, no. 15 (April 10, 2018): 1611–13. http://dx.doi.org/10.1161/circulationaha.118.033558.

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Pilichou, Kalliopi, Connie R. Bezzina, Gaetano Thiene, and Cristina Basso. "Arrhythmogenic Cardiomyopathy." Circulation: Cardiovascular Genetics 4, no. 3 (June 2011): 318–26. http://dx.doi.org/10.1161/circgenetics.110.959031.

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Jallon, P. "Arrhythmogenic Seizures." Epilepsia 38 (November 1997): S43—S47. http://dx.doi.org/10.1111/j.1528-1157.1997.tb06127.x.

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Rawal, Aranyak S., Tara VanCleave, Neeraja Yedlapati, Jeffery E. Saffitz, William James Craigen, and John L. Jefferies. "Arrhythmogenic Ventricular Cardiomyopathy." JACC: Case Reports 3, no. 3 (March 2021): 438–42. http://dx.doi.org/10.1016/j.jaccas.2020.12.012.

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Priori, Silvia G. "Inherited Arrhythmogenic Diseases." Circulation Research 94, no. 2 (February 6, 2004): 140–45. http://dx.doi.org/10.1161/01.res.0000115750.12807.7e.

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Dissertations / Theses on the topic "ARRHYTHMOGENIC"

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BERNARDI, JOYCE. "Arrhythmogenic mechanisms in genetic channelopathies." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/153192.

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Introduzione: Recentemente, varianti minori di SNP del gene NOS1AP sono stati associati a prolungamento del QT e aumentata incidenza di morte improvvisa in pazienti LQT1. Il gene NOS1AP codifica per la proteina CAPON, che localizza NOS1 in prossimità del reticolo sarcoplasmico (SR). L' attività di NOS1 è importante per la modulazione mediate da NO di ICaL, dei canali RyR2 e di SERCA, interferendo così con la regolazione dell’handling del Ca2+ e la stabilità del SR. Perciò abbiamo ipotizzato che gli SNPs di NOS1AP possano alterare la localizzazione/funzione di NOS1 diminuendo la stabilità del SR. In questo contesto, il prolungamento del QT indotto da mutazione, potrebbe indurre un sovraccarico di Ca2+, il cui effetto pro-aritmico potrebbe essere smascherato da un’alterata localizzazione/funzione di NOS1. Scopo: Valutare l’effetto di cambiamenti nell’attività di NOS1 a livello della stabilità funzionale del SR, della ripolarizzazione e aritmogenesi in un contesto di perdita di IKs (LQT1). Metodi: In miociti ventricolari di cavia soggetti a blocco di IKs (per riprodurre il fenotipo LQT1) e a stimolazione adrenergica (Isoproterenolo, ISO), abbiamo misurato l’attività elettrica, le correnti di membrane e il Ca2+ intracellulare, in condizione basale e dopo inibizione selettiva di NOS1 (SMTC 3µM). Risultati: In condizioni basali, l’inibizione di NOS1 prolunga la durata del PA (APD) (152.6  11.7 ms vs 96.1  9.0 ms; 58.8%. p<0.01), aumenta la densità di ICaL (SMTC vs CTRL: -16.61.2 pA/pF vs -13.51.0 pA/pF; p<0.05) ma non altera ne IKs (SMTC vs CTRL: 2.50.4 pA/pF vs 2.60.2 pA/pF) nè IKr (SMTC vs CTRL: 0.840.04 pA/pF vs 0.910.05 pA/pF). L’isoproterenolo, agonista -adrenergico (ISO, 1nM), induce delayed afterdepolarizations (DADs), un indice di instabilità del SR, in una percentuale significativamente maggiore di cellule trattate con SMTC rispetto a quelle di controllo (93% per SMTC vs 22% per CTRL, p<0.01). Inoltre, il tempo medio di comparsa delle DADs è significativamente ridotto in miociti trattati con SMTC rispetto a quelli di CTRL (25.8 ± 3.8 s e 61.5 ± 15.3 s rispettivamente, p<0.01). In aggiunta, la durata del PA è importante per il verificarsi di questi eventi, poiché il passaggio, in AP clamp, da un PA lungo (140 ms) a uno corto (100 ms) durante applicazione di ISO, abolisce le “transient inward currents” (ITI). Conclusioni: Questi risultati indicano che la mancanza di NOS1 può contribuire al prolungamento dell’APD e aumentare l’influsso di Ca2+; questi effetti compromettono la stabilità del SR in presenza di stimolazione adrenergica. Gli effetti dell’inibizione di NOS1 sono tali da poter spiegare l’effetto aritmogenico dei polimorfismi di NOS1AP.
Background: Recently, minor SNP variants of the NOS1AP gene have been reported to be associated with QT prolongation and increased incidence of sudden death in LQT1 patients. The NOS1AP gene encodes for CAPON protein, that localizes NOS1 close to the sarcoplasmic reticulum (SR). NOS1 activity accounts for NO-mediated modulation of ICaL, RyR2 channels and SERCA, thus interfering with regulation of Ca2+ handling and SR stability. Therefore we hypothesize that NOS1AP SNPs might affect NOS1 localization/function to decrease SR stability. In this setting, mutation-induced QT prolongation would induce Ca2+ overload, whose proarrhythmic effect would be unveiled by abnormal NOS1 localization/function. Aim: To evaluate the effect of changes in NOS1 activity on SR functional stability, repolarization and arrhythmogenesis in the context of IKs deficiency (LQT1). Methods: In guinea-pig ventricular myocytes subjected to IKs blockade (to reproduce the LQT1 phenotype) and adrenergic stimulation (Isoproterenol, ISO), we measured electrical activity, membrane currents and intracellular Ca2+, in basal condition and under selective inhibition of NOS1 (SMTC 3µM). Results: Under basal conditions, NOS1 inhibition prolonged AP duration (APD) (152.6  11.7 ms vs 96.1  9.0 ms; 58.8%. p<0.01), enhanced ICaL density (peak current density at +10 mV, SMTC vs CTRL: -16.61.2 pA/pF vs -13.51.0 pA/pF; p<0.05) and did not affect IKs (SMTC vs CTRL: 2.50.4 pA/pF vs 2.60.2 pA/pF) and IKr (SMTC vs CTRL: 0.840.04 pA/pF vs 0.910.05 pA/pF). The -adrenergic agonist isoproterenol (ISO, 1nM) induced delayed afterdepolarizations (DADs), an index of SR instability, in a significantly greater percentage of SMTC treated cells, compared to control ones (93% for SMTC vs 22% for CTRL, p<0.01). Moreover, the average time of DADs appearance was significantly different between SMTC and CTRL myocytes, with a earlier rise after NOS1 inhibition (25.8 ± 3.8 s and 61.5 ± 15.3 s respectively, p<0.01). Furthermore, the duration of the AP is important for the occurrence of these events, as switching from a long AP (140 ms) to a short AP (100 ms) waveform under ISO application in AP clamp mode, transient inward currents (Iti) were abolished. Conclusions: These results indicate that NOS1 deficiency may contribute to APD prolongation and enhance Ca2+ influx; these effects compromise SR stability in the presence of adrenergic stimulation. The effects of NOS1 inhibition are such as to account for the arrhythmogenic effect of NOS1AP polymorphism.
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Egdell, Robin Michael. "Arrhythmogenic phenomena in isolated cardiac myocytes." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322380.

