Pugazhendhi Vijayaraman

Reanalysis of The “Pseudo A‐A‐V” Response to Ventricular Entrainment of Supraventricular Tachycardia: Importance of His‐Bundle Timing

Background: The sequence of atrial and ventricular electrograms following termination of ventricular pacing during supraventricular tachycardia has been shown to reliably differentiate atrial tachycardia from atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). However in patients with long HV intervals, this may be misleading due to a pseudo “A‐A‐V” response. The aim of the present study is to see if inclusion of the timing of the His‐bundle in the electrogram response (ER) following ventricular pacing would reliably identify the mechanism of tachycardia in patients with long HV intervals.

Mahaim fibers: new electrophysiologic insights into an unusual variant.

In 1938, Mahaim described the existence of islands of conducting tissue extending from the atrioventricular (AV) node into the ventricular myocardium.1 Since its original description and subsequent implication as a nodoventricular or nodofascicular fiber in the genesis of preexcited tachycardias, electrophysiologists have held a fascination for the rare and interesting arrhythmias these patients experience.2,3 The presence of right sided accessory pathways with decremental conduction properties and preexcited tachycardias with left bundle branch block pattern were initially explained by bypass tracts originating from the AV node and inserting into the right ventricular apex or right bundle branch as described by Mahaim.4 A series of critical observations were made in the 1980s based on the results of observations made in the electrophysiological,5 surgical,6,7 and histopathological laboratories.8 These observations showed these pathways could be ablated surgically, and unlike traditional atrioventricular accessory pathways were located away from the atrioventricular groove in the majority of cases. Electrophysiology studies confirmed these pathways to be right-sided decrementally conducting atriofascicular accessory pathways with the atrium forming a part of the antidromic tachycardia circuit. With the introduction of radiofrequency ablation for the treatment of tachyarrhythmias, our understanding of the Mahaim fibers has further evolved. Some of the unique electrophysiologic features of this variant of preexcitation according to our current understanding are summarized below:

Postoperative atrial fibrillation: some more answers, some new questions.

Postoperative atrial fibrillation (AF) is a common problem following cardiac surgery, occurring in 11% to 40% of patients after coronary artery bypass grafting1,2 and in up to 50% of patients after valvular surgery.2 Despite advances in surgical techniques, anesthesia, and myocardial protection, the incidence of postoperative AF has not decreased significantly.3 Postoperative AF has been associated with increased length of hospital stay, rates of stroke, and accompanying cost.4 The underlying mechanism for postoperative AF is multifactorial. Proposed causative mechanisms include pericardial inflammation, excessive production of catecholamines, autonomic imbalance during the postoperative period, and interstitial mobilization of fluid with resultant changes in volume, pressure, and neurohumoral environment. All of these physiologic changes likely play some role in altering the electrophysiologic properties of the atria. Abnormal atrial automaticity, prolonged atrial activation, dispersion of atrial refractoriness, and anisotropic conduction5,6 act as potential electrophysiologic substrates for postoperative AF. Various pharmacologic therapies have been aimed at reducing the incidence of postoperative AF, with modest success. Beta-blockers, sotalol, and amiodarone in various randomized trials have been effective in preventing postoperative AF, with odds ratio of 0.39, 0.35, and 0.48, respectively, compared with control groups.7 Medical therapy with beta-blockers as prophylactic agents to decrease the incidence of AF following cardiac surgery may be limited by asthma, hemodynamic instability, and the need for pressors in the postoperative period. It is important to place pacing therapy in perspective for the prevention of AF in the non-postcardiac surgical setting. For patients with sick sinus syndrome and heart block, atrial pacing has been shown to be more effective than ventricular pacing to prevent AF.8-10 The Canadian Trial of Physiologic Pacing prospectively followed 2,568 patients with symptomatic bradycardia who had received either a dualchamber or a ventricular pacer. Dual-chamber pacing significantly decreased the incidence of AF and progression to chronic AF.11,12 Several studies have shown that pacing from the interatrial septum13 or Bachmann’s bundlel4 decreases the incidence of paroxysmal and chronic AF. Several studies have shown that atrial overdrive pacing decreases the incidence and duration of AF episodes,15,16 but other studies have been unable to show a benefit to atrial overdrive pacing.l7 Finally, Saksena et al.18 showed in a cross-over study of 120 patients with AF that long-term, dual-site atrial pacing

A Narrow‐QRS Tachycardia: What is the Mechanism?

