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.
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http://dx.doi.org/10.1016/j.diii.2014.07.009 | DOI Listing |
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.
Heart
January 2025
Department of Cardiology, University Hospital Zurich, Zurich, Switzerland
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 PDFComput Methods Programs Biomed
January 2025
Department of Physiology II, Kanazawa Medical University, Uchinada 920-0293, Japan. Electronic address:
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.
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 PDFJACC Case Rep
January 2025
Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
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.
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