Relevant bibliographies by topics / Arrhythogenic Right Ventricular Cardiomyopathy

Academic literature on the topic 'Arrhythogenic Right Ventricular Cardiomyopathy'

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Published: 22 June 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Arrhythogenic Right Ventricular Cardiomyopathy":

1

Bhardwaj, Parveen, Minoo Sharma, and Neeraj Ganju. "Arrhythmogenic right ventricular cardiomyopathy." Nigerian Journal of Cardiology 12, no. 2 (2015): 142. http://dx.doi.org/10.4103/0189-7969.152035.

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McCullough, Jocelyn, and Rohan G. Perera. "Arrhythmogenic Right Ventricular Cardiomyopathy." New England Journal of Medicine 387, no. 10 (September 8, 2022): e20. http://dx.doi.org/10.1056/nejmicm2119255.

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Jug, Juraj, and Martina Lovrić Benčić. "Arrhythmogenic right ventricular cardiomyopathy." Cardiologia Croatica 14, no. 1-2 (March 2019): 12–20. http://dx.doi.org/10.15836/ccar2019.12.

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4

Tseluyko, V. Y., and O. O. Butko. "Right ventricular arrhythmogenic cardiomyopathy." Medicine of Ukraine, no. 3(249) (May 7, 2021): 38–42. http://dx.doi.org/10.37987/1997-9894.2021.3(249).238044.

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The article describes the questions of prevalence, etiology and pathogenesis, clinical presentation, instrumental diagnostics of arrhythmogenic right ventricular cardiomyopathy (ARVC). Diagnostic criteria, sudden cardiac death risk stratification in patients with ARVC and basic approaches in the treatment of this disease are proposed.
5

Grishina, N. V. "Arrhythmogenic right ventricular cardiomyopathy." PULMONOLOGIYA 32, no. 2 (April 13, 2022): 47–53. http://dx.doi.org/10.18093/0869-0189-2022-32-2s-47-53.

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The article provides current information about the clinical manifestations and diagnosis of arrhythmogenic right ventricular cardiomyopathy, highlights the genetic aspects of the disease, and analyzes the recent scientific research. A clinical case of diagnosis of this rare disease is given.
6

Krahn, Andrew D., Arthur A. M. Wilde, Hugh Calkins, Andre La Gerche, Julia Cadrin-Tourigny, Jason D. Roberts, and Hui-Chen Han. "Arrhythmogenic Right Ventricular Cardiomyopathy." JACC: Clinical Electrophysiology 8, no. 4 (April 2022): 533–53. http://dx.doi.org/10.1016/j.jacep.2021.12.002.

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7

Nogami, Akihiko. "Arrhythmogenic Right Ventricular Cardiomyopathy." Japanese Journal of Electrocardiology 34, no. 3 (2014): 245–63. http://dx.doi.org/10.5105/jse.34.245.

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8

Gallo, Cristina, Alessandro Blandino, Carla Giustetto, Matteo Anselmino, Davide Castagno, Elena Richiardi, and Fiorenzo Gaita. "Arrhythmogenic right ventricular cardiomyopathy." Journal of Cardiovascular Medicine 17, no. 6 (June 2016): 418–24. http://dx.doi.org/10.2459/jcm.0000000000000354.

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Poloni, Giulia, Marzia De Bortoli, Martina Calore, Alessandra Rampazzo, and Alessandra Lorenzon. "Arrhythmogenic right-ventricular cardiomyopathy." Journal of Cardiovascular Medicine 17, no. 6 (June 2016): 399–407. http://dx.doi.org/10.2459/jcm.0000000000000385.

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Graziosi, Maddalena, and Claudio Rapezzi. "Right ventricular arrhythmogenic cardiomyopathy." Journal of Cardiovascular Medicine 18 (January 2017): e157-e160. http://dx.doi.org/10.2459/jcm.0000000000000470.

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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Arrhythogenic Right Ventricular Cardiomyopathy":

1

Laredo, Mikaël. "Nouveaux développements techniques et applications cliniques de l'imagerie par résonance magnétique cardiaque et tomodensitométrie pour le diagnostic et la caractérisation de la cardiomyopathie arythmogène." Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS568.pdf.