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Åström, Aneq Meriam. "Arrhythmogenic right ventricular cardiomyopathy : Is it right?" Doctoral thesis, Linköpings universitet, Klinisk fysiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-70403.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart disease, where sudden cardiac death in young seemingly healthy persons may be the first symptom. There is a need for more sensitive and accurate diagnostic methods to detect signs of disease, at an early stage and in relatives of affected individuals. The aim of this thesis is the evaluation of new non-invasive modalities in assessment of right ventricular (RV) volume and function with focus on patients with ARVC. Clinical and non-invasive follow-up of fifteen patients with ARVC during a mean period of 8 years permitted the evaluation of disease progression. RV volume analysis by magnetic resonance imaging relies on short axis (SA) views. A new axially rotated modality acquisition was tested and its feasibility in assessment of RV volume was evaluated. This acquisition seems to be able to improve the assessment of RV volume and function by reducing the uncertainty in defining the basal slice of the RV. A third study concentrated on analysis of RV regional and general function by echocardiography, using tissue Doppler imaging as well as two dimensional (2D) longitudinal strain based on speckle tracking in patients with ARVC, their first degree relatives and in healthy subjects. 2D strain showed a good feasibility in analysis of the RV function in relatives and controls but less in ARVC patients probably due to the progressive myocardial cell death with fibro-fatty replacement of the RV wall. In order to detect and follow up echocardiographic changes an index was developed combining dimensional and functional parameters for the left and for the right ventricle. Advances in the molecular genetics of ARVC have provided new insights into the understanding of the disease. Hitherto, 9 candidate genes have been identified. A new mutation in the plakophilin 2 gene was detected in a three generation family. The clinical phenotype related to this mutation was investigated. The studies have evaluated and developed methods for studying the right ventricle with special emphasis on ARVC. With the ultimate goal of preventing sudden death in ARVC, a combination of genetic testing and improved diagnostic methods may create an improved algorithm for risk stratification and selection to prophylactic treatment.
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Scridon, Alina. "Atrial fibrillation : insights concerning the arrhythmogenic substrate." Phd thesis, Université Claude Bernard - Lyon I, 2012. http://tel.archives-ouvertes.fr/tel-00933537.

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Atrial fibrillation is the most prevalent form of cardiac arrhythmia. Studies in animal modelshave provided important insights into arrhythmia mechanisms. However, to date, we do not dispose ofanimal models of spontaneous atrial arrhythmia.Thus, we aimed to develop a model of spontaneous atrial arrhythmia in rats and to assesspathophysiological mechanisms of these arrhythmias by using a multidisciplinary approach. We alsoaimed to assess the presence and the extent of inflammation and endothelial dysfunction, incriminatedin atrial fibrillation-related complications such as stroke, in atrial fibrillation patients.The animal study describes the first animal model of spontaneous atrial arrhythmias. We alsoprovide evidence that multiple mechanisms participate in arrhythmia occurrence in this model,particularly autonomic imbalance with relative vagal hyperactivity, left atrial endocardial fibrosis, anddecreased left atrial expression of the Pitx2 gene. In our clinical study, we found high levels ofvascular endothelial growth factor and von Willebrand factor in atrial fibrillation patients compared tosinus rhythm controls. These results suggest specific thromboembolic risk patterns according to theclinical form of arrhythmia and highlight a parallel evolution of atrial fibrillation and endothelialdysfunction. These results add new insights into the understanding of atrial arrhythmias. This new animalmodel could facilitate studies of pathophysiological mechanisms involved in atrial arrhythmias andallow assessment of efficacy and toxicity of therapeutic agents in a setting that faithfully reproducesthe clinical presentation of the arrhythmia
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King, James Harmsworth. "Arrhythmogenic mechanisms in RYR2-P2328S murine hearts." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648837.

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Celeghin, Rudy. "Genomics in Arrhythmogenic Cardiomyopathy: exploring the complexity." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3421844.

