Bharatraj Banavalikar

An unusual case of complete atrioventricular block causing Takotsubo syndrome

Complete atrioventricular (AV) block in association with Takotsubo syndrome (TS) has been well recognized, but the cause and effect relationship has not been elucidated. We describe a 78-year-old female who presented with complete AV block but one week later developed new-onset, diffuse T-wave inversions, QT prolongation, and acceleration of junctional escape rate. Left ventriculogram revealed features typical of TS. One year after permanent pacemaker implantation, complete AV block persisted despite the reversal of wall motion defects implying that conduction abnormality was the trigger of TS rather than its consequence.

Oral quinine sulfate for the treatment of electrical storm and prevention of recurrent shocks in Brugada syndrome after failed cilostazol therapy

Brugada syndrome (BrS), an inherited ion channelopathy with an autosomal mode of inheritance, is associated with an increased risk of ventricular fibrillation (VF) and sudden death in the young. Implantable cardioverter-defibrillator (ICD) is effective in terminating VF and preventing sudden cardiac arrest in high-risk BrS patients but does not prevent recurrences of VF.1 An electrical storm occurs in 5% of asymptomatic BrS patients and in 45% of patients who have survived sudden cardiac arrest.2 Isoproterenol infusion is effective in suppressing VF episodes during electrical storms in BrS patients.3 Quinidine, a class IA drug, is effective in preventing recurrences of ventricular tachycardia (VT) and VF in a patient with BrS.4 However, quinidine is not available in most countries around the world, especially in Southeast Asia, where the disease is more prevalent.5 We present a case of BrS with an electrical storm while on therapy with oral cilostazol and discuss the management with oral quinine sulfate.

Electrocardiographic characteristics and mapping approach of ventricular arrhythmias originating from the left ventricular summit

The left ventricular summit is the most common site of idiopathic epicardial ventricular tachycardia (VT). We report a case of a 48-yr-old lady who presented with VT of RBBB configuration, inferior axis and delayed initial activation. During electrophysiological study, local activation in the distal great cardiac vein (GCV) preceded surface QRS by 56 ms whereas mapping in the aortic sinuses and left ventricular outflow tract endocardially revealed late activation. Ablation in the distal GCV with an irrigated catheter successfully terminated the tachycardia. The 12‑lead electrocardiogram is an invaluable tool for predicting the VT focus and planning the mapping strategy.

Response to the letter to the editor: Complete heart block and Takotsubo syndrome: Dissecting the pathophysiology

We reviewed the letter by John Madias [1] and would like to thank him for the constructive and encouraging remarks regarding our case report. Complete AV block occurring in association with Takotsubo syndrome (TS) has been an enigma, and the cause and effect relationship has not been elucidated. The occurrence of AV block in the context of exaggerated sympathetic activation seems paradoxical. However, we could document the chronological sequence of the occurrence of AV block and the subsequent TS in our patient [2]. As illustrated by our case report, most cases of complete AV block associated with TS that persist on long-term followup are probably the triggers of TS rather than its consequence. Nevertheless, transient AV blocks have also been reported in association with TS, but the pathophysiology of rhythm disturbance in such cases has not been elucidated. Whether AV blocks can occur as a consequence of TS is controversial. Life-threatening stressful stimuli are associated with a generalized autonomic storm, with early events dominated by sympathetic effects and later events by parasympathetic effects [3]. Quantifying sympathetic and parasympathetic activity serially from the time of presentation can provide valuable insights into the pathophysiology of this condition. As proposed by Madias, measuring thoracic skin sympathetic activity employing conventional ECG electrodes represents a novel noninvasive surrogate of stellate ganglion activity and the extent of cardiac sympathetic activation [4,5]. We hope that future studies of TS and AV block will incorporate careful assessment of autonomic function that can help in unraveling the association between the two conditions.

