Key result
In patients with ARVC, superimposed myocarditis was identified in 36% to 87.5% and mutations in 11% to 50% across four clinical forms, with inflammation predominating in the latent arrhythmic form.
Why the study?
The study was conducted to assess the contribution of genetic and inflammatory factors to the development of arrhythmogenic right ventricular cardiomyopathy.
Population
54 patients with ARVC
Design
Observational cohort study
Follow-up
Mean 21 [6; 60] months
Authors
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Different ARVC phenotypes may reflect varying genetic versus inflammatory contributions; leaves open targeted therapy implications.
Observational (n=54)
In ARVC, inflammation plays a leading role in the latent arrhythmic form, whereas pathogenic mutations prevail in the manifested arrhythmic form.
Lutokhina et al. (2021) conducted an observational in arrhythmogenic right ventricular cardiomyopathy (n=54). Genetic mutations and superimposed myocarditis was evaluated on Prevalence of superimposed myocarditis and mutations across clinical types of ARVC. In patients with ARVC, superimposed myocarditis was identified in 36% to 87.5% and mutations in 11% to 50% across four clinical forms, with inflammation predominating in the latent arrhythmic form.
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