The relationship between vigorous physical activity (PA) and the development of coronary atherosclerosis has remained less explored for many years. Recently, literature data have focused on coronary atherosclerosis in athletes showing that prevalence is not trivial, that there are differences among various types of sport, and that there are some peculiar features. As a matter of fact, plaque composition in athletes seems to be characterized by calcium rather than soft components. Specific mechanisms through which vigorous PA influences coronary artery disease are not yet fully understood. However, the prevalent calcific nature of coronary plaques in athletes could be related with a trend in a lower cardiovascular event rate.

Arrhythmogenic cardiomyopathy (ACM) is a rare cardiac disease, characterized by the progressive replacement of myocardial tissue with fibrous and fatty deposits. It can involve both the right and left ventricles. It is associated with the development of life-threatening arrhythmias and culminates in sudden cardiac death. Electrocardiography (ECG) has emerged as a pivotal tool, offering diagnostic insights and prognostic information. The specific ECG abnormalities observed in ACM not only contribute to early detection but also hold the key to the prediction of the likelihood of severe complications. The recognition of these nuanced ECG manifestations has become imperative for clinicians as it guides them in the formulation of tailored therapeutic strategies that address both the present symptoms and the potential future risks.

Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disease characterized by fibrofatty replacement of the ventricular myocardium, with an estimated prevalence of 1:5000 people in the general population. Sudden cardiac death is the first manifestation of this disease in 16–23% of patients with ACM. Fibrofatty infiltration can be identified with noninvasive cardiac magnetic resonance. Studies of epicardial fat deposits have suggested pathogenic roles of epicardial fats in mediating cardiac diseases and arrhythmias. Although myocardial fat infiltration has been well described in ACM, changes in epicardial fat deposits with this disease have not been well investigated. Our study shows that patients with ACM have a higher amount of EAT compared to controls. Additionally, the EAT amount seems to increase with the evolution of the disease.

Anodal capture, characterized by a different QRS morphology compared to cathodal capture, is a well-known issue in cardiac resynchronization therapy (CRT). Left bundle branch area pacing (LBBAP), a novel physiological pacing technique, is also used as a bailout strategy following failed conventional CRT implantation. In LBBAP, QRS transition, defined by a change in paced QRS morphology, serves as a key marker of successful lead placement. This clinical case highlights the importance of recognizing both anodal capture and QRS transition in patients receiving LBBAP combined with an implantable cardioverter-defibrillator (ICD) as bailout strategy for failed cardiac resynchronization therapy with defibrillator (CRT-D) implantation, in order to optimize pacing parameters and device programming.

Anodal capture, characterized by a different QRS morphology compared to cathodal capture, is a well-known issue in cardiac resynchronization therapy (CRT). Left bundle branch area pacing (LBBAP), a novel physiological pacing technique, is also used as a bailout strategy following failed conventional CRT implantation. In LBBAP, QRS transition, defined by a change in paced QRS morphology, serves as a key marker of successful lead placement. This case report is the first to document both high-output anodal capture and LBBAP-induced QRS transition in a single individual receiving LBBAP with an implantable cardioverter–defibrillator (ICD) as a bailout strategy for failed cardiac resynchronization therapy with defibrillator (CRT-D) implantation. Their coexistence underscores unique device optimization challenges in this emerging approach.