Ventricular Fibrillation Resulting from Synchronized Internal Atrial Defibrillation in a Patient with Ventricular Preexcitation

VF After Synchronized Internal Atrial Defibrillation. This case describes ventricular proarrhythmia as a result of a synchronized internal atrial defibrillation shock in a 29-year-old man with Ebstein's anomaly referred for radiofrequency ablation of a right posterior accessory pathway. During the electrophysiologic study, atrial fibrillation was induced and 3/3 msec shocks of various strengths were delivered between two decapolar defibrillation catheters in the coronary sinus and right atrial appendage. A 2.0-J biphasic shock synchronized to an R wave after a short-long-short ventricular cycle length pattern with a preshock coupling interval of 245 msec induced ventricular fibrillation, which was externally defibrillated with 200 J. This observation has implications for the development of implantable atrial defibrillators.     

Atrial Fibrillation-triggered Ventricular Fibrillation in a Patient with Early Repolarization Syndrome

A 54-year-old man with early repolarization syndrome (ERS) implanted with an implantable cardioverter-defibrillator (ICD) developed persistent atrial fibrillation (AF) three years after the implantation. Similarly, the remote monitoring system begun frequently detecting ventricular fibrillation (VF) and polymorphic ventricular tachycardia (PVT). Longer RR intervals were repeatedly observed just before the initiation of PVT/VF. Catheter ablation for AF successfully diminished both the PVT and VF events.     

Intermittent Preexcitation and Mesothelioma of the Atrioventricular Node: A Hitherto Undescribed Entity

Mesothelioma of AV Node with WPW. This is the first documented case of spontaneous intermittent preexcitation associated with mesothelioma of the atrioventricular (AV) node. A 66-year-old male with recurrent atrial arrhythmias, palpitations, heart failure, and marked intra-atrial conduction defect that required a pacemaker died during sleep. Electrophysiologic study revealed left free-wall bypass tract with marked intra-atrial conduction defect and prolonged conduction across the bypass tract. With atrial pacing, high degrees of block were noted in the bypass tract. Serial section of the conduction system and both AV rims revealed two left posterior and lateral bypass pathways with patchy areas of fibrosis. A large mesothelioma (benign AV nodal tumor) almost completely replaced the AV node. In addition, there was marked fatty infiltration of the atria. In summary: (1) the intermittent preexcitation with prolonged conduction across the bypass tract and block with atrial pacing were probably related to the incomplete patchy degenerative changes in the bypass tract, and/or almost complete replacement of the AV node by the tumor; (2) the intra-atrial conduction defect was probably related to the replacement of the AV node by mesothelioma and/or the fatty infiltration of the atria: and (3) the paroxysmal atrial arrhythmias probably reflect the marked atrial pathology.     

Rapid Ventricular Response Due to Treatment of Atrial Flutter or Fibrillation with Class IC Antiarrhythmic Drugs

The Class IC antiarrhythmic drugs, propafenone and flecainide, may slow the atrial rate during atrial flutter permitting 1:1 AV conduction. This effect is well known to occur soon after starting treatment for atrial fibrillation or atrial flutter with these Class IC drugs. We report two patients who had adverse effects after prolonged treatment with either propaienone or flecainide. In addition, we illustrate that this adverse effect can occur despite concomitant treatment with drugs that act on the AV node to prevent rapid AV conduction. A.N.E. 2000;5(1):101–104     

Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.     

Clinical Value of Noninducibility by High-Dose Isoproterenol Versus Rapid Atrial Pacing After Catheter Ablation of Paroxysmal Atrial Fibrillation

