Cardiac magnetic resonance imaging in athletes with suspected structural myocardial disease: results of a high volume single-center study

• Published in: European heart journal Vol. 44; no. Supplement_2
• Main Authors: Vago, H, Balla, D, Szabo, L, Juhasz, V, Bodor, C S, Fekete, B, Csonka, K, Sydo, N, Csulak, E, Kiss, O, Czimbalmos, C S, Suhai, F, Dohy, Z S, Becker, D, Merkely, B
• Format: Journal Article
• Language: English
• Published: 09.11.2023
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/eurheartj/ehad655.2610

Abstract Introduction Structural heart disease is one of the leading causes of sudden cardiac death in athletes. Cardiac magnetic resonance imaging (CMR) has a key role in the diagnosis, providing accurate functional and morphological information. Aim To investigate the prevalence of structural heart disease and the etiology of sudden cardiac death (SCD) in athletes. Methods We enrolled athletes (training ≥6 hours/week) who underwent CMR due to suspected structural myocardial disease at our Heart and Vascular Center between 2009 and 2022. We also performed cardiogenetic testing with new-generation sequencing (174 genes) in athletes with confirmed structural heart disease and/or malignant arrhythmia who gave consent. Results CMR was performed on a total of 556 athletes (445 male, 24±10 age). The indications for CMR were as follows: aborted sudden cardiac death/sustained ventricular tachycardia (3%), ECG (46%) or echocardiographic abnormality (36%), positive family history of SCD or cardiomyopathy (CMP) (3%), or athletes' complaints (31%). Structural myocardial abnormalities were confirmed in 99 athletes: hypertrophic (HCM) in 27, arrhythmogenic (AC) in 11, dilated (DCM) CMP in 7, and left ventricular non-compaction (LVNC) in 9 cases. MR images consistent with Fabry disease were found in 5 patients. We have discovered post-myocardial infarction scars in 10 cases, and atypical non-ischemic scarring (excluding hinge point fibrosis) was observed in 32 athletes. Besides pathological abnormalities, minor alterations were identified in 76 patients. Among the athletes examined after aborted sudden cardiac death/sustained ventricular tachycardia (n=18), we found structural heart disease in 14 patients, AC was confirmed in 7, HCM in two, non-ischemic fibrosis in three cases and LVNC in one athlete. Cardiogenetic test was performed in 26 athletes, we found pathogenic or likely pathogenic mutations in 5 cases, typical of HCM, AC, DCM (MYBPC3, PKP2, LMNA, TTN). The genetic test showed VUS (variant of unknown significance) in 15 additional athletes. Conclusions HCM was identified as the most frequent CMP, whereas AC and nonischaemic scar was the leading cause of SCD or SVT in our athletes.Figure A)Short axis late gadolinium ehancement CMR image of a 26-year-old female tennis player with hypertrophic cardiomyopathy and nonischemic fibrosis (arrow) and MYBPC3 pathogenic variant.Figure B)Short axis late gadolinium enhancement CMR image of a 40-year-old male elite discus thrower with sustained ventricular tacchycardia and nonischaemic scar formation (arrows). LMNA and titin pathogenic variants could be detected.