Case details: A 30-year-old man with a structurally normal heart presented with sudden-onset rapid palpitations due to wide complex tachycardia, which spontaneously reverted to sinus rhythm. He was referred to us for an electrophysiological (EP) study.

Title: Sudden QRS widening while ablating a concealed left accessory pathway during left ventricular pacing

A 30-year-old man with a structurally normal heart was referred to us with a 2-year history of recurrent episodes of rapid paroxysmal palpitations. A few episodes required hospitalization and were terminated with intravenous diltiazem. During electrophysiology (EP) study done twice before in other hospitals, the patient was diagnosed as typical atrioventricular nodal reentrant tachycardia (AVNRT) and underwent radiofrequency ablation of the slow pathway. However, the episodes recurred.  Because of the patient’s persistent symptoms, an EP study was performed again. Tachycardia was easily induced using atrial extrastimuli, ventricular extrastimuli and with rapid atrial pacing.

The classification of AVNRT is based on HA and VA interval. Typical AVNRT is diagnosed in presence of HA ≤70 ms OR VA interval ≤60 ms and HA>70ms or VA >60ms is required to diagnose atypical AVNRT. This might be fallacious in some clinical situations. The septal VA and the “shortest” VA may be also different depending on clinical scenario .

Background: Cardiac Sympathetic Denervation (CSD) involves surgical removal of lower half of the stellate ganglion and the T1-T4 ganglia for reducing sympathetic discharge to the heart. CSD is a useful therapeutic option in patients with ventricular tachycardia (VT) when they are non-responsive to standard drug therapy or catheter ablation. We report here the clinical profile and long-term outcome of all our patients who underwent CSD for refractory VT or VT storm. Method: Data of all patients who underwent CSD from 2010 to 2019 was analysed. They were regularly followed up, focusing on arrhythmia recurrence. Complete response to CSD was defined as more than 75% decrease in the frequency of VT. Results: A total of 65 patients (50 male, 15 female) underwent CSD in the above-mentioned period and the duration of follow-up was 27±24 months. The underlying substrate was for VT was coronary artery disease in 30 (46.2%) patients and 35 (53.8%) patients had a variety of other causes. Complete response to CSD was attained in 47 (72.3%) patients. There was a significant decline in the incidence of number shocks after CSD (24±37 vs 2±4; p <0.01). Freedom from a combined end point of ICD shock or death at the end of two years was 51.5%. Advanced NYHA class (III and IV) was the only parameter shown to have significant association with this combined end point. Conclusion: The current retrospective analysis reemphasize the role of surgical CSD in the treatment of patients with refractory VT or VT storm.

EP Rounds

A 44-year-old lady, a follow up case of idiopathic dilated cardiomyopathy and cardiac resynchronization therapy defibrillator (CRT-D) device implantation with epicardial left ventricular (LV) lead, underwent a transvenous LV lead revision in view of epicardial lead malfunction. A chest X-ray after this, done for worsening dyspnoea, revealed pneumopericardium along with left pneumothorax. The CT revealed a communication between the left pleural and pericardial cavities, around the old epicardial lead. Drainage of the left pleural cavity resolved both the pneumothorax and pneumopericardium and the patient remained well on follow up.

A 53- year old woman presented with recurrent episodes of paroxysmal tachycardia with a structurally normal heart. She had undergone an electrophysiology study in an outside hospital which revealed orthodromic atrioventricular reentrant tachycardia (ORT) using a concealed left posterolateral accessory pathway (AP), for which radiofrequency ablation was performed. But tachycardia recurred three months later. In view of significant symptoms, she came to us for a repeat procedure. The AH and HV intervals were 77 ms and 45 ms respectively. Narrow complex tachycardia with a cycle length (CL) of 300 ms was easily and repeatedly induced and terminated (Figure 1, left panel) by a premature ventricular complex (PVC). Shortly another tachycardia with CL of 255 ms was induced and terminated (Figure 1, right panel) by a premature ventricular complex. Later, during another tachycardia, a spontaneous change was seen (Figure 2). Are we dealing with a single tachycardia mechanism?