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Background Arrhythmogenic cardiomyopathy (AC) is a rare heart muscle disease characterized by fibrofatty myocardial replacement, prominent impairment of ventricular systolic function and arrhythmias. AC phenotypic spectrum was revealed wider than previously thought thanks to genotype–phenotype correlation. Combining multiple sources of clinical information, such as genetic, electrocardiographic, arrhythmic, morphofunctional, and histopathologic findings resulted the best approach to untangle the complexity of this disease. Aim The aim of our study was to assess AC genetic heterogeneity, applying appropriate genetic screening and performing a multiparametric genotype-phenotype correlation taking into account AC variants classification. Materials and Methods A total of 224 consecutive patients, with a clinical (n.192) or post mortem (n.32) diagnosis of AC, underwent genetic screening by using a 174 cardiac-related genes panel (Trusight Cardio, Illumina). The prevalence of Copy Number Variations (CNVs) and newly AC-associated genes such as FLNC and CDH2, were investigated. Detailed clinical data were obtained on 12-lead elettrocardiography, echocardiography, and cardiac magnetic resonance with the purpose of performing a multiparametric genotype-phenotype correlation. TTN variants were evaluated separately, due the magnitude of the gene, as well as rare variants in AC-unrelated genes. Finally, WES was carried out on 10 AC genotype negative patients in order to identify new candidate genes involved in the disease pathogenesis. Results We identified 95 different rare genetic variants in 97 (43%) of the 224 index cases. Of them, 79 variants were found in 5 major desmosomal genes (83%), whereas 16 in AC-related non desmosomal genes (17%). American College of Medical Genetics (ACMG)-based variant classification made evident that half of desmosomal variants (39/79, 49%) were classified as pathogenic/likely pathogenic and were predominantly radical (32/39, 78%). Comprehensive sequencing, including newly AC associated genes (FLNC and CDH2) and CNVs analysis, led to the identification of the genetic cause in 10 more patients increasing the overall yield of genetic screening from 43% to 48%. No pathogenic variants were identified in 117 (52%) patients. Overall we re-evaluated based on the current International Task Force Criteria (ITC) the clinical phenotype of 188 out of 224 AC (84%) index cases. Of these, 94 index cases received a definite AC diagnosis at the outpatient clinic, 16 were heart-transplanted (HTx) patients and 32 sudden death (SD) victims. The remaining 18 were borderline and 28 were possibly affected by AC. 78 of the 142 (55%) definite index cases carried at least a rare variant in AC related genes whereas, only 13 of the 46 (28%) borderline/possible index cases were genotype positive. Genotype analysis focusing on ventricular involvement highlighted that patients with Left Dominant variant (LDAC) were significantly less positive for desmosomal variants (11/42, 26%) compared to the “classic” AC cases (75/182, 41%)(p-value 0.0065). More in deep, 19 of the 42 (45%) LDAC patients were SD victims, of whom only 4 cases (21%) were genotype positive for desmosomal rare variants. Based on previous transcriptome studies from our laboratory we identified rare variants in LGALS3. Specifically, sequencing of 10 index cases through WES and 140 by direct sequencing, led to the identification of 5 LGALS3 rare nucleotide variants in 7 probands (4%, 5 males, mean age 39±11 years). Of note, two missense variants occurred in the protein carbohydrate recognition domain (CRD) conferring the loss of its binding site. Conclusions Comprehensive genetic analysis revealed a genetic cause in nearly half (48%) of AC patients, of which only half could be classified as P/LP. A proper phenotypic characterization increased variant finding likelihood in definite AC patients (55%). Nevertheless, half of AC patients still missed a genetic cause. Specifically, genetic testing achieved to identify a causative variant in only ~25% of LDAC cases. Finally a new candidate gene was identified in 4% of AC cases, supporting the fact that other genetic factors might be involved in disease pathogenesis. Most of identified genetic variants were variants of unknown significance (VUS), highlighting that cascade genetic screening remains mandatory to understand their significance in disease pathogenesis.
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Cason, Marco. "Application of omic technologies in Arrhythmogenic Cardiomyopathy." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3427282.

