Objective: Arrhythmogenic right ventricular dysplasia (ARVD) is one of the most difficult to diagnose and manage of the cardiomyopathies. Physical exercise can be a contributing factor and may accelerate the pro-gression of the disease.
Methods: We present the case of a 49-year-old, a for-mer professional football player, with a history of car-diac arrest in 2011 by ventricular tachycardia (VT) (normal coronary arteries). Between 2011 and 2019 the patient didn’t present for reevaluation and resu-med endurance sports activity in spite of doctor re-commendation. In 2019 he was directed to our clinic for a syncope followed by constrictive anterior chest pain and palpitations, the clinical expression of a VT with LBBB morphology and inferior axis, most likely originated in the RVOT, for which cardioversion was required. Upon admission, the patient was hemodyna-mically and respiratory stable, at sinus rhythm 60/min with left anterior hemiblock and negative T waves in V1-V2. Biologically, myocardial and hepatic cytolysis enzymes were within normal limits, with mild hypoka-lemia. Echocardiography showed significant dilatation of RV and RVOT with RV dysfunction (TAPSE 16 mm, FAC 20%, s’ 8.6 cm/s). LV was nondilated, with normal systolic function and kinetic, but with trabeculation of the apex. To confirm the diagnosis of ARVD, cardiac MRI was performed and confirmed fat infiltration in the RV free wall with biventricular involvement. Given the high arrhythmic risk (two resuscitated VT episo-des, syncope), a two-chamber ICD was implanted, wi-thout immediate post-procedural complications.
Results: In the second postprocedural day, the pati-ent suddenly installed important epigastric pain with thoracic irradiation. The ECG showed sensing and pacing malfunction and radioscopy showed evidence of ventricular probe displacement. The echocardiogra-phy confirmed the myocardial perforation. Emergency surgery by median thoracotomy was performed, with successful extraction of the electrode and myocardial suture. Postoperative progression was favorable under treatment with beta-blocker and amiodarone. A sub-cutaneous ICD will be implanted as soon as available.
Conclusions: In conclusion, this case is a very parti-cular one. First of all, we’ve documented two distinct phases in the evolution of the ARVD (electrical phase and structural phase). Moreover, by resuming endu-rance sports activity and in concordance with the li-terature data, we can only assume that the progression of the disease was accelerated and the arrhythmic risk was greater. Complications related to probe stability are common in this population, but myocardial perforati-on is a very rare and dangerous one. The therapeutic management of patients with ARVD has evolved over the years and continues to be an important challenge. To further improve risk stratification and treatment of patients, more information is needed on the natural history, long-term prognosis and risk assessment.