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Les cardiomyopathies arythmogènes (CMA) sont une famille de pathologies cardiaques d’origine génétique dont la principale conséquence est le risque d’arythmie ventriculaires pouvant conduire à la mort subite cardiaque. Les CMA présentent une variété de phénotypes constamment en évolution incluant des modifications structurelles cachées nécessitant une évaluation multiparamétrique. L’imagerie par résonance magnétique cardiaque (IRMC) est essentielle à leur évaluation, compte tenu de l'identification croissante des formes de CMA biventriculaires et touchant le ventricule gauche (VG) de manière prédominante. La tomodensitométrie cardiaque (TDMC), bien que moins établie, présente une utilité potentielle comme outil complémentaire ou alternatif. Dans cette thèse, nous avons profité de notre large cohorte de patients porteur d’une CMA pour poursuivre trois objectifs permettant d'étendre les limites de l'imagerie cardiaque pour le diagnostic et la caractérisation fonctionnelle des CMA. Premièrement, nous avons développé et évalué un nouveau paramètre d’IRMC de suivi de textures intégrant les dynamiques longitudinales et radiales du ventricule droit (VD), qui s'est avéré efficace pour distinguer les patients atteint de CMA, en particulier ceux qui manquent de critères structurels majeurs, des sujets sains, impliquant qu'une analyse bidimensionnelle de la dynamique VD est essentielle pour saisir la physiologie complexe des CMA. Deuxièmement, nous avons décrit les caractéristiques à l’IRMC de la CMA liée aux variants pathogéniques dans Desmoplakine (DSP), une entité spécifique associée à un pronostic particulièrement défavorable au sein de la vaste diversité des CMA, et pour la première fois les avons comparées à celles trouvées dans d’autres formes de CMA avec atteinte du VG. Nous avons constaté que la présence d'un rehaussement tardif diffus s'étendant au-delà du VG inferolatéral associée à un rapport de volume VG-VD en fin de systole ≥ 0,8 pourrait être considérée comme indicatrice d'une forte probabilité pré-test génétique de CMA liée à DSP. Troisièmement, à travers une étude multimodalité, nous avons montré qu'il y avait généralement une faible concordance spatiale entre le substrat arythmogène et les anomalies morpho-fonctionnelles ou la graisse VD, à un niveau segmentaire. Ce résultat ouvre la voie à une intégration de données électrophysiologiques dans les critères diagnostics des CMA et suggère que l'imagerie cardiaque en pratique courante ne peut pas exclure de manière fiable la présence d'un substrat arythmogène à un certaine localisation du VD. Des améliorations déterminantes sont actuellement entreprises pour augmenter l'impact et la généralisabilité des trois ensembles de résultats
Arrhythmogenic cardiomyopathies (ACM) constitute a spectrum of genetically-determined cardiac diseases of which the main consequence are ventricular arrhythmias potentially leading to sudden cardiac death. Arrhythmogenic cardiomyopathies have a diverse range of clinical-imaging phenotypes, and a continuously evolving landscape including concealed structural changes requiring multiparametric assessment. Cardiac magnetic resonance (CMR) is central in their evaluation, given the growing identification of biventricular and left-ventricular(LV)-predominant ACM variants. Multidetector computed tomography (MDCT), while not as established, offers potential utility as either an adjunct or alternative tool. In this thesis, we took advantage on our large ACM cohort to pursue three aims able to extend the boundaries of cardiac imaging for ACM diagnosis and functional characterization. First, we developed and evaluated a novel feature-tracking CMR parameter that integrates both longitudinal and radial right ventricular (RV) dynamics, which was effective in distinguishing ACM patients, particularly those lacking major structural criteria, from healthy subjects, implying that a two-dimensional representation of RV dynamics is crucial to capture the complex physiology of ACM. Second, we described the CMR features of Desmoplakin (DSP)-related ACM, a specific entity associated with particularly worse outcomes amidst the wide diversity of ACMs, and for the first time compared them to those found in ACM with LV involvement. We found that the presence of diffuse late gadolinium enhancement extending beyond the inferolateral LV combined with an end-systolic LV-to-RV volume ratio ≥0.8 may be considered as indicative of a high pre-genetical test results likelihood for DSP-ACM. Third, through a transversal multimodality study, we showed there was overall a low spatial concordance between the arrhythmogenic substrate and morpho-functional abnormalities or RV fat, at a segmental level. This finding paves the way for an integration of EP data into ACM diagnostic criteria and suggest that routine practice cardiac imaging cannot reliably exclude the presence of an EP substrate in a given RV location. Determinant improvements are currently being undertaken to increase the impact and generalizability of the three sets of results
2

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.
3

Fish, Maryam. "Analysis of desmoplakin in arrythmogenic right ventricular cardiomyopathy." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/10466.

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Includes bibliographical references (leaves 71-79).
It has been shown that all forms of cardiomyopathy, including the dilated, hypertrophic, restrictive, and right ventricular arrhythmogenic forms, are found in African populations. Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare muscle disease characterised by fibrofatty replacement of the right ventricular myocardium, leading to electrical instability and eventual heart failure. Dilated cardiomyopathy (DCM) is a disease characterised by a reduction in ventricular wall thickness which leads to reduced contractility and impaired ventricular function. Mutations that cause ARVC have been reported in five desmosomal and three non-desmosomal genes.
4

Fish, Maryam. "Analysis of genetic variations associated with arrhythmogenic right ventricular cardiomyopathy." Doctoral thesis, University of Cape Town, 2016. http://hdl.handle.net/11427/20350.