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Background. Arrhythmogenic cardiomyopathy (AC) is an inherited myocardial disease characterized by fibro-fatty replacement of the myocardium and life-threatening arrhythmias. This genetically and phenotypically heterogeneous condition, caused mainly by mutations in desmosomal genes (JUP, DSP, PKP2, DSG2 and DSC2), exhibits reduced penetrance making challenging the diagnosis and the identification of a molecular mechanism underlying disease pathogenesis. Aims. (1) To identify one or more altered molecular pathways in AC carriers of desmosomal mutations; (2) to evaluate the diagnostic role of JUP immune analysis in AC; (3) to study the frequency of genetic variants in the five major AC-related genes in a healthy population of Veneto region in order to evaluate their role in the pathogenesis of the disease. Materials and methods. (1) Differential expression analysis was carried out on myocardial tissue of 7 transplanted AC patients harbouring a pathogenic mutation in desmosomal genes and 3 controls. Genetic/epigenetic interference-factors were unbiased analyzing also 3 mouse groups: 8 over-expressing NS-dsg2 mutation [TgNS], 6 over-expressing wild type dsg2 [TgWt] and 2Wt); each group was further subdivided in two age-groups (<2 weeks and >3 weeks) before and after the onset of disease. Data confirmation was obtained by quantitative-PCR. (2) Heart specimens (HS, either autopsy or transplants) and endomyocardial biopsies (EMB) formalin-fixed from 44 AC unrelated patients and 30 non-AC matched-subjects were evaluated both by conventional immunoperoxidase analysis (IPOX) and immunofluorescence (IF) using two different JUP antibody (Ab) dilutions. Reduced JUP signal level was defined as 50% reduction in distribution and/or intensity of the immunostained areas compared to the control samples. To exclude time-dependent tissue decay, control staining for N-Cadherin was also performed. (3) 200 unrelated young athletes (mean age 20 yrs, male/female ratio 3:1), eligible at the pre-participation clinical evaluation, underwent conventional genetic screening for major disease causative genes. Variants selection was based on the current ACMG guidelines and the absence or low frequency (minor allele frequency, MAF <0.0002) of the genetic variants in the general population. Results. (1) 1136 and 822 differentially expressed genes (DEGs) were respectively identified in the right and left human myocardium of AC compared to controls. 204 DEGs were identified comparing TgNS<2 weeks and TgNS>3 weeks gene expression profiling. 82 DEGs were identified comparing human and murine (TgNS>3 weeks) expression-profiling including genes most associated with canonical WNT/β-catenin and TGF-β pathways. On the contrary only 29 DEGs were identified in the comparison between TgNS<2 weeks to age-matched controls (WT and TgWt <2 weeks) mostly associated with inflammatory and pro-apoptotic process, but none with WNT and TGF-β pathways. (2) Test sensitivity (Se) of 70.6% and specificity (Sp) of 50%, with an Ab dilution 1:50.000 were found among HS, whereas with a 5-fold higher (1:250.000) Ab dilution the test Se was increased to 79.4% and the Sp decreased to 35%. Same analysis was performed on EMB samples showing different results: 40% Se; 80% Sp with 1:50.000 Ab dilution, whereas Se was 50% and Sp 70% with 1:250.000 Ab dilution. IF data were similar both with 1:1000 and 1:50.000 JUP-Ab dilution, indicating a Se of 61.8% and a Sp of 45% Sp in HS and a Se 50% and a Sp 70% in EMB samples. (3) Genetic screening identified rare genetic desmosomal variants in 20 healthy subjects (10%) reduced to 12 (6%) after appropriate filtering. Conclusions. Our findings demonstrated the interaction between WNT and TGF pathways at early disease stages, triggering cardiac remodelling. Specifically, we identified probably the ‘culprit molecules’ of disease onset. Routine IPOX and IF analysis of JUP signal is associated with low Se and limited Sp to be advocated as a diagnostic test. The absolute Se range was much higher in HS than EMB samples. The same for IF, HS specimens showed higher Se and lower Sp than EMB samples. Finally, high Ab dilutions confer higher Se but reduce test Sp. Comprehensive mutation screening and filtering in a large cohort of unrelated consecutive healthy subjects identified a lower rate of rare variants than the rates (16 and 18%) reported in literature for AC probably due to our selected cohort of healthy subjects.
Introduzione. La cardiomiopatia aritmogena (AC) è una patologia ereditaria del miocardio caratterizzata da sostituzione fibrosa e adiposa dei cardiomiociti e da aritmie potenzialmente letali. Questa condizione geneticamente e fenotipicamente eterogenea, causata principalmente da varianti genetiche a livello dei geni desmosomiali (JUP, DSP, PKP2, DSG2 e DSC2), mostra una penetranza incompleta; queste caratteristiche rendono difficile non solo la corretta diagnosi, ma anche l'identificazione di un meccanismo molecolare alla base della patogenesi della malattia. Obiettivi. (1) Identificare uno o più pathway molecolari alterati in pazienti AC portatori di mutazioni desmosomiali; (2) valutare il ruolo diagnostico dell'analisi immunologica della JUP; (3) studiare la frequenza delle varianti genetiche nei cinque principali geni correlati alla malattia in una popolazione sana della regione Veneto al fine di valutare il loro ruolo nella patogenesi dell’AC. Materiali e metodi. (1) L'analisi dell'espressione differenziale è stata condotta su tessuto miocardico di 7 pazienti AC precedentementi sottoposti a trapianto cardiaco, portatori di una variante patogena nei geni desmosomiali e 3 controlli. Al fine di eliminare i fattori di interferenza genetica/epigenetica sono stati analizzati anche 3 gruppi di un modello murino: 8 topi sovra-esprimenti la mutazione NS-dsg2 [TgNS], 6 sovra-esprimenti la dsg2 wild-type [TgWt] e 2 Wt; ciascun gruppo è stato ulteriormente suddiviso in base all’età (<2 settimane e >3 settimane) prima e dopo l'insorgenza della malattia. La conferma dei dati è stata ottenuta mediante PCR quantitativa. (2) Le analisi immunoistochimiche sono state eseguite sia su sezioni di miocardio (HS, autoptici o da trapianto) che su biopsie endomiocardiche (EMB) di 44 pazienti con diagnosi di AC e 30 soggetti non-AC. Tutti i casi sono stati valutati sia mediante colorazione con immunoperossidasi (IPOX) che mediante immunofluorescenza (IF) utilizzando due diverse diluizioni dell'anticorpo (Ab) che lega specificatamente la proteina JUP. Per escludere il decadimento tissutale tempo dipendente, è stata anche eseguita l’analisi di controllo sulla N-Caderina. (3) Lo screening genetico convenzionale per i principali geni responsabili delle patologia è stato eseguito su 200 giovani atleti (età media 20 anni, rapporto maschi / femmine 3: 1), considerati idonei all’attività sportiva. La selezione delle varianti era basata sulle attuali linee guida della ACMG e sull'assenza/bassa frequenza (frequenza allelica minore, MAF <0,0002) delle varianti genetiche nella popolazione generale. Risultati. (1) 1136 e 822 geni differenzialmente espressi (DEGs) sono stati identificati rispettivamente nel ventricolo destro e nel ventricolo sinistro dei pazienti AC. Sono stati identificati inoltre, 204 DEGs comparando il profilo di espressione genica di TgNS<2 settimane e TgNS> 3 settimane. Infine, confrontando il profilo di espressione umano con quello murino sono stati identificati 82 DEGs in comune; molti di questi geni sono associati ai pathway WNT e TGF-β. Al contrario, solo 29 DEGs sono stati identificati nel confronto tra TgNS <2 settimane e i controlli di età corrispondente (WT e TgWt <2 settimane); questi geni sono per lo più associati a processi infiammatori e pro-apoptotici, ma nessuno ai pathway WNT e TGF-β. (2) L’analisi IPOX eseguita sui campioni HS con una diluizione dell’Ab 1: 50.000 mostra una sensibilità (Se) del 70,6% e la specificità (Sp) del 50%, mentre con una diluizione Ab 5 volte più alta (1: 250.000) la Se del test aumenta al 79,4% e la Sp diminuisce al 35%. La stessa analisi eseguita su campioni EMB restituisce come risultato: 40% Se; 80% Sp con diluizione anticorpale di 1: 50.000, mentre alla diluizione 1: 250.000 la Se si attesta a 50% e la Sp al 70%. I dati risultanti dall’analisi IF sono simili sia con diluizione dell’anticorpo 1: 1000 che 1: 50.000, indicando una Se del 61.8% e una Sp del 45% per gli HS e una Se 50% e una Sp 70% nei campioni EMB. (3) Lo screening genetico dei 5 geni desmosomiali ha identificato varianti genetiche rare in 20 soggetti sani (10%) ridotti a 12 (6%) dopo un appropriato filtraggio. Conclusioni. I nostri risultati hanno dimostrato l'interazione tra WNT e TGF-β nelle fasi iniziali della malattia, determinando il rimodellamento cardiaco. Nello specifico, abbiamo identificato probabilmente le "molecole colpevoli" dell'insorgenza della malattia. L'analisi del segnale immunologico della JUP mostra in generale una bassa Se e ad una limitata Sp. Nello specifico, nell’analisi la Se risulta più elevata nei campioni HS rispetto ai campioni EMB. Alte diluizioni anticorpali conferiscono valori di Se superiori ma riducono la Sp del test. Lo screening genetico e la successiva analisi delle varianti individuate in un'ampia coorte di soggetti sani ha identificato un tasso minore di varianti rare rispetto a quanto riportato in letteratura per la AC (16 e 18%), probabilmente ciò è dovuto alla pre-selezione fatta sui soggetti inseriti nella coorte analizzata.
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Lazzarini, Elisabetta. "Diagnostic Implications of Arrhythmogenic Cardiomyopathy Genetic Testing." Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3424161.

