Acute Myocarditis Associated With Desmosomal Gene Variants.
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Ammirati Enrico, Raimondi Francesca, Piriou Nicolas, Sardo Infirri Loren, Mohiddin Saidi A, Mazzanti Andrea, Shenoy Chetan, Cavallari Ugo A, Imazio Massimo, Aquaro Giovanni Donato, Olivotto Iacopo, Pedrotti Patrizia, Sekhri Neha, Van de Heyning Caroline M, Broeckx Glenn, Peretto Giovanni, Guttmann Oliver, Dellegrottaglie Santo, Scatteia Alessandra, Gentile Piero, Merlo Marco, Goldberg Randal I, Reyentovich Alex, Sciamanna Christopher, Klaassen Sabine, Poller Wolfgang, Trankle Cory R, Abbate Antonio, Keren Andre, Horowitz-Cederboim Smadar, Cadrin-Tourigny Julia, Tadros Rafik, Annoni Giuseppe A, Bonoldi Emanuela, Toquet Claire, Marteau Lara, Probst Vincent, Trochu Jean Noël, Kissopoulou Antheia, Grosu Aurelia, Kukavica Deni, Trancuccio Alessandro, Gil Cristina, Tini Giacomo, Pedrazzini Matteo, Torchio Margherita, Sinagra Gianfranco, Gimeno Juan Ramón, Bernasconi Davide, Valsecchi Maria Grazia, Klingel Karin, Adler Eric D, Camici Paolo G, Cooper Leslie T
Аннотация
OBJECTIVES: The purpose of this study was to ascertain the risk of death, ventricular arrhythmias, recurrent myocarditis, and heart failure (main endpoint) in patients with AM and pathogenic or likely pathogenetic DGV.
METHODS: In a retrospective international study from 23 hospitals, 97 patients were included: 36 with AM and DGV (DGV[+]), 25 with AM and negative gene testing (DGV[-]), and 36 with AM without genetics testing. All patients had troponin elevation plus findings consistent with AM on histology or at cardiac magnetic resonance (CMR). In 86 patients, CMR changes in function and structure were re-assessed at follow-up.
RESULTS: In the DGV(+) AM group (88.9% DSP variants), median age was 24 years, 91.7% presented with chest pain, and median left ventricular ejection fraction (LVEF) was 56% on CMR (P = NS vs the other 2 groups). Kaplan-Meier curves demonstrated a higher risk of the main endpoint in DGV(+) AM compared with DGV(-) and without genetics testing patients (62.3% vs 17.5% vs 5.3% at 5 years, respectively; P < 0.0001), driven by myocarditis recurrence and ventricular arrhythmias. At follow-up CMR, a higher number of late gadolinium enhanced segments was found in DGV(+) AM.
CONCLUSIONS: Patients with AM and evidence of DGV have a higher incidence of adverse cardiovascular events compared with patients with AM without DGV. Further prospective studies are needed to ascertain if genetic testing might improve risk stratification of patients with AM who are considered at low risk.