Clinical expression of plakophilin-2 mutations in familial arrhythmogenic right ventricular cardiomyopathy

Circulation. 2006 Jan 24;113(3):356-64. doi: 10.1161/CIRCULATIONAHA.105.561654. Epub 2006 Jan 16.

Abstract

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiac disorder characterized by loss of cardiomyocytes and their replacement by adipose and fibrous tissue. It is considered a disease of cell adhesion because mutations in desmosomal genes, desmoplakin and plakoglobin, have been implicated in the pathogenesis of ARVC. In a recent report, mutations in plakophilin-2, a gene highly expressed in cardiac desmosomes, have been shown to cause ARVC.

Methods and results: We investigated 100 white patients with ARVC for mutations in plakophilin-2. Nine different mutations were identified by direct sequencing in 11 cases. Five of these mutations are novel (A733fsX740, L586fsX658, V570fsX576, R413X, and P533fsX561) and predicted to cause a premature truncation of the plakophilin-2 protein. Family studies showed incomplete disease expression in mutation carriers and identified a number of individuals who would be misdiagnosed with the existing International Task Force and modified diagnostic criteria for ARVC.

Conclusions: In this study, we provide new evidence that mutations in the desmosomal plakophilin-2 gene can cause ARVC. A systematic clinical evaluation of mutation carriers within families demonstrated variable phenotypic expression, even among individuals with the same mutation, and highlighted the need for a more accurate set of diagnostic criteria for ARVC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Arrhythmogenic Right Ventricular Dysplasia / genetics*
  • Arrhythmogenic Right Ventricular Dysplasia / pathology
  • Child
  • Codon, Nonsense
  • Death, Sudden, Cardiac
  • Desmosomes / pathology
  • Family Health
  • Female
  • Frameshift Mutation
  • Gene Deletion
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Mutation, Missense
  • Pedigree
  • Phenotype
  • Plakophilins / genetics*
  • RNA Splice Sites

Substances

  • Codon, Nonsense
  • PKP2 protein, human
  • Plakophilins
  • RNA Splice Sites