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Background & Aims: Arrhythmogenic Cardiomyopathy (AC) is a rare inherited heart muscle disease associated with mutations in genes encoding mainly components of the cardiac desmosome. We performed a comprehensive study of genetic variants in a cohort of AC subjects and the assessment of Next Generation Sequencing (NGS) strategies for molecular diagnosis of AC. Methods: Ninety-nine unrelated index cases, of which 26 sudden cardiac death cases, underwent genetic screening for 5 desmosomal genes by denaturing high performance liquid chromatography and direct sequencing, whereas 46 probands were additionally screened for 3 extra desmosomal genes. A complementary analysis for copy number variants (CNVs) was performed by multiplex ligation-dependent probe amplification and quantitative real-time PCR in the entire cohort. A 4-step variant filtering strategy based on mutation type, frequency, evolutionary conservation and in silico analysis, was used. Whole Exome and Targeted NGS strategies were performed on Illumina platforms in order to test methods efficacy. Results: Screening of 8 AC genes and subsequent 4-step variants filtering identified 37 different point desmosomal mutations in 42 AC probands (42%). The most frequently mutated genes resulted PKP2 and DSP, with “radical” mutation type accounting for the 80% of the PKP2 variants. No pathogenic mutations were identified in the extra desmosomal genes analyzed. CNVs analysis further revealed 3 different large genomic rearrangements in 5 probands (4%), increasing to 46 (46%) the number of positively genotyped patients. PKP2 and DSP single mutation accounted respectively for 20% and 11% of the cohort, with DSP carriers showing a higher risk of sudden cardiac death. Eight multiple mutations carriers were observed (8%). NGS approaches identified 4 variants in extra desmosomal genes allowing a differential diagnosis in 4 patients. Conclusions: A fine variant filtering avoids overrepresentation of putative pathogenic mutations and shows that radical and missense mutations should be equally interpreted with great caution in the setting of clinical diagnosis. NGS and CNVs analysis increased significantly the diagnostic yield in AC genetic testing. The genetics of AC is more complex than previously appreciated, with frequent requirement for more than one ‘hit’ for penetrant disease.
Introduzione & Scopo: La Cardiomiopatia Aritmogena (AC) è una malattia rara del muscolo cardiaco associata a mutazioni a carico di geni che codificano principalmente per componenti del desmosoma cardiaco. Abbiamo realizzato l`analisi genetica in una coorte di soggetti affetti da AC e lo sviluppo di strategie in Next Generation Sequencing (NGS) per la diagnosi molecolare di AC. Metodi: Novantanove casi indice, di cui 26 soggetti di morte improvvisa, sono stati sottoposti a screening genetico per 5 geni desmosomiali mediante cromatografia denaturante in fase liquida ad alto rendimento e sequenziamento diretto, 46 probandi sono stati analizzati anche per 3 geni extra desmosomiali. Abbiamo inoltre ricercato nell`intera popolazione varianti del numero di copie (CNVs) mediante la tecnica MLPA (Multiplex Ligation-Dependent Probe Amplification) e PCR quantitativa. La strategia di filtraggio si è basata sul tipo di mutazione, frequenza, conservazione, e analisi in silico. Gli approcci NGS “Whole Exome” e “Targeted” sono stati eseguiti su piattaforme Illumina. Risultati: L`analisi di 8 geni associati alla AC e il successivo filtraggio delle varianti ha individuato 37 diverse mutazioni puntiformi in 42 soggetti (42%). I geni più frequentemente mutati sono la PKP2 e la DSP, le mutazioni “radicali” costituiscono l`80% delle varianti della PKP2. Non sono state riscontrate mutazioni patogene nei geni extra desmosomiali studiati. La ricerca di CNVs ha identificato 3 diversi riarrangiamenti cromosomici in 5 probandi (4%), portando a 46 (46%) i soggetti genotipo positivi. Si sono osservate mutazioni singole nei geni PKP2 e DSP nel 20% e nell`11% dei soggetti, i portatori di mutazioni nella DSP presentano un rischio maggiore di morte improvvisa, 8 (8%) soggetti presentano mutazioni multiple. Le analisi mediante NGS hanno indentificato 4 varianti in geni extra desmosomiali permettendo la diagnosi differenziale in 4 pazienti. Conclusioni: La diagnosi molecolare in ambito clinico rende necessaria un`attenta interpretazione del potenziale patogeno tanto delle mutazioni missenso quanto di quelle radicali soprattutto dopo il cospicuo aumento di varianti identificate con NGS e la ricerca di CNVs. La base genetica di AC è molto più complessa di quanto finora apprezzato, con una frequente presenza di più di una mutazione per una penetranza completa della malattia.
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Spier, Alan W. "The electrocardiographic evaluation of arrhythmogenic cardiomyopathy in boxers /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486462702466123.