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Cardiomyopathy accounts for 20-30% of acute heart failure cases in adult Africans. Several types of cardiomyopathy have been identified; this study focused primarily on the genetic causes of arrhythmogenic right ventricular cardiomyopathy (ARVC). Many genes are implicated in ARVC pathogenesis, but many remain to be identified. We investigated a South African family (ACM2) with autosomal dominant ARVC, for whom the genetic cause of disease was unknown. Extensive genetic analysis was previously performed using genome-wide linkage analysis, but no disease-causing genetic variant was identified. We subsequently performed candidate gene screening of the phospholamban (PLN) gene, genome-wide copy number variant (CNV) analysis and whole exome sequencing to identify the causal genetic variant. The ACM2 family harboured no disease-causing PLN variants. However, on screening all cardiomyopathy cases in our registry (ARVC, dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy and peripartum cardiomyopathy), we identified a known pathogenic PLN variant (c.25C>T; p.R9C) in a DCM family of European descent. This variant was reported in an American DCM family of European descent. Haplotype analysis revealed independent variant origins in these families. CNV analysis revealed no disease-causing variants in the ACM2 family. Whole exome sequencing of two affected ACM2 family members revealed 38 variants shared by these individuals. Variants were verified in family members and population controls by high resolution melt analysis and Sanger sequencing, and by bioinformatics analysis to predict variant pathogenicity. A novel N-cadherin (CDH2) c.686A>C (p.Q229P) variant segregated with ARVC in the ACM2 family and was bioinformatically predicted to be deleterious. An additional pathogenic CDH2 variant (c.1219G>A (p.D407N)) was identified in another individual with ARVC after screening 85 cases. These CDH2 variants were absent in normal population controls. Furthermore, alterations in Cdh2 are known to cause cardiomyopathy in rodent models. Taken together, these findings support the causal role of N-cadherin gene variants in human cardiomyopathy.
5

ElMaghawry, Mohamed. "Advances in Electrocardiographic Features in Arrhythmogenic Right Ventricular Cardiomyopathy." Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3423899.

