Poster Session 2.Q - Cardiovascular Medicine and Research
Balla, Dorottya
Heart and Vascular Centre, Semmelweis University
Dr. Dorottya Balla1, Dr. Szabó Liliána1, Dr. Dohy Zsófia1, Dr. Drobni Zsófia1, Dr. Vincze Viktória1, Dr. Meskó Csongor1, Dr. Kovács Árpád1, Dr. Sydó Nóra1, Dr. Csulak Emese1, Dr. Kiss Orsolya1, Prof. Dr. Bödör Csaba2, Dr. Suhai Ferenc1, Dr. Tóth Attila1, Prof. Dr. Merkely Béla1, Prof. Dr. Vágó Hajnalka1
1: Heart and Vascular Centre, Semmelweis University
2: Department of Pathology and Experimental Cancer Research, Semmelweis University
Introduction: Sudden cardiac death (SCD) in young athletes is most commonly related to underlying structural myocardial disorders. Cardiac magnetic resonance imaging (CMR) has emerged as a key diagnostic modality for detailed myocardial tissue characterization and for identifying substrates associated with malignant ventricular arrhythmias.
Aims: To assess the prevalence and spectrum of structural myocardial diseases detected by CMR in athletes and to evaluate the underlying etiologies associated with SCD and life-threatening ventricular arrhythmias.
Methods: Athletes performing ≥6 hours of weekly training who were referred to our center for CMR due to suspected structural heart disease were included. Genetic testing was performed in athletes with confirmed myocardial disease or documented malignant ventricular arrhythmias.
Results: A total of 857 athletes (752 males; mean age 25.3±11.3 years) underwent CMR evaluation. Structural myocardial abnormalities were identified in 142 athletes (115 males; mean age 30.2±12.6 years; weekly training volume 12.3±6.5 hours). Among cardiomyopathies, hypertrophic cardiomyopathy (HCM) was diagnosed in 42 athletes, arrhythmogenic cardiomyopathy (AC) in 16, and dilated cardiomyopathy (DCM) in 12 cases. Non-ischemic myocardial fibrosis or scarring was detected in 52 athletes, including patterns consistent with acute or previous myocarditis and atypical fibrosis. Among athletes evaluated following resuscitation or sustained ventricular tachycardia, structural abnormalities were identified in 17 individuals, including AC (8 cases), HCM (1 case), mitral annular disjunction (1 case), ischemic injury (2 cases), and atypical fibrosis (5 cases). Genetic testing was performed in 53 athletes, revealing pathogenic or likely pathogenic variants in 14 cases and variants of uncertain significance in 25 cases.
Conclusions: In this large athlete cohort, HCM was the most frequent cardiomyopathy, while AC was the predominant substrate associated with SCD. Beyond classical cardiomyopathies, atypical non-ischaemic myocardial scar represents a relevant structural finding in athletes undergoing CMR and may constitute an important arrhythmogenic substrate.