Associazione Nazionale Medici Cardiologi Ospedalieri




Roagna Edoardo Torino(Torino) – Cardiology, Department of Medical Sciences, University of Turin, Italy | Visalli Andrea Torino(Torino) – Cardiology, Department of Medical Sciences, University of Turin, Italy | Tribuzio Anna Torino(Torino) – Cardiology, Department of Medical Sciences, University of Turin, Italy

Introduction: Intense exercise training has been recently associated with QTc prolongation and morphologic repolarization abnormalities, whereas detraining, in asymptomatic genotype negative patients, was associated with ECG normalization. Data about this condition and its best management are scant.

Case: an asymptomatic, 16 years old, competitive basketball player (training load 11 hours/week, significantly increased in the previous 6 months), with negative family history was referred to our Center for the appearance of notched T waves in V2-V3 and of late T wave peak in the other leads, with mild QTc prolongation in DII (455 msec), severe in V2-V3. Holter ECG (12 leads) confirmed the presence of a 2nd dynamic component of ventricular repolarization leading to a markedly prolonged QT (QTc max> 550 ms), that was more evident after sudden heart rate (HR) increases. A genetic test was performed using in silico long QT panel by next-generation sequencing (NGS) and then multiplex-ligation dependent probe amplification (MLPA) to exclude deletions/duplications, and turned out negative. A complete 6-month detraining was recommended. At the reassessment, QTc and morphological abnormalities had both normalized at resting ECG (QTc in DII 401 msec) and for most of Holter ECG (QTc mostly between 375 and 400 msec). A 2nd dynamic component of ventricular repolarization with U wave characteristics could be detected only after sudden HR increases. Exercise stress test confirmed preserved QTc adaptation during exercise and recovery (with a 4th minute recovery QTc of 401 msec). Cardiac ultrasound in detraining showed preserved LVEF (62%) and global longitudinal strain (-23%), with a global electromechanical dispersion of 34 ms and an electromechanical window of -11 ms at 73 bpm. Return to play was granted with a reduced training load (6 hours/week) and mandatory complete cardiological assessment after 6 months (pending). Resting ECG after 3 months was within normal limits.

Conclusion: Our case confirms that intense exercise training can induce dynamic non physiological abnormalities in ventricular repolarization with QTc prolongation, in genotype negative patients. Detraining is therefore mandatory before definitive long QT diagnosis every time this condition is suspected and, if the level of suspicion of an expert Center is high, beta-blocker therapy initiation may be temporarily deferred. Return to play and best subsequent monitoring are still a matter of debate.