Transient Early Repolarization Pattern and Recurrent Ventricular Fibrillation in a Young Survivor of Sudden Cardiac Arrest: Diagnostic Challenges in Suspected Malignant Channelopathy

Malignant early repolarization syndrome (ERS) and inherited cardiac channelopathies are important causes of sudden cardiac arrest (SCA) in young individuals with structurally normal hearts. Diagnosis remains challenging due to dynamic electrocardiographic findings and the absence of overt structural abnormalities. We report the case of a 22–year–old male with no prior medical history admitted after out–of–hospital cardiac arrest due to ventricular fibrillation (VF), successfully resuscitated with bystander basic life support and two automated external defibrillator shocks. Total resuscitation time was 21 minutes. After return of spontaneous circulation, the patient was comatose with generalized tonic–clonic seizures, requiring deep sedation and mechanical ventilation. Baseline ECG showed sinus rhythm with slurred QRS downstroke and J waves without ST–segment elevation in inferior and lateral leads (Figure 1). Toxicological screening was positive for cannabinoids. Extensive diagnostic evaluation excluded structural heart disease: transthoracic echocardiography showed normal biventricular function; coronary angiography ruled out coronary artery disease; cardiac magnetic resonance imaging demonstrated no myocardial edema or fibrosis. Neurological assessment, including EEG and brain CT, was unremarkable. During hospitalization, transient ECG features consistent with malignant early repolarization were documented on a single tracing but were absent on subsequent recordings. Continuous monitoring revealed frequent monomorphic premature ventricular complexes with short coupling intervals, followed by recurrent episodes of polymorphic ventricular tachycardia and VF requiring external defibrillation. Given the recurrence of malignant ventricular arrhythmias in the absence of structural heart disease, a diagnosis of suspected inherited arrhythmogenic syndrome was established. After appropriate evaluation, a subcutaneous implantable cardioverter–defibrillator (S–ICD) was implanted for secondary prevention (Figure 2). Genetic testing is currently ongoing. This case highlights the diagnostic complexity of malignant ERS and inherited channelopathies when ECG abnormalities are transient. In survivors of unexplained VF, a structured diagnostic pathway including advanced imaging, prolonged rhythm monitoring, and comprehensive genetic evaluation is essential. Early ICD implantation and genetic counselling remain key strategies for secondary prevention according to current guidelines.Figure 1 Figure 2