Noninducibility by High‐Dose Isoproterenol. Objective: To determine the relative clinical value of noninducibility of atrial fibrillation (AF) by isoproterenol (ISO) and by rapid atrial pacing (RAP) in patients with paroxysmal AF (PAF). Background: AF can be induced by RAP or ISO in >85% of patients with PAF. Methods: ISO was administered in escalating doses of 5, 10, 15, and 20 μg/min in 112 patients (age = 56 ± 13 years) with PAF before radiofrequency catheter ablation. AF was inducible in 97 of 112 patients (87%) at a mean dose of 15 ± 5 μg/min. RAP induced AF in the remaining 14 of 15 patients. Antral pulmonary vein (PV) isolation (APVI) was followed by ablation of complex fractionated atrial electrograms (CFAEs) as necessary to terminate AF and render AF noninducible in response to ISO. Results: AF terminated during APVI in 72 of 111 patients (65%) and after APVI plus ablation of CFAEs in 11 of 111 patients (10%). In the remaining 28 patients (25%), sinus rhythm was restored by transthoracic cardioversion. RAP was performed in the last 61 consecutive patients who were rendered noninducible by ISO. RAP initiated AF in 20 of 61 patients (33%) and atrial flutter in 6 patients (10%). No additional ablation was performed if AF was induced with RAP; however, atrial flutter was targeted. At 12 ± 5 months, 63/75 patients (84%) who were noninducible by ISO and 2 of 8 (25%) who still were reinducible by ISO were free from recurrent AF after a single ablation procedure without antiarrhythmic drugs (P = 0.001). AF recurred in 20 of 36 patients (56%) who required cardioversion for persistent AF after ablation (P < 0.001). Among the 61 patients who also underwent RAP, 12 of 20 (60%) who were, and 31 of 41 (76%) who were not inducible by RAP were free from recurrent AF (P = 0.21). The accuracy of noninducibility as a predictor of clinical outcome was 83% with ISO and 64% by RAP (P = 0.03). Conclusions: The response to isoproterenol after catheter ablation of PAF more accurately predicts clinical outcome than the response to RAP. (J Cardiovasc Electrophysiol, Vol. 21, pp. 13–20, January 2010)     

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex-trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)     

Radiofrequency Catheter Ablation Versus Modification of the AV Node for Control of Rapid Ventricular Response in Atrial Fibrillation

AV Node Modification vs Ablation in AF. Atrial fibrillation is a common arrhythmia, which is frequently difficult to control. Symptoms and ventricular dysfunction may be caused by a rapid ventricular response to atrial fibrillation. Radiofrequency catheter ablation techniques for ventricular rate control have been developed, including AV node modification and AV node ablation with pacemaker implantation. For both AV node modification and ablation, radiofrequency energy is applied via a 4-mm tipped electrode catheter. For AV node ablation radiofreqnency energy is applied near the compact AV node or His bundle via the right atrium, or occasionally at the His bundle via the left ventricle. For AV node modification radiofrequency energy is applied in the low middle or posterior septal right atrium near the tricuspid valve annulus. Both techniques can effectively control ventricular response to atrial fibrillation and the associated symptoms, although AV node modification is effective in only about 70% of patients compared to AV node ablation, which is effective in nearly 100%. In patients responding to AV node modification, maximal and mean ventricular response to atrial fibrillation is reduced by 25% to 35% chronically. Inadvertent AV block may occur during attempted AV node modification. It seems appropriate to attempt AV node modification prior to AV node ablation in patients with refractory atrial fibrillation and rapid ventricular response, in order to avoid the need for permanent pacemaker implantation. Although unproven, studies suggest that the mechanism by which AV node modification achieves ventricular rate control may he slow-pathway ablation in the low posterior septal right atrium.     

Rapidly Conducted Atrial Fibrillation Complicating Surgical Coronary Revascularization in a Patient with Intermittent Pre-Excitation

This report describes a case of atrial fibrillation conducted rapidly over a bypass tract postoperatively in a 73-year-old man subsequently shown to have intermittent pre-excitation. The determinants of atrioventricular bypass tract conduction and potential for dynamic functional change in bypass properties are reviewed. This article challenges the widely held clinical belief thai patients with intermittent pre-excitation are unlikely to experience rapidly conducted atrial fibrillation.     

Post Mortem Analysis of a Left Atrial Appendage Occlusion Device (PLAATO) in a Patient with Permanent Atrial Fibrillation

Thromboemoblism is the most feared complication of atrial fibrillation. Percutaneous left atrial appendage occlusion is a new interventional procedure for reducing thromboembolic risk in patients with atrial fibrillation. The paper reports of a post mortem analysis of the device demonstrating that one year after implantation the atrial surface of the device is completely covered by neo-endothelium and the device occludes the appendage completely.     

