Exploring the intricate relationship between IL-1β and IL-18 in the context of osteoarthritis.

Arrhythmogenic cardiomyopathy (ACM) and Brugada syndrome (BrS) are inherited, genetically determined disorders characterized by an increased risk of ventricular arrhythmias (VA) and sudden cardiac death (SCD). ACM, caused by pathogenic variants in desmosomal proteins, induces structural myocardial alterations that progress from the epicardium to the endocardium (). Depending on the specific desmosomal involvement, the disease may predominantly affect the right, the left, or both ventricles. In contrast, BrS results from variants affecting cardiac ion-channel proteins (); the resulting ionic-current abnormalities mirror the regional expression of the affected channels and are most pronounced in the epicardial layer of the right ventricular outflow tract (RVOT) (, ). On the basis of overlapping phenotypic and pathophysiological features, a unifying hypothesis has been proposed in which ACM and BrS represent different expressions of a shared disease spectrum (, ). Historically, clinical interest has focused on ventricular arrhythmias and SCD risk in both conditions. More recently, attention has shifted to atrial involvement, which is present in both diseases, although to varying degrees. These observations delineate a spectrum of atrioventricular involvement and underscore the need to investigate the underlying mechanisms in both atrial and ventricular myocardium. The aim of the present systematic review is to summarize the current evidence on atrial substrate and on the prevalence, mechanisms, and prognostic implications of supraventricular tachyarrhythmias (SVT) in ACM and BrS, and to outline the clinical implications for risk stratification and management.