| Literature DB >> 25037680 |
Elena Biagini1, Iacopo Olivotto2, Maria Iascone3, Maria I Parodi4, Francesca Girolami5, Giulia Frisso6, Camillo Autore7, Giuseppe Limongelli8, Massimiliano Cecconi4, Barry J Maron9, Martin S Maron10, Stefania Rosmini11, Francesco Formisano12, Beatrice Musumeci7, Franco Cecchi2, Attilio Iacovoni13, Tammy S Haas9, Maria L Bacchi Reggiani11, Paolo Ferrazzi14, Francesco Salvatore6, Paolo Spirito12, Claudio Rapezzi11.
Abstract
End-stage hypertrophic cardiomyopathy (ES-HC) has an ominous prognosis. Whether genotype can influence ES-HC occurrence is unresolved. We assessed the spectrum and clinical correlates of HC-associated mutations in a large multicenter cohort with end-stage ES-HC. Sequencing analysis of 8 sarcomere genes (MYH7, MYBPC3, TNNI3, TNNT2, TPM1, MYL2, MYL3, and ACTC1) and 2 metabolic genes (PRKAG2 and LAMP2) was performed in 156 ES-HC patients with left ventricular (LV) ejection fraction (EF) <50%. A comparison among mutated and negative ES-HC patients and a reference cohort of 181 HC patients with preserved LVEF was performed. Overall, 131 mutations (36 novel) were identified in 104 ES-HC patients (67%) predominantly affecting MYH7 and MYBPC3 (80%). Complex genotypes with double or triple mutations were present in 13% compared with 5% of the reference cohort (p = 0.013). The distribution of mutations was otherwise indistinguishable in the 2 groups. Among ES-HC patients, those presenting at first evaluation before the age of 20 had a 30% prevalence of complex genotypes compared with 19% and 21% in the subgroups aged 20 to 59 and ≥60 years (p = 0.003). MYBPC3 mutation carriers with ES-HC were older than patients with MYH7, other single mutations, or multiple mutations (median 41 vs 16, 26, and 28 years, p ≤0.001). Outcome of ES-HC patients was severe irrespective of genotype. In conclusion, the ES phase of HC is associated with a variable genetic substrate, not distinguishable from that of patients with HC and preserved EF, except for a higher frequency of complex genotypes with double or triple mutations of sarcomere genes.Entities:
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Year: 2014 PMID: 25037680 DOI: 10.1016/j.amjcard.2014.05.065
Source DB: PubMed Journal: Am J Cardiol ISSN: 0002-9149 Impact factor: 2.778