Endocardial Transcatheter Stimulation of the AV Nodal Fat Pad: Stabilization of Rapid Ventricular Rate Response During Atrial Fibrillation in Left Ventricular Failure

Introduction: Recent acute studies demonstrated that atrioventricular (AV) node vagal stimulation during atrial fibrillation (AF) decreases the mean ventricular rate, thus improving hemodynamics.
Methods and Results: We report a case of a woman with acute heart failure (HF), chronic AF with untreatable ventricular rapid response, in severe hypotensive state due to a cardiogenic shock. The patient underwent left ventricular (LV) pacemaker implantation and received 50 Hz AV node stimulation, delivered through a posteroseptal atrial lead, thus allowing a 100% pacing. Hemodynamics improvements allowed carvedilol titration; the rate was below 85 bpm after 4 days, then the atrial lead was removed.
Conclusions: This novel strategy may allow controlling the rapid AV response in patients undergoing pacemaker implantation.     

Maintenance of Sinus Rhythm after Cardioversion of Atrial Fibrillation in Patients with Lone Atrial Fibrillation and Patients with Hypertension

Background: The success rate and prognosis of cardioversion of atrial fibrillation (AF) in patients with organic heart disease is well known. In contrast, little data exist about cardioversion success and maintenance of sinus rhythm (SR) in patients with lone AF and in patients with hypertension as the only underlying cardiovascular disease. Methods: In a prospective cardioversion registry 148 of 181 patients (81.8%) with lone AF (age 58 ± 13 years, duration of AF 7.6 ± 19 weeks) and 120 of 148 patients (81.1%) with hypertension (age 62 ± 10 years, duration of AF 6.6 ± 21 weeks) had successful cardioversion and were followed for 7.7 ± 1.9 months. Results: At follow-up, 120 patients (81.1%) with lone AF were in SR, and 18 of these patients had had repeated cardioversion during follow-up (AF total recurrence rate 31.1%). In stepwise regression analysis, the number of previous cardioversions was predictive of rhythm at follow-up (P = 0.0453). Rhythm at follow-up did not differ between patients who were or were not on antiarrhythmic drugs. At follow-up 96 patients (80%) with hypertension were in SR, and 9 of these had had repeated cardioversion during follow-up (AF total recurrence rate 27.5%). As in lone AF, the recurrence rate of AF did not differ between patients with or without antiarrhythmic drug treatment, and in multivariate regression analysis, the number of previous cardioversions was the only clinical predictor of rhythm at follow-up (P = 0.0284). Conclusions: Even in patients with such benign conditions as lone AF or hypertension as the only underlying disease, the prognosis of cardioversion in terms of maintenance of SR is poor. Future studies of rhythm control versus rate control need to include not only patients with organic heart disease but also patients with lone AF and patients with hypertension, since the long-term benefits of these two strategies remain unclear even in these subsets of patients.     

Incidence of Atrial Fibrillation Following Ventricular Defibrillation with Transvenous Lead Systems in Man

Atrial Fibrillation After Ventricular Defibrillation. Introduction: The induction of atrial fibrillation (AF) following implantable defibrillator therapy of ventricular fibrillation carries multiple risks. The frequency of shock-induced AF may be more problematic in patients with transvenous defibrillators because current is often delivered through atrial tissue. Thus, the purpose of this study was to determine the incidence of AF following transvenous ventricular defibrillation. Methods and Results: Atrial electrograms were recorded before and after energy delivery in patients undergoing intraoperative testing of transvenous defibrillation lead systems. A total of 114 tracings were examined from 21 patients following ventricular defibrillation. Transvenous deflbrillation shock strength ranged between 200–800 volts (2–40 joules). Bipolar atrial electrograms were obtained from atrial electrodes with 1-cm interelectrode spacing located on one of the defibrillation catheters. The timing of the ventricular defibrillation shock was expressed as a percentage of the preceding sinus PP interval. Three of the 114 transvenous shocks (2.6%) generated AF. Each episode of AF occurred in a different patient. The shocks responsible for AF occurred at 21%, 43%, and 84% of the preceding sinus PP interval. No relation was found between AF induction and the timing of pulse delivery, pulse strength, or pulse number. Conclusion: We conclude that transvenous ventricular defibrillation infrequently causes AF and that timing shock delivery to the atrial cycle is likely to be of marginal or no benefit in the prevention of shock-induced AF. (J Cardiovasc Electrophysiol, Vol. 3, pp. 411–417, October 1992)     