An 83-year-old man was admitted after an episode of syncope. In the emergency room, he was documented to have episodes of supraventricular tachycardia (SVT) at 130 to 140 beats/min associated with systolic blood pressures of 70 to 80 mmHg. An electrophysiologic procedure was performed. Baseline sinus cycle length, atrial-His (AH) interval, and His-ventricular (HV) interval were 760, 130, and 50 msec, respectively. Programmed atrial stimulation established the presence of anterograde dual AV nodal physiol-

Apparent Inappropriate Shocks from an Implantable Cardioverter Defibrillator

A 72-year-old man with a history of hypertension, dilated cardiomyopathy, and sustained ventricular tachycardia (VT) underwent placement of an implantable cardioverter defibrillator (ICD) in 1995. The patient’s ICD was interrogated as a result of an ICD shock delivered 24 hours earlier. The interrogation revealed 149 episodes of nonsustained VT, 9 episodes of sustained VT successfully terminated by antitachycardia pacing (ATP), and one episode of ventricular fibrillation (VF) terminated by a 22-J shock. All the episodes occurred in the past 48 hours. He was admitted to the hospital for further management and amiodarone loading. His ICD device was a Marquis DR 7274 (Medtronic, Inc., Minneapolis, MN, USA) programmed to DDDR mode at a rate 60 to 120 beats/min. The VT detection interval was set at 430–320 ms, FVT at 320–280 ms, and VF at <320 ms, with ventricular sensitivity of 0.3 mV. The VF detection duration was programmed to 18 of 24 beats, with redetection at 9 of 12 beats. VT detection was programmed to 40 beats, with redetection to 20 beats.

Supraventricular tachycardia upon termination of atrial flutter: what is the mechanism?

A 67-year-old man with coronary artery disease and persistent atrial flutter of 1-year duration was referred for radiofrequency ablation of atrial flutter. A multipolar catheter with 10 bipoles (2-10-2 spacing; Daig Corp., MN) was placed along the tricuspid annulus (TA) with the distal bipole at the coronary sinus os, just septal to the intended ablation line. The right atrial activation sequence and entrainment pacing from the cavo-tricuspid isthmus confirmed the rhythm to be isthmus-dependent counter-clockwise flutter. The atrial flutter cycle length was 260 ms and the HV interval was 70 ms. Linear radiofrequency ablation at the isthmus was performed using an 8-mm ablation catheter (EP Technologies, Inc., San Jose CA). The atrial flutter terminated during the ablation, and another supraventricular tachycardia (SVT) ensued (Fig. 1). The atrial activation sequence changed spontaneously 10 seconds later during the tachycardia (Fig. 2). Is the flutter ablation complete? What is the mechanism for the change in the atrial activation sequence? Overdrive ventricular pacing was performed during the SVT and the response is shown in Figure 3. What is the tachycardia mechanism?

Wide complex tachycardia: what is the mechanism?

A 57-year-old man was admitted to the hospital following an implantable cardioverter defibrillator (ICD) discharge. The patient had a history of an old inferior wall myocardial infarction, severely reduced left ventricular systolic function, paroxysmal atrial fibrillation, and sustained ventricular tachycardia (VT) for which he received an ICD a few years ago. ICD interrogation revealed the patient had multiple episodes of VT at a cycle length of 360 msec, all but one of which was terminated with antitachycardia pacing (ATP). On this one occasion, the tachycardia accelerated to 200 beats/min with ATP and subsequently was terminated