Female patient, 58 years old.

The patient had a history of acute myocardial infarction in 1992; after the event, she developed heart failure with reduced ejection fraction (35%), New York Heart Association (NYHA) functional class II. She reported no other comorbidities and denied smoking and alcoholism. She was being treated with carvedilol 12.5 mg twice daily, enalapril 10 mg twice daily, simvastatin 20 mg, acetylsalicylic acid 100 mg, furosemide 40 mg, and spironolactone 25 mg once daily. In April 2015, she was hospitalized for an episode of monomorphic ventricular tachycardia (VT) with a heart rate (HR) of 170 bpm, blood pressure of 93/52 mmHg, and persistent chest pain, characterizing unstable VT. She underwent synchronized electrical cardioversion at a 200 J charge, with reversion to sinus rhythm. During the same hospitalization, she was started on amiodarone and underwent implantation of a single-chamber cardioverter-defibrillator.

During outpatient follow-up after cardioverter-defibrillator implantation, she presented recurrent episodes of slow VT, with HR of 100 to 110 bpm (Figure 1). The VT episodes were interrupted by antitachycardia cardioverter-defibrillator pacing. In April 2016, she was referred for VT ablation. During the procedure, an extensive area of fibrosis was identified in the apical region of the left ventricle. During ventricular pacing, the induction of 3 different VT morphologies was observed, with HR of 110 bpm, without hemodynamic instability. Radiofrequency ablation was performed based on entrainment and pace mapping. No attempt was made to induce VT at the end of the procedure.

After ablation, while using carvedilol 12.5 mg twice daily and amiodarone 200 mg once daily, the patient continued to experience recurrent episodes of slow VT, interrupted by antitachycardia pacing. She progressed with frequent hospitalizations due to decompensated heart failure, NYHA functional class III to IV, and recurrent episodes of VT, and she was listed for heart transplantation.

She received heart transplantation in April 2017 from a 41-year-old female donor. During the procedure, she required mechanical mitral valve replacement due to severe acute mitral regurgitation due to valve tethering, possibly caused by ischemic injury. The cardioverter-defibrillator leads were removed during transplantation, and the generator was maintained. During the postoperative period, she presented with primary graft dysfunction, transient atrioventricular block, sepsis due to Klebsiella pneumoniae, and cardiac tamponade due to pericardial effusion requiring drainage and pericardiotomy. She required implantation of new atrial and ventricular pacemaker leads due to chronotropic incompetence. The cardioverter-defibrillator generator was preserved, functioning exclusively as a pacemaker. The patient was discharged after 25 days of hospitalization. The discharge echocardiogram showed preserved ejection fraction (66%) and good functioning of the mechanical mitral valve prosthesis, with no relevant abnormalities.

The patient continued outpatient follow-up with favorable progress. During this period, she was monitored by the electrophysiology team, as the cardioverter-defibrillator remained implanted, functioning as a pacemaker, with the arrhythmia monitoring function deactivated. In October 2024, 7 years after the transplant, during elective hospitalization for orthopedic surgery due to a rotator cuff tear, she presented an episode of tachycardia with a wide QRS complex and a heart rate of 150 bpm (Figure 2). The QRS morphology was similar to her electrocardiogram in sinus rhythm (Figure 3). Analyzing the QRS morphology according to the Brugada criteria, the patient's QRS would be compatible with VT based on the morphological criteria for right bundle branch block (due to the qR pattern in V1). During the arrhythmia episode, she reported only anxiety, without palpitations, angina, dyspnea, or other complaints. Given the patient's native QRS morphology and the suspected diagnosis of paroxysmal supraventricular tachycardia, 6 mg of adenosine was administered intravenously, with immediate reversal of the tachycardia. The carvedilol dose was increased from 12.5 mg to 25 mg twice daily after the episode.

In March 2025, the patient was hospitalized for dengue fever, in the context of immunosuppression, warfarin use with prolonged prothrombin time, and associated acute kidney injury. During hospitalization, two new oligosymptomatic episodes of supraventricular tachycardia were recorded, which were reversed with 6 mg adenosine. The patient did not develop severe dengue or any major associated complications. When questioned about previous arrhythmia symptoms in recent years, the patient reported occasional anxiety similar to the tachycardia episodes she experienced in the hospital, but never more intense symptoms that prompted her to seek hospital care. Given this account, coupled with the fact that cardioverter-defibrillator event monitoring remained disabled in the years following transplantation, it was not possible to determine the exact timing of her first episode of paroxysmal supraventricular tachycardia. According to the team's assessment, the patient had already been experiencing rather vague symptoms of arrhythmia (anxiety, nonspecific discomfort), delaying diagnosis, which was eventually made in a timely manner during hospitalization for another reason.

After recovering from dengue, she was referred for ablation of supraventricular tachycardia. During the procedure, the presence of dual nodal physiology was identified, with easy and reproducible induction of typical atrioventricular nodal reentrant tachycardia with a cycle length of 414 ms. Slow-pathway ablation was performed with a 4 mm catheter. After ablation, the patient did not have any new episodes of supraventricular tachycardia.