Atrial Fibrillation/Flutter Induced by Implantable Ventricular Defibrillator Shocks:

Atrial Fibrillation/Flutter Induced by Defibrillator Shocks. Introduction : We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.
Methods and Results : Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak® lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 ± 6 shocks (mean ± SD) per patient compared with the endocardial group, which received 181 total shocks and 6 ± 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41 %) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 ± 9 J, lower than the endocardial mean energy of 20 ± 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 ± 6 defibrillator shocks < 15 J and 4 ± 2 shocks ≥ 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and ≥ 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J.
Conclusions : In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.     

Adverse Effects of Continuous Ventricular Pacing in Patients with Slower Atrial Fibrillation and Normal Left Ventricular Systolic Function

Background: Both heart rate irregularity during chronic atrial fibrillation (AF) and ventricular desynchronization imposed by ventricular pacing may compromise ventricular function. We investigated whether heart rhythm regularization achieved through ventricular overdrive pacing (VP) gives additional benefit over rate control alone in patients with AF. Methods: We studied 27 patients (mean age 72 ± 7 years) with AF and normal left ventricular (LV) systolic function who were implanted with a common VVIR pacemaker. Cardiac function was assessed by using serial echocardiographic conventional, tissue Doppler imaging (TDI) and color M‐Mode (CMM) examinations, together with B‐type natriuretic peptide (BNP) measurements. Baseline data were obtained during AF (mean heart rate 58 ± 5 beats/minute) with the pacemakers programmed to ventricular mere back‐up pacing. These data were compared to the corresponding measurements following a 2‐week VP period after the devises had been programmed to a lower rate of 70 beats/min, ensuring most of the time continuing VP. Results: Continuous VP compared to AF, reduced the LV cardiac index (2.28 ± 0.44 l/min/m² vs 2.33 ± 0.39 l/min/m², P < 0.05), increased the LV end‐systolic volume (38 ± 14 mL vs 35 ± 11 mL, P < 0.05), and decreased the TDI‐derived systolic and diastolic mitral velocity (8.1 ± 1.8 cm/s vs 8.3 ± 1.6 cm/s, and 8.1 ± 1.8 cm/s vs 8.3 ± 1.6 cm/s, respectively, both P < 0.05) and the CMM‐derived transmitral early diastolic flow propagation velocity (37.6 ± 9.2 vs 41.5 ± 9.7, P < 0.05). Following VP, both ratios E/Ea and E/Vp showed a trend toward increase (P = NS), whereas BNP rose up to 25.5% (median value, from 111 pg/mL to 165 pg/mL, P < 0.01). Conclusion: VP may be considered disadvantageous compared to slower AF.     

Amiodarone in Atrial Fibrillation

ABSTRACT Twenty-seven patients with atrial fibrillation without any concomitant conduction abnormality have been treated with oral amiodarone in a daily maintenance dose of 200 mg. The drug has been used for three purposes: 1) to block atrioventricular conduction, thereby decreasing the ventricular rate during atrial fibrillation (9 patients), 2) as prophylaxis against paroxysmal atrial fibrillation (8 patients), 3) as prophylaxis against recurrence of atrial fibrillation after DC conversion to sinus rhythm (13 patients). All patients were considered refractory to other antiarrhythmic drugs in these respects. In the second group, 4 of the 8 patients reported complete cessation of attacks and the others a marked reduction of the attack rate. In the third group, 10 of the 13 patients have maintained sinus rhythm for a longer period on treatment with amiodarone than with other drugs, resulting more than a triple prolongation of the time in sinus rhythm. In 3 patients the drug has been discontinued because of side-effects. In conclusion, amiodarone affords protection from episodes of paroxysmal atrial fibrillation, as well as from recurrence of atrial fibrillation after DC conversion to sinus rhythm. If the drug is ineffective in either of these respects, it may still be useful as a means of moderating the ventricular response in atrial fibrillation.