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Bueno, Marinas Maria. "MicroRNA profiling in Arrhythmogenic Cardiomyopathy and prognostic markers." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3427265.

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Background: Arrhythmogenic cardiomyopathy (AC) is a clinically and genetically heterogeneous myocardial disease, characterised by a progressive myocardial dystrophy with fibro-fatty replacement, and represents one of the major causes of sudden cardiac death in the young and athletes. Although half of AC patients harbour private desmosomal gene mutations, their low and age-dependent penetrance suggests the involvement of other regulatory molecules. MicroRNAs (miRNAs) are a group of endogenous short noncoding RNAs that regulate gene expression by sequence-specific recognition of their target transcripts. They have been associated with numerous pathophysiological conditions, including cardiovascular diseases; however, their role as key regulatory molecules in AC as well as their impact on the onset and progression of the disease is largely unknown. Purpose: miRNA profiling in genotype-positive AC-patients with different gene mutations in order to identify their potential as AC biomarkers. Methods: The study involved 59 subjects with a definite AC diagnosis, previously genotyped, and 14 healthy controls. 84-miRNA array was applied on 8 frozen right-ventricle (RV) myocardial tissue samples, from heart transplanted AC patients; 9 whole blood samples, from patients with definite AC diagnosis, and 6 healthy controls (HC). In the validation study, seven miRNAs were analysed on 42-AC and 8-HC blood samples. miRNA analysis was performed by qPCR, relative quantification ΔΔCt method and in silico target prediction. All data were expressed in fold-change values. Receiver operating characteristic (ROC) analysis was performed on validated miRNAs. Results: miRNA profiling on AC-tissue samples displayed a genotype-related profile, 19 miRNAs were differentially expressed in PKP2 carriers, 15 in DSP carriers and 14 in DSG2 carriers, when compared to healthy controls. A common signature between PKP2 and DSP carriers was identified with 14 miRNAs in common (PKP2/DSP profile). None of these miRNAs were shown within DSG2 profile. In silico target prediction identified Hippo Signaling Pathway as a common target for both profiles. Analysis of AC-tissue samples as a unique group confirmed 26 differentially expressed miRNAs (AC-tissue profile) with predicted targets in the AC pathway. AC-blood miRNA profiling demonstrated a 14-miRNA signature, with 10 miRNAs differentially expressed in common with AC-tissue profile. Hsa-miR-144-3p, -122-5p, -208a-3p and -494-3p as well as hsa-miR-21-5p, -155-5p and -320a were analysed on a larger cohort of 42-AC and 8-HC. Only hsa-mir-122-5p was significantly overexpressed (p-value<0,05). ROC analysis showed hsa-miR-122-5p to be a potential AC biomarker (area under the curve: 0.83). Conclusions: A genotype-related miRNA profile was observed in AC-tissue samples, as to reflect clinical variability. In addition, 10 miRNAs in common were identified between AC-tissue and AC-blood profiles, proving a specific miRNA signature for AC. These miRNA profiles targeted pathways involved in AC pathogenesis demonstrating their key roles in the onset and progression of the disease. Circulating level of hsa-miR-122-5p was significantly elevated in AC subjects, demonstrating its potential as a prognostic marker for heart failure in AC.
Introduzione. La Cardiomiopatia Aritmogena (AC) è una malattia clinicamente e geneticamente eterogenea del miocardio, caratterizzata da una progressiva distrofia miocardica con sostituzione fibro-adiposa, e rappresenta una delle principali cause di morte improvvisa nei giovani e negli atleti. Nonostante circa la metà dei pazienti affetti da AC presentino mutazioni nei geni desmosomiali, la bassa penetranza e dipendenza dall’età della patologia suggeriscono il coinvolgimento di altre molecole regolatrici. I microRNA (miRNA) sono un gruppo di molecole endogene, di RNA non codificante, che regolano l'espressione genica mediante lo specifico riconoscimento di sequenze target dei trascritti. Sono stati associati a numerose condizioni patofisiologiche, tra cui malattie cardiovascolari; tuttavia, il loro ruolo come molecole regolatrici nella AC e il loro impatto sull'insorgenza e sulla progressione della malattia è in gran parte sconosciuto. Scopo dello studio. Analizzare il profilo di espressione dei miRNA in pazienti affetti da AC genotipicamente positivi allo scopo di studiare il loro potenziale come biomarcatori prognostici. Materiali e metodi. Lo studio ha coinvolto 59 soggetti con una diagnosi clinica di AC, precedentemente genotipizzati, e 14 controlli sani (HC). Un array composto da 84-miRNA è stato testato su: 8 campioni di tessuto miocardico congelato del ventricolo destro, proveniente da pazienti trapiantati affetti da AC; 9 campioni di sangue intero congelato, da pazienti con diagnosi clinica di AC e 6 controlli sani. Nella fase di validazione sono stati analizzati sette miRNA su campioni di sangue provenienti da 42-AC e 8-HC. L'analisi è stata eseguita mediante qPCR seguita da quantificazione relativa con il metodo ΔΔCt e predizione in silico dei geni target. I risultati sono stati espressi in valori di “fold-change” e le curve ROC (Receiver Operating Characteristic) analizzate sui miRNA validati. Risultati. L’analisi dei miRNA su 8 campioni di tessuto di pazienti affetti da AC mostrava un profilo correlato al genotipo rispetto ai controlli sani, in particolare: 19 miRNA erano differenzialmente espressi nei portatori di una mutazione in PKP2, 15 nei portatori di una mutazioni in DSP e 14 nei portatori di una mutazione in DSG2. E’ stato identificato un profilo d’espressione in comune tra i portatori della mutazione in PKP2 e i portatori della mutazione in DSP, con 14 miRNA alterati (profilo PKP2/DSP). Nessuno di questi miRNA è stato trovato nel profilo DSG2. Lo studio in silico dei possibili geni target ha identificato la via di segnale “Hippo Signaling Pathway” come target comune per entrambi i profili (PKP2/DSP- DSG2). Considerando i campioni di tessuto AC come un unico gruppo indipendentemente dal gene mutato sono emersi 26 miRNA differenzialmente espressi (profilo AC-tessuto) che hanno come target geni coinvolti nel pathway AC. Lo studio dei miRNA nei 9 campioni di sangue dei pazienti affetti da AC ha dimostrato un profilo costituito 14-miRNA alterati, dei quali 10 alterati anche nel profilo AC-tessuto. Hsa-miR-144-3p, -122-5p, -208a-3p e -494-3p così come hsa-miR-21-5p, -155-5p e -320a sono stati infine validati su una coorte più ampia di 42-AC e 8-HC. Solo hsa-mir-122-5p è stato riscontrato come significativamente sovraespresso (valore p <0,05). L'analisi di curve ROC ha mostrato che hsa-miR-122-5p è un potenziale biomarcatore di AC (AUC: 0.83). Conclusione. Nei campioni AC di tessuto è stato osservato un profilo di miRNA correlato al genotipo, tale da rispecchiare la variabilità clinica della patologia. Inoltre, sono stati identificati 10 miRNA in comune tra i profili dei campioni AC di tessuto e sangue, evidenziando un profilo di espressione di miRNA specifico per AC. Entrambi i profili infatti (tessuto e sangue) hanno come target vie di segnale coinvolte nella patogenesi della AC, dimostrando un ruolo chiave nella insorgenza e la progressione della malattia. In particolare il livello di hsa-miR-122-5p in circolo era significativamente elevato nei soggetti affetti da AC, dimostrando il suo potenziale come marcatore prognostico della malattia.
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Books on the topic "ARRHYTHMOGENIC"