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Introduction Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic heart muscle disease characterized by electrical instability leading to ventricular arrhythmias and sudden cardiac death. The hallmark pathological lesion of ARVC is the transmural loss of the myocardium of the right ventricular (RV) free wall with replacement by fibro-fatty tissue. Three-dimensional electroanatomic voltage mapping (EVM) by CARTO system (Biosense-Webster, Diamond Bar, California) allows identification and characterization of low-voltage regions, i.e. "electroanatomical scars" (EAS), which in patients with ARVC correspond to areas of fibro-fatty replacement. Although the technique has been demonstrated to enhance the accuracy for diagnosing ARVC, its value for arrhythmic risk stratification remains to be established. Furthermore, the clinical utility of EVM for scar quantification and risk assessment is limited by its invasive nature, low availability and high costs. Thus, in daily clinical practice there is the need of a non-invasive test such as 12-lead electrocardiogram (ECG) for prediction of the amount of RV myocardial scar lesion and assessment of arrhythmic risk. Previous studies demonstrated an association between ECG repolarization/depolarization abnormalities and RV mechanical dilation/dysfunction. In fact, T wave inversion in right pericardial leads is the most common ECG abnormality of ARVC. However, the presence of T wave inversion in leads V1-V3, known as persistence of the juvenile pattern of repolarization, may also be observed in about 3% of healthy adults. The current perspective is that, at variance with healthy subjects, right precordial NTWs persist with exercise in ARVC patients. However, this view is not supported by systematic scientific data. Objective In this work, we aimed to further study some of the electrocardiographic features of ARVC. First, we assessed the prognostic value of EAS detected by EVM and its correlation with various non-invasive characteristics of ARVC, including abnormalities detected by surface ECG. Second, we studied the exercise-induced changes in right precordial negative T waves in patients with ARVC and in a group of healthy young individuals with persistence of the juvenile repolarization pattern Methods and results We first studied 69 consecutive ARVC patients (47 males; median age 35 years [28-45]) who underwent electrophysiological study and both bipolar and unipolar EVM. The extent of confluent bipolar (<1.5 mV) and unipolar (<6.0 mV) low-voltage electrograms was estimated using the CARTO-incorporated area calculation software. Fifty-three patients (77%) showed ≥1 RV electroanatomic scars with an estimated burden of bipolar versus unipolar low voltage areas of 24.8% (7.2-31.5) and 64.8% (39.8-95.3), respectively (P=0.009). In the remaining patients with normal bipolar EVM (n=16; 23%), the use of unipolar EVM unmasked ≥1 region of low-voltage electrogram affecting 26.2% (11.6-38.2) of RV wall. During a median follow-up of 41 (28-56) months, 19 (27.5%) patients experienced arrhythmic events. At multivariate analysis, the only independent predictor was the bipolar low-voltage electrogram burden (hazard ratio=1.6 per 5%; 95% confidence interval, 1.2-1.9; P<0.001). Patients with normal bipolar EVM had an uneventful clinical course. Then we further analyzed a subgroup including 49 patients [38 males, median age 35 years] with ARVC and an abnormal EVM by CARTO system. At univariate analysis, the presence of epsilon waves, the degree of RV dilation, the severity of RV dysfunction and the extent of negative T-waves correlated with RV-EAS% area. At multivariate analysis, the extent of negative T-waves remained the only independent predictor of RV-EAS% area (B=4.4, 95%CI 1.3-7.4, p=0.006) and correlated with the arrhythmic event-rate during follow-up (p=0.03). In a different cohort, we assessed the prevalence and relation to the clinical phenotype of exercise-induced right precordial negative T wave changes in 35 ARVC patients (19 males, mean age 22.2±6.2 years). Forty-one healthy individuals with right-precordial negative T waves served as controls. At peak of exercise, negative T waves persisted in 3 ARVC (9%) patients, completely normalized in 12 (34%) and partially reverted in 20 (57%). ARVC patients with or without negative T waves normalization showed a similar clinical phenotype. The overall prevalence of right precordial T-waves changes during exercise (normalization plus partial reversal) did not differ between ARVC patients and controls (92% versus 88%, p=1.0), while there was a statistically non significant trend towards a higher prevalence of complete normalization in controls (59% versus 34%, p=0.06). Conclusion In conclusion, our results showed that the extent of bipolar RV endocardial low-voltage area was a powerful predictor of arrhythmic outcome in ARVC independently of arrhythmic history and RV dilatation/dysfunction. A normal bipolar EVM characterized a low-risk subgroup of ARVC patients. Patients with abnormal ECG have a more severe RV EAS involvement, which is proportional to the extent of T wave inversion across ECG 12-leads and a higher arrhythmic risk. The absence of negative T waves characterizes a low-risk subgroup of ARVC patients with a more favorable clinical course because of a low rate of arrhythmic events. The results also showed that exercise-induced changes of negative T waves were unrelated to ARVC phenotypic manifestations and were of limited value for the differential diagnosis between ARVC and benign persistence of the juvenile repolarization pattern
Introduzione La cardiomiopatia aritmogena del ventricolo destro (CAVD) è una patologia genetica del muscolo cardiaco caratterizzata da instabilità elettrica che può portare a aritmie ventricolari e morte improvvisa. Dal punto di vista patologico, la CAVD si caratterizza per una progressiva perdita di tessuto miocardico della parete libera del ventricolo destro (VD) con sostituzione fibro-adiposa. Il mapaggio elettroanatomico tridimensionale (endocardial voltage mapping, EVM) col sistema CARTO (Biosense-Webster, Diamond Bar, California) consente di identificare e caratterizzare aree di basso-voltaggio, dette "cicatrici elettroanatomiche" (CEA), che in pazienti affetti da CAVD corrispondono ad aree di sostituzione fibro-adiposa. Nonostante la tecnica abbia dimostrato di migliorare l"accuratezza per la diagnosi di CAVD, il suo valore per la stratificazione del rischio aritmico rimane da dimostrate. Inoltre, l"utilità dell"EVM per la quantificazione della cicatrice e la valutazione del rischio è limitata dalla natura invasiva, bassa disponibilità ed alti costi. Quindi, nella pratica clinica quotidiana è auspicabile la disponibilità di un esame non-invasivo, come l"elettrocardiogramma (ECG), per la stima dell'estensione della CEA e la stratificazione del rischio aritmico. Studi precedenti hanno dimostrato un"associazione tra la presenza di anomalie della ripolarizzazione o della depolarizzazione all"ECG e l"entità della dilatazione e della disfunzione del VD. In particolare, l"inversione delle onde T nelle derivazioni precordiali destre V1-V3 è uno dei segni distintivi della CAVD. Tuttavia, lo stesso segno ECG può essere riscontrato come "persistenza del pattern giovanile di ripolarizzazione" fino al 3% degli adulti sani. La prospettiva attuale è che le T negative persistano con l'esercizio nei pazienti con CAVD ma non nei soggetti sani. Tuttavia, questa idea non è supportata da dati scientifici. Obbiettivo L"obbiettivo dell"attività di ricerca è stato quello di caratterizzare ulteriormente alcune delle caratteristiche ECG della CAVD. Inizialmente, abbiamo valutato il valore prognostico della CEA all"EVM e la sua correlazione con vari esami non invasivi, in particolare l"ECG. In secondo luogo, abbiamo studiato le modificazioni indotte dall"esercizio nella T negative nelle derivazioni precordiali destre in un gruppo di pazienti con CAVD ed in un gruppo di soggetti sani con "persistenza del pattern giovanile di ripolarizzazione". Metodi e risultati Sono stati studiati 69 pazienti consecutivi affetti da CAVD (47 maschi, età mediana 35 [28-45] anni) che sono stati sottoposti a studio elettrofisiologico endocavitario con mappa di voltaggio unipolare e bipolare. L"estensione delle aree contenenti elettrogrammi di basso voltaggio bipolari (<1.5 mV) e/o unipolari (<6.0 mV) è stata stimata usando un software incorporato nel sistema CARTO. Cinquantatre pazienti (77%) mostravano ≥1 CEA con un"estensione pari a 24.8% (7.2-31.5) dell"estensione del VD alla mappa bipolare e del 64.8% (39.8-95.3) alla mappa unipolare (p=0.009). Nei rimanenti 16 pazienti con mappa bipolare normale, la mappa unipolare è risultata alterata con un"estensione delle lesioni pari al 26.2% (11.6-38.2) del VD. Nel corso di un follow-up medio di 41 (28-56) mesi, 19 (27.5%) pazienti hanno avuto un evento aritmico maggiore. All'analisi multivariata, l'unico predittore indipendente di eventi aritmici è risultata l'estensione della CEA alla mappa di voltaggio bipolare (hazard ratio=1.6 per 5%; intervallo di confidenza 95%: 1.2-1.9; P<0.001). I pazienti con mappa di voltaggio bipolare negativa hanno avuto un follow-up privo di eventi. Successivamente, abbiamo analizzato un sottogruppo di 49 pazienti (38 maschi, età mediana 35 anni) con CAVD e mappa di voltaggio bipolare positiva. All'analisi univariata, la presenza di onde epsilon, il grado di dilatazione del VD, la severità della disfunzione del VD e l'estensione delle T negative all'ECG correlavano con l'estensione della CEA alla mappa bipolare. All'analisi multivariata, l'estensione delle onde T negative è rimasta l'unico predittore di estensione della CEA (B=4.4, 95%CI 1.3-7.4, p=0.006). Questo parametro si è inoltre dimostrato correlare con il rischio di eventi aritmici durante il follow-up (p=0.03). In una coorte differente, abbiamo valutato il comportamento durante test da sforzo delle T negative nelle derivazioni precordiali destre V1-V4 in 35 pazienti con CAVD (19 maschi, età media 22.2"±6.2 anni) ed in 41 controlli appaiati per età e sesso con benigna "persistenza del pattern giovanile di ripolarizzazione". Al picco dell'esercizio, le onde T negative persistevano in 3 (9%) pazienti con CAVD, normalizzavano completamente in 12 (34%) e normalizzavano parzialmente in 20 (57%). I pazienti affetti da CAVD con e senza normalizzazione delle onde T durante l'esercizio mostravano un fenotipo simile. La prevalenza di normalizzazione (parziale o completa) delle onde T era simile nei pazienti e nei controlli (92% e 88%, p=1,0), mentre si è notato un trend non significativo verso una più alta prevalenza di normalizzazione completa nei controlli sani rispetto ai pazienti con CAVD (59% e 34%, p=0,06). Conclusioni In conclusione, i nostri risultati hanno mostrato che l'estensione della CEA bipolare alla mappa di voltaggio del VD è un potente predittore di rischio aritmico nei pazienti con CAVD, indipendentemente dalla storia aritmica e dal grado di disfunzione/dilatazione del VD. Una mappa di voltaggio bipolare normale caratterizza una popolazione di pazienti con CAVD a basso rischio. Abbiamo inoltre dimostrato che l'estensione della CEA bipolare può essere stimata dall'estensione delle anomalie della ripolarizzazione (T negative) all'ECG. I pazienti che non mostrano T negative all'ECG dimostrano un basso rischio aritmico. Infine, abbiamo dimostrato che il comportamento delle T negative nelle derivazioni precordiali destre V1-V3 non è un utile strumento di diagnosi differenziale tra CAVD e benigna "persistenza del pattern giovanile di ripolarizzazione"
6

