For example, the participating centres in our study were predominantly cardiomyopathy units compared with the electrophysiology focused units that participated in the 2019 study, which could predispose to a more arrhythmia-prone population.10 This can potentially explain the lower annual incidence rate of VA and thus the risk overestimation that we have observed compared with the 2019 model development study.10 In addition, the genotype composition between the two studies differs; for example, the prevalence of PKP2 variants in our cohort is 21.7% compared with 48.9% in the 2019 study10. This evidence concerns the gene PKP2 and cardiac arrhythmia.