Long term effects of cardiac resynchronization therapy on electrical remodeling in heart failure ‐ a prospective study

Effects of cardiac resynchronization therapy (CRT) on arrhythmogenicity and sudden death have not been fully ascertained. CRT has been shown to increase transmural dispersion of repolarization (TDR) immediately on implantation, which may favorably remodel on long‐term follow‐up. However, such a hypothesis has not been prospectively evaluated.

Takotsubo syndrome presenting as syncope in a patient with permanent pacemaker

Takotsubo syndrome is an acute reversible heart failure syndrome triggered by physical or emotional stress, especially in postmenopausal women. Herein, we describe a case of a 31-year-old pacemaker dependent lady who presented with syncope after she was bereaved of her father. Electrocardiogram at admission revealed ventricular paced rhythm at 60/min, prolonged QT interval and frequent runs of torsades de pointes. Transthoracic echocardiogram and left ventriculogram revealed findings typical of Takotsubo syndrome. QT prolongation and torsade de pointes in the context of fixed-rate ventricular pacing imply direct catecholamine toxicity on the ventricular myocardium independent of heart rate.

Electrical Cardioversion of an Irregular Narrow QRS Tachycardia to a Regular Narrow QRS Tachycardia

A 45-year-old woman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead ECG was normal during sinus rhythm. The electrophysiological study showed an AH interval of 68 ms and histoventricular (HV) interval of 42 ms during sinus rhythm. Ventricular pacing showed concentric activation of the atrium with decremental conduction. Anterograde dual atrioventricular (AV) node physiology was demonstrated. Burst atrial pacing induced atrial fibrillation (AF). Upon cardioversion, AF terminated

Observations During Parahisian Entrainment

A 45-year-old man has undergone electrophysiological study for paroxysmal palpitation. Surface electrocardiogram during sinus rhythm was consistent with left lateral accessory pathway. The atriohisian (AH) and hisioventricular (HV) intervals during sinus rhythm were 84 ms and 10 ms, respectively, and earliest ventricular activation was recorded at coronary sinus (CS) distal dipole that was placed at the distal CS. A regular narrow QRS tachycardia was easily and reproducibly induced with atrial pacing and ventricular pacing protocols that was confirmed to be orthodromic atrioventricular reentrant tachycardia (ORT) involving the left lateral pathway. ParaHisian entrainment was performed during tachycardia that showed an interesting response (Figs. 1 and 2). During paraHisian entrainment, there are 3 competing and interacting waves, namely the AV reentrant tachycardia circuit, His bundle-right bundle (HB-RB) capture circuit, and right ventricular (RV) paraHisian myocardial capture circuit. The retrograde atrial (A) activation sequence (RAAS) during tachycardia, HB-RB capture, and RV capture are the same with earliest atrial electrogram being recorded at CS distal dipole. On the other hand, the net stim to A (S-A) interval prolonged after loss of His capture. This is best explained

Response of Narrow QRS Tachycardia to Late Coupled PVC: What Is the Mechanism?: Arrhythmia Rounds

A 45-year-old gentleman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiogram (ECG) was normal during sinus rhythm. The electrophysiological study showed an atriohisian (AH) interval of 84 ms and hisioventricular (HV) interval of 37 ms during sinus rhythm. Ventricular pacing showed concentric activation of the atrium with nondecremental conduction. Atrial pacing reproducibly induced regular narrow QRS tachycardia. A late coupled premature ventricular extra delivered during tachycardia demonstrated an interesting phenomenon (Fig. 1). What is the likely mechanism?

Narrow QRS Tachycardia with Spontaneous Switch. What Is the Mechanism

doi: 10.1111/pace.12874 study showed a normal atrioHisian (AH) interval of 88 ms and His-ventricular interval of 48 ms during sinus rhythm. There was evidence of dual atrioventricular (AV) node physiology. Atrial burst pacing reproducibly induced narrow QRS tachycardia. Figures 1 and 2 show spontaneous switch of tachycardia 1 to tachycardia 2. What are the likely mechanisms of the tachycardia and the transition?