Kaplan, S.R., Gard, J.J., Protonotarios, N., Tsatsopoulou, A., Spiliopoulou, C., Anastasakis, A., Squarcioni, C.P., McKenna, W.J., Thiene, G., Basso, C., Brousse, N., Fontaine, G. and Saffitz, J.E. (2004) Remodeling of Myocyte Gap Junctions in Arrhythmogenic Right Ventricular Cardiomyopathy Due to a Deletion in Plakoglobin (Naxos Disease). Heart Rhythm, 1, 3-11.
http://dx.doi.org/10.1016/j.hrthm.2004.01.001

has been cited by the following article:

• TITLE: Arrhythmogenic Ventricular Dysplasia/Cardiomyopathy: Insights from the Rationale of Disease Nomenclature and Clinical Perspectives

  AUTHORS: Aimé Bonny, Mohammed A. Talle, Guy Fontaine

  KEYWORDS: Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, Arrhythmogenic Cardiomyopathy, Ventricular Arrhythmia, Sudden Cardiac Death

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.5 No.8, August 26, 2015

  ABSTRACT: “Arrhythmogenic right ventricular dysplasia” (ARVD), a heart muscle disorder characterized by the presence of fibro-fatty tissue and ventricular electrical vulnerability related to sudden death, was first described in 1977 by a French team. Since then, other terms such as “arrhythmogenic right ventricular cardiomyopathy” (ARVC), “arrhythmogenic cardiomyopathy” (AC), “left-dominant arrhythmogenic cardiomyopathy” (LDAC), and “arrhythmogenic left ventricular dysplasia” (ALVD) have been introduced. These changes in nomenclature of the same disease entity are based on different explanations of pathomorphologic patterns. The dysplasia theory claims cardiac growth “maldevelopment” whereas the cardiomyopathy has been seen as an atrophy from acquired injury (myocyte death) and repair (fibrofatty replacement). The other area of divergent opinion is with regards to involvement of both ventricles rather than being an isolated right ventricular anomaly that may result in increased likelihood of diagnosing the concealed form manifesting with pre-dominant left ventricular arrhythmias. Multiple line of evidences support common disease path-ways: Presence of fibro-fatty and superimposed myocarditis, desmosome mutations and malfunc-tion. These compelling data regarding the heart growth, and pathological, clinical, phenotype/ genotype correlates have advanced our understanding of arrhythmogenic ventricular dysplasia/ cardiomyopathy and increased the diagnostic accuracy as well as providing an avenue for future development of new mechanism-based therapies.