Norman, Mark. "Investigation of the familial nature of arrhythmogenic right ventricular cardiomyopathy." Thesis, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511949.

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7

Blanckenberg, Janine. "Molecular genetics of arrhythmogenic right ventricular cardiomyopathy in South Africa." Doctoral thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/10130.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable disorder characterised by progressive degeneration of the right ventricular myocardium, arrhythmias and an increased risk of sudden death at a young age. Fourteen chromosomal loci have been linked to ARVC and nine disease genes have been identified. Linkage analysis of a South African family was previously performed at ARVC loci 1 to 6. ARVC loci 1 to 5 were excluded as disease loci in this family based on lack of evidence for linkage. However, a peak lod score of 2.93 was obtained for the ARVC-6 locus which is highly suggestive of linkage. Subsequently another locus (ARVC-7) and five ARVC disease genes (ARVC loci 8 to 12) have been reported. The aim of this project was to identify the disease gene that causes ARVC in this family.
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Du, Preez Janine. "A candidate gene analysis of arrhythmogenic right ventricular cardiomyopathy (ARVC)." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/3092.

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Includes bibliographical references (leaves 84-90).
Heart failure is a major public health problem throughout the world. In South Africa 17% of mortality is attributed to cardiovascular disease (CVD). Heart failure may be either ischemic or non-ischemic in origin. A significant proportion of non-ischemic heart failur is due to cardiomyopathy. There are currently five types of cardiomyopathy recognised, of which arrhythmogenic right ventricular cardiomyopathy (ARVC) is one. ARVC is familial in 30 to 50% of cases and it is inherited in an autosomal dominant or an autosomal recessive manner. Twelve chromosomal loci have been linked to ARVC and six genes have been identified. In 2004 Asano and colleagues reported a mouse model of ARVC that established LAMRI and CBX5 as candidate genes for the human form of ARVC.
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MIGLIORE, FEDERICO. "Arrhythmogenic Right Ventricular Cardiomyopathy: Prognostic Value of Electroanatomic Voltage Mapping." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3426170.