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Markus, Frank I., Andrea Nava, and Gaetano Thiene, eds. Arrhythmogenic RV Cardiomyopathy/Dysplasia. Milano: Springer Milan, 2007. http://dx.doi.org/10.1007/978-88-470-0490-0.

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Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center., and United States. Agency for Healthcare Research and Quality., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center., and United States. Agency for Healthcare Research and Quality., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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United States. Agency for Healthcare Research and Quality., ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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Harmon, Jordan, United States. Agency for Healthcare Research and Quality., and New England Medical Center Hospital. Evidence-based Practice Center., eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Healthcare Research and Quality, 2004.

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United States. Agency for Healthcare Research and Quality. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. Rockville, Md.]: Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services, 2004.

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United States. Agency for Healthcare Research and Quality, ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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United States. Agency for Healthcare Research and Quality., ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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United States. Agency for Healthcare Research and Quality, ed. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2004.

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Harmon, Jordan, Tufts-New England Medical Center. Evidence-based Practice Center, and United States. Agency for Healthcare Research and Quality, eds. Effects of omega-3 fatty acids on arrhythmogenic mechanisms in animal and isolated organ/cell culture studies. [Rockville, Md: Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, 2004.

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Book chapters on the topic "ARRHYTHMOGENIC"

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Proost, V. M., and Arthur A. Wilde. "Arrhythmogenic Cardiomyopathy." In Electrocardiography of Inherited Arrhythmias and Cardiomyopathies, 85–115. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-52173-8_7.

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Cox, Moniek G. P. J., Ardan M. Saguner, Anneline S. te Riele, J. Peter van Tintelen, Firat Duru, Corinna Brunckhorst, and Richard N. W. Hauer. "Arrhythmogenic Cardiomyopathy." In Clinical Cardiogenetics, 91–111. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44203-7_6.

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Cox, Moniek G. P. J., Anneline S. J. M. te Riele, and Richard N. W. Hauer. "Arrhythmogenic Cardiomyopathy." In Clinical Cardiogenetics, 99–114. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45457-9_6.

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Vaideeswar, Pradeep. "Arrhythmogenic Cardiomyopathy." In Tropical Cardiovascular Pathology, 243–46. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3720-0_44.

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Horacek, B. Milan, Terrence J. Montague, Martin J. Gardner, and Eldon R. Smith. "Arrhythmogenic Conditions." In Body Surface Electrocardiographic Mapping, 167–89. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4613-1769-2_13.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Arrhythmogenic Cardiomyopathy." In Encyclopedia of Molecular Mechanisms of Disease, 147. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7470.

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Basso, Cristina, Monica De Gaspari, Stefania Rizzo, and Gaetano Thiene. "Arrhythmogenic Cardiomyopathy." In Sport-related sudden cardiac death, 57–67. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80447-3_5.

