Using the 12-Lead ECG to Localize the Origin of Atrial and Ventricular Tachycardias: Part 2—Ventricular Tachycardia

Monomorphic ventricular tachycardia (VT) can arise from multiple different ventricular locations in the context of several different underlying myocardial substrates. Despite this variability, the surface 12-lead electrocardiograph (ECG) has proven to be a robust and reproducible initial mapping tool that can provide useful information in localizing the origin of both focal and reentrant forms of VT. The second part of this review series will look at the use of the ECG in mapping the various forms of VT encountered in clinical practice.     

Observations From Intraatrial Recordings on the Termination of Electrically Induced Atrial Fibrillation in Humans

Background: The circulating wavelet hypothesis suggests that atrial fibrillation could terminate by either progressive fusion or simultaneous block of all wavelets. Methods: Intraatrial recordings from the right atrial free wall were made during procainamide induced (n = 8) or spontaneous (n = 7) termination of electrically induced atrial fibrillation in 14 patients. Atrial rate, mean magnitude squared coherence, and direction of activation during sequential electrograms were measured. Rate and coherence were calculated from the earliest point within 5 minutes prior to termination as well as from the 4-second interval just prior to termination. Results: Termination was directly to sinus rhythm (13 episodes) or to atrial flutter (2 episodes). For the eight procainamide induced terminations, rate decreased between the first measurement and the measurement just prior to termination, from 443 ±127 beats/ min to 322 ± 119 beats/min. For the seven spontaneous terminations, rate also decreased from 373 ± 119 beats/min to 323 ± 88 beats/min; however, a slight increase in atrial rate prior to termination was observed in three episodes. No specific patterns of atrial cycle lengths were seen during the final few seconds of fibrillation. No increase in coherence was observed. In seven episodes, recordings were made using orthogonal bipoles in the x, y, and z directions, allowing direction of activation of wavefronts to be measured. Three episodes showed multiple instances where direction of activation remained similar over several electrograms as we have previously reported for chronic fibrillation. However, no such instances precipitated termination in any of the seven episodes. Conclusions: Atrial fibrillation usually terminates directly to sinus rhythm and does so abruptly and without forewarning. While we and others have previously reported that the rate of atrial fibrillation decreases with procainamide infusion, a decrease in the rate of atrial fibrillation is not required for the rhythm to terminate and consequently may not be a part of the termination process at all. Coherence does not demonstrate a progressive increase in the organization of atrial fibrillation prior to termination. Lack of stabilization in the direction of activation of wavefronts in the final few seconds also fails to support fusion of wavefronts as the mechanism of termination of atrial fibrillation. Simultaneous block of all wavelets is consistent with, but not proven by our observations.     

Epicardial Maps of Atrial Fibrillation After Linear Ablation Lesions

Maps of AF After Ablation. Introduction: The purpose of this study was to investigate the mechanisms by which atrial linear ablation lesions eliminate atrial fibrillation (AF).
Methods and Results: With an array of 112 unipole, epicordial maps of electrically induced AF in 6 dogs (acute group), self-sustained AF in 6 dogs (chronic group), and sinus rhythm and atrial pacing in 3 dogs (control group) were analyzed before and after creating linear radiofrequency ablation lesions in both atria that eliminated the AF. In the acute and chronic groups, activation maps showed multiple wavelets with complex patterns of activation and reentry during AF. Conduction velocity and the number, size, and complexity of wavelets did not change, whereas median fibrillatory cycle length increased with the number of linear lesions. In the control group, refractoriness and conduction velocity were unaffected by the number of lesions.
Conclusions: In these models of AF, linear lesions that eliminate AF increase the cycle length of AF without changing conduction velocity, number or size of wavelets, or complexity of activation patterns.     