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Background: Endocardial voltage mapping (EVM) identifies low-voltage right ventricular (RV) areas, which may represent the electroanatomic scar substrate of life-threatening tachyarrhythmias. We prospectively assessed the prognostic value of EVM in a consecutive series of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods: We studied 69 consecutive ARVC patients [47 males; median age 35 years(28-45)] who underwent electrophysiological study and both bipolar and unipolar EVM. The extent of confluent bipolar (<1.5mV) and unipolar (<6.0mV) low-voltage electrograms was estimated using the CARTO-incorporated area calculation software. Results: Fifty-three patients (77%) showed ≥1 RV electroanatomic scars with an estimated burden of bipolar vs unipolar low-voltage areas of 24.8% (7.2-31.5) and 64.8% (39.8-95.3), respectively (P=0.009). In the remaining patients with normal bipolar-EVM (n=16;23%), the use of unipolar EVM unmasked ≥1 region of low-voltage electrogram affecting 26.2% (11.6-38.2) of RV wall. During a median follow-up of 41 (28-56) months, 19(27.5%) patients experienced arrhythmic events, such as sudden death (n=1), appropriate ICD interventions (n=7), or sustained ventricular tachycardia (n=11). Univariate predictors of arrhythmic outcome included previous cardiac arrest or syncope (HR=3.4; 95%CI:1.4-8.8; P=0.03) and extent of bipolar low-voltage areas (HR=1.7 per 5%; 95%CI=1.5-2; P<0.001), while the only independent predictor was the bipolar low-voltage electrogram burden (HR=1.6 per 5%; 95% CI:1.2-1.9; P<0.001). Patients with normal bipolar-EVM had an uneventful clinical course. Conclusions: The extent of bipolar RV endocardial low-voltage area was a powerful predictor of arrhythmic outcome in ARVC, independently of history and RV dilatation/dysfunction. A normal bipolar-EVM characterized a low-risk subgroup of ARVC patients.
Introduzione: Il mappaggio elettroanatomico mediante sistema CARTO permette di identificare e quantificare aree di basso voltaggio del ventricolo destro che corrispondono a cicatrici elettroanatomiche, substrato di aritmie ventricolari pericolose per la vita. Lo scopo dello studio era di valutare, in modo prospettico, il valore prognostico del mappaggio elettroanatomico in una coorte di pazienti affetti da Cardiomiopatia Aritmogena del Ventricolo Destro. Materiali e Metodi: La popolazione di studio includeva 69 pazienti (47maschi; età mediana 35 anni; 28-35) affetti da Cardiomiopatia Aritmogena del Ventricolo Destro. Tutti i pazienti sono stati sottoposti ad un completo work up clinico che includeva: elettrocardiogramma, ecocardiografia, cateterismo cardiaco, studio elettrofisiologico e mappaggio elettroanatomico del ventricolo destro, utilizzando sia mappe bipolari sia unipolari. L’estensione degli elettrogrammi confluenti di basso voltaggio bipolari (<1.5 mV) e unipolari (<6.0 mV) è stata stimata usando un software incorporato nel sistema CARTO. Risultati: In cinquantatre pazienti (77%) è stata riscontrata ≥1 regione cicatriziale a carico del ventricolo destro con una percentuale stimata di aree di basso voltaggio bipolari e unipolari rispettivamente di 24.8% (7.2-31.5) e 64.8 (39.8-95.3), rispettivamente (P=0.009). In tutti pazienti con una normale mappa bipolare (n= 16; 23%) l’utilizzo del mappaggio unipolare ha identificato ≥1 regione con elettrogrammi di basso voltaggio che interessava il 26.2% (11.6-38.2) del ventricolo destro. Durante un follow-up di 41 (28-56) mesi 19 (27.5%) pazienti subirono eventi aritmici maggiori, quali morte improvvisa (n=1), intervento appropriato dell’ICD (n=7), o tachicardia ventricolare sostenuta (n=11). All’analisi univariata i predittori dell’outcome aritmico includevano: sincope (HR=3.4; 95%CI: 1.4-8.8; P=0.03), e l’estensione delle aree di basso voltaggio bipolare (HR=1.7 per 5%; 95%CI: 1.5-2; P<0.001). All’analisi multivariata, l’unico predittore indipendente risultava l’estensione delle aree di basso voltaggio al mappaggio bipolare (HR=1.6 per 5%;95% CI:1.2-1.9; P<0.001). Tutti i pazienti con un mappaggio bipolare normale presentavano un decorso clinico privo di eventi aritmici. Conclusioni: l’estensione delle aree endocardiche di basso voltaggio nel ventricolo destro risulta essere un potente predittore di eventi aritmici maligni nella Cardiomiopatia Aritmogena del Ventricolo Destro indipendentemente dalla storia clinica e dalla dilatazione/disfunzione del ventricolo destro. La presenza di un normale mappaggio elettroanatomico bipolare rapprestanta un sottogruppo di pazienti affetti da Cardiomiopatia Aritmogena del Ventricolo Destro a basso rischio aritmico.
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Huang, Hsin-Chi. "Cardiovascular magnetic resonance and right ventricular angiography in assessment of right ventricular volumes, function and wall motion abnormalities in arrhythmogenic right ventricular cardiomyopathy: a comparative study." Master's thesis, Faculty of Health Sciences, 2019. https://hdl.handle.net/11427/31643.

