Electrocardiographic Difference between Ventricular Arrhythmias from the Right Ventricular Outflow Tract and Idiopathic Right Ventricular Arrhythmias

Ren, Lixin; Liu, Zheng; Jia, Yuhe; Fang, Pihua; Pu, Jielin; Zhang, Shu

doi:10.1111/pace.12463

Cited by 8 publications

(3 citation statements)

References 27 publications

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“…The ECG morphology of the OT‐VA and the sinus beat was assessed and measured offline by using electronic calipers on the recording system or on the electronic version of the paper electrocardiogram as the previously reported methodology . Care was taken to ensure uniform lead gains at a paper speed of 50 mm/s.…”

Section: Methodsmentioning

confidence: 99%

Multiple Intercostal Space Electrocardiogram Allows Accurate Localization of Outflow Tract Ventricular Arrhythmia Origin

Liu

Jia

Ren

et al. 2015

Pacing Clinical Electrophis

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Section: Methodsmentioning

confidence: 99%

Multiple Intercostal Space Electrocardiogram Allows Accurate Localization of Outflow Tract Ventricular Arrhythmia Origin

Liu

Jia

Ren

et al. 2015

Pacing Clinical Electrophis

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“…Several diseases may mimic ACM making its diagnosis even more challenging. Early phases of ACM are often misdiagnosed as idiopathic right ventricular outflow tract (RVOT) tachycardia ( 19 ) or Brugada syndrome ( 20 ). In the more advanced biventricular form of the disease, ACM is indistinguishable from dilated cardiomyopathy (DCM) ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

Histopathological Features and Protein Markers of Arrhythmogenic Cardiomyopathy

Bueno-Betí

Asimaki

2021

Front. Cardiovasc. Med.

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Arrhythmogenic cardiomyopathy (ACM) is a heritable heart muscle disease characterized by syncope, palpitations, ventricular arrhythmias and sudden cardiac death (SCD) especially in young individuals. It is estimated to affect 1:5,000 individuals in the general population, with >60% of patients bearing one or more mutations in genes coding for desmosomal proteins. Desmosomes are intercellular adhesion junctions, which in cardiac myocytes reside within the intercalated disks (IDs), the areas of mechanical and electrical cell-cell coupling. Histologically, ACM is characterized by fibrofatty replacement of cardiac myocytes predominantly in the right ventricular free wall though left ventricular and biventricular forms have also been described. The disease is characterized by age-related progression, vast phenotypic manifestation and incomplete penetrance, making proband diagnosis and risk stratification of family members particularly challenging. Key protein redistribution at the IDs may represent a specific diagnostic marker but its applicability is still limited by the need for a myocardial sample. Specific markers of ACM in surrogate tissues, such as the blood and the buccal epithelium, may represent a non-invasive, safe and inexpensive alternative for diagnosis and cascade screening. In this review, we shall cover the most relevant biomarkers so far reported and discuss their potential impact on the diagnosis, prognosis and management of ACM.

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“…Early ACM can be misdiagnosed as idiopathic RVOT tachycardia 9 or Brugada syndrome. 10 Nevertheless, current research indicates that idiopathic RVOT tachycardia may not be as benign as originally thought.…”

Section: Natural History Of Arrhythmogenic Cardiomyopathymentioning

confidence: 99%

Pathogenesis of Arrhythmogenic Cardiomyopathy

Asimaki

Kléber

Saffitz

2015

Canadian Journal of Cardiology

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Arrhythmogenic cardiomyopathy (ACM) is a primary myocardial disease. It is characterized by frequent ventricular arrhythmias and increased risk of sudden cardiac death typically arising as an early manifestation before the onset of significant myocardial remodeling. Myocardial degeneration, often confined to the right ventricular free wall, with replacement by fibrofatty scar tissue, develops in many patients. ACM is a familial disease but genetic penetrance can be low and disease expression is highly variable. Inflammation may promote disease progression. It also appears that exercise increases disease penetrance and accelerates its development. More than 60% of probands harbor mutations in genes encoding desmosomal proteins, which has raised the possibility that defective cell-cell adhesion may play a role in disease pathogenesis. Recent advances have implicated changes in the canonical Wnt/β-catenin and Hippo signaling pathways and defects in forwarding trafficking of ion channels and other proteins to the intercalated disk in cardiac myocytes. This review summarizes current understanding of the pathogenesis of ACM and highlights future research directions.

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Electrocardiographic Difference between Ventricular Arrhythmias from the Right Ventricular Outflow Tract and Idiopathic Right Ventricular Arrhythmias

Abstract: Longer QRS duration, later precordial R/S transition, and QRS notching in lateral leads (leads Ⅰ and aVL) are useful in discriminating ARVD/C from idiopathic RVOT-VA.

Cited by 8 publications

References 27 publications

Multiple Intercostal Space Electrocardiogram Allows Accurate Localization of Outflow Tract Ventricular Arrhythmia Origin

Multiple Intercostal Space Electrocardiogram Allows Accurate Localization of Outflow Tract Ventricular Arrhythmia Origin

Histopathological Features and Protein Markers of Arrhythmogenic Cardiomyopathy

Pathogenesis of Arrhythmogenic Cardiomyopathy

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