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Hedrich, Olaf, Gianfranco Buja, Domenico Corrado, Mark S. Link, Thomas Wichter, and N. A. Mark Estes. "The Role of the Implantable Cardiac Defibrillator in the Management." In Arrhythmogenic RV Cardiomyopathy/Dysplasia, 189–97. Milano: Springer Milan, 2007. http://dx.doi.org/10.1007/978-88-470-0490-0_21.

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Czarnowska, Elzbieta, Mila Della Barbera, Gaetano Thiene, Marialuisa Valente, and Cristina Basso. "Ultrastructural Substrates." In Arrhythmogenic RV Cardiomyopathy/Dysplasia, 53–60. Milano: Springer Milan, 2007. http://dx.doi.org/10.1007/978-88-470-0490-0_7.

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Young, David B. "Arrhythmogenic Significance of Hypokalemia." In Basic Science for the Cardiologist, 155–67. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1443-5_10.

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Conference papers on the topic "ARRHYTHMOGENIC"

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Nasir, U., T. A. Waheed, K. Syed, and R. Reddy. "Pulmonary Arterial Hypertension and Arrhythmogenic Right Ventricular Cardiomyopathy." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3517.

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Vives-Gilabert, Yolanda, Jorge Sanz, Antonio Cebrián, Raquel Cervigón, Jose Millet, Esther Zorio, and Francisco Castells. "Dyssynchrony Assessment in Arrhythmogenic Cardiomyopathy With Left Ventricular Involvement." In 2018 Computing in Cardiology Conference. Computing in Cardiology, 2018. http://dx.doi.org/10.22489/cinc.2018.073.

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CHEN, YAO-CHANG, YI-JEN CHEN, SHIH-ANN CHEN, and CHENG-I. LIN. "LOSARTAN DECREASES THE ARRHYTHMOGENIC ACTIVITY OF PULMONARY VEIN CARDIOMYOCYTE." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0011.

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Bocharin, I., A. Martusevich, and L. Dilenyan. "COMPLEX SCRINING OF SPECIALTIES OF HEART RATE VARIABILITY IN STUDENTS AT MEGAPOLIS." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c9d03c8.92975024.

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The aim of the study was to study the state of systemic hemodynamics in students of the main higher educational institutions of Nizhny Novgorod during the inter-sessional period. It was found that this group of individuals has good adaptive reserves, but some of the surveyed students have signs of sympathicotonia and a moderate risk of arrhythmogenic events
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Ščurek, Martin, Martin Pešl, Jan Přibyl, Šimon Klimovič, Tomáš Urban, Šárka Jelínková, Vladimír Rotrekl, and Kristián Brat. "Arrhythmogenic and chronotropic effects of bronchodilator drugs on human cardiomyocytes." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3297.

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Cohen, Mark H., Giora Ben-Shachar, Stanley D. Beder, Mark Sivakoff, and Thomas A. Riemenschneider. "Epicardial Application Of Laser Energy In Vivo: Acute Arrhythmogenic Potential." In 29th Annual Technical Symposium, edited by Abraham Katzir. SPIE, 1986. http://dx.doi.org/10.1117/12.950733.

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Vives-Gilabert, Yolanda, Bego�a Igual, Santiago Jim�nez-Serrano, Jorge Sanz, Raquel Cervig�n, Antonio Cebri�n, Jose Manuel Santab�rbara, Jos� Millet, Esther Zorio, and Francisco Castells. "Bayesian Classification Applied to Strain in Arrhythmogenic Left-Ventricle Cardiomyopathy." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.079-088.

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Wonham, Andrew, and Jan Till. "1396 Arrhythmogenic flecainide toxicity in Neonatal Atrio-ventricular Re-entry Tachycardia." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference, Liverpool, 28–30 June 2022. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2022. http://dx.doi.org/10.1136/archdischild-2022-rcpch.695.

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Gharbia, Omar, Susumu Tao, Albert C. Lardo, Henry Halperin, and Linwei Wang. "Electrical and Anatomical Imaging of Arrhythmogenic Substrates for Scar-related Ventricular Tachycardia." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.042-345.

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Gliner, Vadim, and Yael Yaniv. "Identification of Features for Machine Learning Analysis for Automatic Arrhythmogenic Event Classification." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.170-101.

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Reports on the topic "ARRHYTHMOGENIC"

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Shalganov, Tchavdar, Milko Stoyanov, and Vassil Traykov. Outcomes following catheter ablation for ventricular tachycardia in adult patients with structural heart disease and implantable cardioverter-defibrillator: protocol for an updated systematic review and meta-analysis of randomized studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0080.

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Review question / Objective: Does catheter ablation for scar-related monomorphic ventricular tachycardia improve outcomes (defined as any appropriate ICD therapy, appropriate ICD shocks, all-cause mortality, VT storm, cardiovascular mortality, cardiovascular hospitalizations, complications) in adult patients with ischemic or non-ischemic cardiomyopathy and implantable cardioverter-defibrillator? Condition being studied: Ventricular tachycardia in patients with structural heart disease is usually an arrhythmia using the myocardial scar as a substrate for reentry. It poses a risk of syncope and sudden cardiac death, especially in patients with reduced ejection fraction. Most antiarrhythmic drugs are of little value and their use is restricted in patients with LV systolic dysfunction. Catheter ablation is a viable option for the treatment of ventricular tachycardia. In patients with previous myocardial infarction the arrhythmogenic scar is located most frequently subendocardially and is readily accessible using endocardial approach, while in non-ischemic cardiomyopathy the scar is frequently located in the midmyocardial or subepicardial layers. This is the reason endocardial catheter ablation to be less effective in those patients and to more often necessitate epicardial approach.
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