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Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy characterised by structural changes to mostly the right ventricle (RV) that predisposes to ventricular arrhythmias heart failure and sudden cardiac death. ARVC is diagnosed using the 2010 Task Force Criteria which include RV angiography (RVA) and cardiovascular magnetic resonance (CMR). There has been a dearth of studies to document the comparison of the performance of CMR and RVA, and none undertaken in Africa. The aim of this study was to compare CMR and RVA in the assessment of ARVC in the South African ARVC registry. Methods: The study is a retrospective analysis of definite, possible and borderline ARVC cases from the South African ARVC registry and the African Cardiomyopathy and Myocarditis Registry Program (IMHOTEP) that have both CMR and RVA data. RV end-systolic and diastolic volumes, RV ejection fractions and the presence of absence of structural abnormalities derived from RVA and CMR are compared. Sensitivity of CMR and RVA for the diagnosis of definite, possible and borderline ARVC was also calculated. Results: A total of 11 patients out of 62 from the registry met the inclusion criteria. The Spearman’s coefficient for RV end-systolic volume was 0.48 (p=0.12). The Spearman’s coefficient for RV enddiastolic volume was 0.28 (p=0.4). The Spearman’s coefficient for RV ejection fraction was 0.06 (p=0.85). CMR detected regional wall abnormalities in 4 out of 11 patients while RVA did not detect any regional wall abnormalities. Sensitivity of CMR and RVA for the diagnosis of definite, possible and borderline ARVC was 48% and 55%, respectively. Conclusions: We show that South African ARVC patients had poor correlation between CMR and RVA parameters, and CMR was also more likely to reveal RV free wall regional wall motion abnormalities.
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Books on the topic "Arrhythogenic Right Ventricular Cardiomyopathy":

1

Hariharan, Venkatesh. The Effects of Arrhythmogenic Right Ventricular Cardiomyopathy-Causing Proteins on the Mechanical and Signaling Properties of Cardiac Myocytes. [New York, N.Y.?]: [publisher not identified], 2014.

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Elliott, Perry, Kristina H. Haugaa, Pio Caso, and Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.
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Syrris, Petros, and Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0359.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder of the heart muscle which is typically inherited in an autosomal dominant manner. It is believed to be familial in over 50% of cases. A recessive mode of inheritance has also been reported in syndromic cases with cardiocutaneous features. The classic form of the disorder is considered to be ‘a disease of the desmosome’ as pathogenic variants have been identified in five genes encoding key desmosomal proteins: plakoglobin, desmoplakin, plakophilin-2, desmoglein-2, and desmocollin-2. Mutations in these genes account for 30–50% of ARVC cases. A further eight non-desmosomal genes have also been implicated in the pathogenesis of the disorder but only account for rare cases. Studies of patients with ARVC-associated gene mutations have revealed marked genetic heterogeneity and very limited genotype–phenotype correlation. Disease expression often varies significantly amongst individuals carrying the same mutation. It has been proposed that the presence of more than one sequence variant is required to determine overt clinical disease and patients with multiple variants have a more severe phenotype compared to single variant carriers. Identification of a potentially pathogenic variant comprises a major criterion in the diagnosis of ARVC but informative integration of genetic testing into clinical practice remains challenging. Gene testing should be used to identify asymptomatic family members at risk and only aids diagnosis in cases of high suspicion for ARVC, along with other evident features of the disease already present. However, genetic findings should be used with caution in clinical practice and their interpretation must be performed in expert centres.
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Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Arrhythmogenic right ventricular cardiomyopathy/dysplasia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0918_update_004.

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Touboul, Paul, and Marjaneh Fatemi. Touboul Arrhythmogenic Right Ventricular Cardiomyopathy. Wiley & Sons, Incorporated, John, 2008.

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(Editor), Frank I. Marcus, Andrea Nava (Editor), and Gaetano Thiene (Editor), eds. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: Recent Advances. Springer, 2007.

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Arrythmogenic Right Ventricular Cardiomyopathy: ARVC and Related Disorders. Springer, 2007.

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Brunckhorst, Corinna, Firat Duru, and Ardan M. Saguner. Current Concepts in Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia. Cardiotext Publishing, 2014.

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Brunckhorst, Corinna, Firat Duru, and Ardan M. Saguner. Current Concepts in Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia. Cardiotext Publishing, 2014.