Itraconazole‐induced Torsade de Pointes in a patient receiving methadone substitution therapy

Issues. Methadone, a pharmacological agent used to treat heroin dependence is relatively safe, but may cause cardiac arrhythmias in the concurrent presence of other risk factors. Approach and Key Findings. This case report highlights the risk of Torsade de Pointes, a life‐threatening cardiac arrhythmia, in a heroin‐dependent patient receiving methadone substitution therapy who was prescribed itraconazole for vaginal thrush. The patient presented to the accident and emergency department for chest discomfort and an episode of syncope following two doses of itraconazole (200 mg). Electrocardiogram monitoring at the accident and emergency department showed prolonged rate‐corrected QT interval leading to Torsade de Pointes. The patient was admitted for cardiac monitoring, and electrocardiogram returned to normal upon discontinuation of methadone. Implication. This cardiac arrhythmia was most likely as a result of a drug interaction between methadone and itraconazole because the patient presented with no other risk factors. Conclusion. Given the benefits of methadone as a substitution treatment for heroin‐dependent individuals, the association between methadone and cardiac arrhythmias is of great concern. Physicians treating heroin‐dependent patients on methadone substitution therapy should therefore be cautious of the potential risk of drug interactions that may lead to fatal cardiac arrhythmias.[NoorZurani MHR, Vicknasingam B, Narayanan S. Itraconazole‐induced Torsade de Pointes in a patient receiving methadone substitution therapy. Drug Alcohol Rev 2009;28:688–690]     

Ventricular Arrhythmia Inducibility Predicts Subsequent ICD Activation in Nonischemic Cardiomyopathy Patients: A DEFINITE Substudy

Objectives: We evaluated whether electrophysiologic (EP) inducibility predicts the subsequent occurrence of spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) in the Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial.
Background: Inducibility of ventricular arrhythmias has been widely used as a risk marker to select implantable cardioverter defibrillator (ICD) candidates, but is believed not to be predictive in nonischemic cardiomyopathy patients.
Methods: In DEFINITE, patients randomized to the ICD arm, but not the conventional arm, underwent noninvasive EP testing via the ICD shortly after ICD implantation using up to three extrastimuli at three cycle lengths plus burst pacing. Inducibility was defined as monomorphic or polymorphic VT or VF lasting 15 seconds. Patients were followed for a median of 29 ± 14 months (interquartile range = 2–41). An independent committee, blinded to inducibility status, characterized the rhythm triggering ICD shocks.
Results: Inducibility, found in 29 of 204 patients (VT in 13, VF in 16), was associated with diabetes (41.4% vs 20.6%, P = 0.014) and a slightly higher ejection fraction (23.2 ± 5.9 vs 20.5 ± 5.7, P = 0.021). In follow-up, 34.5% of the inducible group (10 of 29) experienced ICD therapy for VT or VF or arrhythmic death versus 12.0% (21 of 175) noninducible patients (hazard ratio = 2.60, P = 0.014).
Conclusions: In DEFINITE patients, inducibility of either VT or VF was associated with an increased likelihood of subsequent ICD therapy for VT or VF, and should be one factor considered in risk stratifying nonischemic cardiomyopathy patients.     

Linear Ablation of Right Atrial Free Wall Flutter: Demonstration of Bidirectional Conduction Block as an Endpoint Associated With Long‐Term Success

Ablation of Right Atrial Free Wall Flutter. Introduction: Ablation for atypical atrial flutter (AFL) is often performed during tachycardia, with termination or noninducibility of AFL as the endpoint. Termination alone is, however, an inadequate endpoint for typical AFL ablation, where incomplete isthmus block leads to high recurrence rates. We assessed conduction block across a low lateral right atrial (RA) ablation line (LRA) from free wall scar to the inferior vena cava (IVC) or tricuspid annulus in 11 consecutive patients with atypical RA free wall flutter. Method and results: LRA block was assessed following termination of AFL, by pacing from the ablation catheter in the low lateral RA posterior to the ablation line and recording the sequence and timing of activation anterior to the line with a duodecapole catheter, and vice versa for bidirectional block. LRA block resulted in a high to low activation pattern on the halo and a mean conduction time of 201 ± 48 ms to distal halo. LRA conduction block was present in only 2 out of 6 patients after termination of AFL by ablation. Ablation was performed during sinus rhythm (SR) in 9 patients to achieve LRA conduction block. No recurrence of AFL was observed at long‐term follow‐up (22 ± 12 months); 3 patients developed AF. Conclusion: Termination of right free wall flutter is often associated with persistent LRA conduction and additional radiofrequency ablation (RFA) in SR is usually required. Low RA pacing may be used to assess LRA conduction block and offers a robust endpoint for atypical RA free wall flutter ablation, which results in a high long‐term cure rate. (J Cardiovasc Electrophysiol, Vol. 21, pp. 526‐531, May 2010)