MR imaging of arrhythmogenic right ventricular dysplasia: What the radiologist needs to know.

Diagn Interv Imaging

Department of Radiology, université Marseille Méditerranée, hôpital universitaire de la Timone, 264, rue Saint-Pierre, 13385 Marseille cedex 5, France.

Published: May 2015

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited heart muscle disease that predominantly affects the right ventricle. Clinical manifestations are related to severe ventricular arrhythmia that may lead to sudden death, mostly in young patients. Magnetic resonance imaging (MRI), included in the new diagnostic criteria since 2010, aims to detect segmental and global wall motion abnormalities, reduced ejection fraction, right ventricular dilatation and right ventricular diastolic/systolic dysfunction. An MRI assessment of the right ventricle is often challenging, partly because the MRI diagnostic criteria have some limitations, and also because it requires a significant learning curve due to the low prevalence of the disease. Therefore, this article aims to review the pathophysiology of the disease, the cardiac MRI protocol, images of the various stages of this affection as well as the differential diagnosis.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.diii.2014.07.009DOI Listing

Publication Analysis

Top Keywords

arrhythmogenic ventricular
8
diagnostic criteria
8
ventricular
5
imaging arrhythmogenic
4
ventricular dysplasia
4
dysplasia radiologist
4
radiologist arrhythmogenic
4
ventricular dysplasia/cardiomyopathy
4
dysplasia/cardiomyopathy arvd/c
4
arvd/c inherited
4

Similar Publications

Identification of Key Genes and Pathways in Lenvatinib-resistant Hepatocellular Carcinoma using Bioinformatic Analysis and Experimental Validation.

Curr Med Chem

January 2025

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Gastrointestinal Oncology, Peking University Cancer Hospital and Institute, Beijing, 100142, China.

Background: Resistance to lenvatinib poses a serious threat to the therapy of patients with Hepatocellular Carcinoma (HCC). The mechanism by which HCC develops resistance to lenvatinib is currently unknown.

Objective: The aim of this study was to identify key genes and pathways involved in lenvatinib resistance in HCC using bioinformatic analysis and experimental validation.

View Article and Find Full Text PDF

Background: Cardiac sarcoidosis (CS) is a chronic inflammatory disease characterised by non-caseating granulomas, while arrhythmogenic cardiomyopathy (ACM) is a genetic condition mainly affecting desmosomal proteins. The coexistence of CS and genetic variants associated with ACM is not well understood, creating challenges in diagnosis and management. This study aimed to describe the clinical, imaging and genetic features of patients with both conditions.

View Article and Find Full Text PDF

Background And Objective: It has been believed that polymorphic ventricular tachycardia (VT) such as torsades de pointes (TdP) seen in patients with long QT syndromes is triggered by creating early afterdepolarization (EAD)-mediated triggered activity (TA). Although the mechanisms creating the TA have been studied intensively, characteristics of the arrhythmogenic (torsadogenic) substrates that link EAD developments to TA formation are still not well understood.

Methods: Computer simulations of excitation propagation in a homogenous two-dimensional ventricular tissue with an anisotropic conduction property were performed to characterize torsadogenic substrates that potentially form TA.

View Article and Find Full Text PDF

Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca channel (Ca1.2) and reduce Ca-dependent inactivation.

Acta Physiol (Oxf)

February 2025

Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.

Aim: Long QT syndrome (LQTS) and catecholaminergic polymorphism ventricular tachycardia (CPVT) are inherited cardiac disorders often caused by mutations in ion channels. These arrhythmia syndromes have recently been associated with calmodulin (CaM) variants. Here, we investigate the impact of the arrhythmogenic variants D131E and Q135P on CaM's structure-function relationship.

View Article and Find Full Text PDF

Structural abnormalities within the right ventricular outflow tract (RVOT) can present similarly to Brugada syndrome. A 34-year-old woman with no medical history presented with polymorphic ventricular tachycardia/ventricular fibrillation cardiac arrest and initial electrocardiogram showed type I Brugada pattern. Cardiac magnetic resonance imaging revealed prominent tissue thickening at the RVOT with late gadolinium enhancement.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!