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Book chapters on the topic "Arrhythogenic Right Ventricular Cardiomyopathy":

1

Zorzi, Alessandro, and Domenico Corrado. "Arrhythmogenic Right Ventricular Cardiomyopathy." In IOC Manual of Sports Cardiology, 217–30. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119046899.ch20.

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Wang, Jian, Yining Wang, and Zheng-yu Jin. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Cardiac CT, 157–61. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5305-9_29.

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Côté, Etienne, Kristin A. MacDonald, Kathryn M. Meurs, and Meg M. Sleeper. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Feline Cardiology, 189–92. West Sussex, UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118785782.ch14.

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Brambatti, Michela, and Matilda Shkoza. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Clinical Cases in Cardiology, 153–63. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19926-9_14.

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Hutchinson, Mathew D. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Cardiac Electrophysiology, 493–97. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28533-3_117.

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Mattesi, Giulia, Alberto Cipriani, Alessandro Zorzi, and Domenico Corrado. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Contemporary Cardiology, 791–810. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41967-7_32.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Arrhythmogenic Right Ventricular Cardiomyopathy." In Encyclopedia of Molecular Mechanisms of Disease, 147–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3113.

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Cowan, Mitchell A., and Karin Chia. "Right Ventricular Outflow Tract/Arrhythmogenic Right Ventricular Cardiomyopathy Ventricular Tachycardia." In Cardiac Electrophysiology, 487–91. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28533-3_116.

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Marcus, Frank I., and Peter Ott. "Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy." In Molecular Genetics of Cardiac Electrophysiology, 239–50. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4517-0_15.

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Bevilacqua, Michela, Federico Migliore, Cristina Basso, Gaetano Thiene, and Domenico Corrado. "Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia." In Clinical Approach to Sudden Cardiac Death Syndromes, 163–71. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-927-5_13.

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Conference papers on the topic "Arrhythogenic Right Ventricular Cardiomyopathy":

1

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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KAWANO, HIROAKI, NORIHIRO KOMIYA, SATOKI FUKAE, REIICHIRO NAKAMIZO, YUJI KOIDE, GENJI TODA, and KATSUSUKE YANO. "ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY WITH RIGHT BUNDLE BRANCH BLOCK AND RIGHT PRECORDIAL ST-SEGMENT ELEVATION -A CASE REPORT-." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0127.

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Ruisch, Janna, Machteld Boonstra, Rob Roudijk, Peter van Dam, Cornelis Herman Slump, and Peter Loh. "Disease-Specific Electrocardiographic Lead Positioning for Early Detection of Arrhythmogenic Right Ventricular Cardiomyopathy." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.334.

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Pieles, G., L. Grosse-Wortmann, M. Hader, M. Fatah, P. Chungsomprasong, C. Sloarach, L. Mertens, R. Hamilton, and M. Friedberg. "Association of Echocardiographic Parameters of Right Ventricular Remodeling and Myocardial Performance with Modified Task Force Criteria in Adolescents with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)." In 50th Annual Meeting of the German Society for Pediatric Cardiology (DGPK). Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1628333.

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Mallappa, A., R. Reddy, and D. Ninjagal Shivanna. "G397(P) Hypertrophic cardiomyopathy with right and left ventricular outflow tract obstruction in a child." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.383.

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Damani, Devanshi N., Anoushka Kapoor, Priyadharshini Sivasubramaniam, Nasibeh Farahani, Moein Enayati, Jeffrey B. Geske, Michael J. Ackerman, et al. "Biventricular Involvement In Hypertrophic Cardiomyopathy: Preliminary Analysis Of Cardiac MRIs With Visual Right Ventricular Hypertrophy." In 2022 IEEE 10th International Conference on Healthcare Informatics (ICHI). IEEE, 2022. http://dx.doi.org/10.1109/ichi54592.2022.00031.

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Aljehani, Areej, Richard Steeds, Laura sommerfeld, Shanat Baig, and Larissa Fabritz. "173 Progression of arrhythmogenic right ventricular cardiomyopathy (arvc) and risk of major adverse cardiac events." In British Cardiovascular Society Annual Conference, ‘Future-proofing Cardiology for the next 10 years’, 5–7 June 2023. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2023-bcs.173.

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Malik, Jahanzeb. "118 Validation of arrhythmogenic right ventricular cardiomyopathy risk calculator for sudden cardiac death: a systematic review." In British Cardiovascular Society Annual Conference, ‘Future-proofing Cardiology for the next 10 years’, 5–7 June 2023. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2023-bcs.118.

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Tollit, Jennifer, Gabrielle Norrish, Olga Boleti, Ella Field, and Juan Pablo Kaski. "5 Diagnostic yield of arrhythmogenic right ventricular cardiomyopathy (ARVC) in paediatric relatives of probands with sads versus non-diagnostic post-mortems." In British Cardiovascular Society Annual Conference, ‘Back to the patient’, 3–5 June 2024. BMJ Publishing Group Ltd and British Cardiovascular Society, 2024. http://dx.doi.org/10.1136/heartjnl-2024-bcs.5.

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