Pathogenic variants in plakophilin-2 gene (PKP2) are associated with better survival in arrhythmogenic right ventricular cardiomyopathy

Journal of Applied Genetics - Tập 62 - Trang 613-620 - 2021
Olgierd Woźniak1, Maria Franaszczyk2, Witold Śmigielski3, Marta Roszczynko2, Piotr Hoffman1, Karolina Borowiec1, Elżbieta K. Biernacka1, Anna Lutyńska4, Alessandra Rampazzo5, Małgorzata Szperl2
1Department of Congenital Heart Diseases, National Institute of Cardiology, Warsaw, Poland
2Molecular Biology Laboratory, Department of Medical Biology, National Institute of Cardiology, Warsaw, Poland
3Department of Demography, University of Lodz, Lodz, Poland
4Department of Medical Biology, National Institute of Cardiology, Warsaw, Poland
5Department of Biology, University of Padua, Padua, Italy

Tóm tắt

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is mainly caused by mutations in genes encoding desmosomal proteins. Variants in plakophilin-2 gene (PKP2) are the most common cause of the disease, associated with conventional ARVC phenotype. The study aims to evaluate the prevalence of PKP2 variants and examine genotype–phenotype correlation in Polish ARVC cohort. All 56 ARVC patients fulfilling the current criteria were screened for genetic variants in PKP2 using denaturing high-performance liquid chromatography or next-generation sequencing. The clinical evaluation involved medical history, electrocardiogram, echocardiography, and follow-up. Ten variants (5 frameshift, 2 nonsense, 2 splicing, and 1 missense) in PKP2 were found in 28 (50%) cases. All truncating variants are classified as pathogenic/likely pathogenic, while the missense variant is classified as variant of uncertain significance. Patients carrying a PKP2 mutation were younger at diagnosis (p = 0.003), more often had negative T waves in V1–V3 (p = 0.01), had higher left ventricular ejection fraction (p = 0.04), and were less likely to present symptoms of heart failure (p = 0.01) and left ventricular damage progression (p = 0.04). Combined endpoint of death or heart transplant was more frequent in subgroup without PKP2 mutation (p = 0.03). Pathogenic variants in PKP2 are responsible for 50% of ARVC cases in the Polish population and are associated with a better prognosis. ARVC patients with PKP2 mutation are less likely to present left ventricular involvement and heart failure symptoms. Combined endpoint of death or heart transplant was less frequent in this group.

Tài liệu tham khảo

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