Philip Mathew

Prevention of recurrent atrial fibrillation with chronic dual-site right atrial pacing.

OBJECTIVES We investigated 1) the feasibility, safety and efficacy of multisite right atrial pacing for prevention of atrial fibrillation (AF); and 2) the ability of atrial pacing in single- and dual-site modes to increase arrhythmia-free intervals in patients with drug-refractory AF. BACKGROUND We recently developed and applied a novel technique of dual-site right atrial pacing in an unselected group of consecutive patients with AF requiring demand pacing. A prospective crossover study design was used to evaluate single- and dual-site right atrial pacing modes. METHODS The frequency of AF during the 3 months before pacemaker implantation was analyzed. Consecutive consenting patients underwent insertion of two atrial leads and one ventricular lead with a DDDR pulse generator. Patients were placed in a dual-site pacing mode for the first 3 months and subsequently mode switched to single site pacing for 3 months. Mode switching was repeated at 6-month intervals thereafter. RESULTS Atrial pacing resulted in a marked decline in AF recurrences (p < 0.001). During dual-site pacing with an optimal drug regimen, there was no AF recurrence in any patient compared with five recurrences in 12 patients during single-site pacing (p = 0.03). The mean (+/-SD) arrhythmia-free interval before pacing (14 +/- 14 days) was prolonged with dual- (89 +/- 7 days, p < 0.0001) and single-site pacing (76 +/- 27 days, p < 0.0001). Symptomatic AF episodes showed a declining trend during dual- and single-site pacing compared with those during the preimplantation period (p = 0.10). Mean antiarrhythmic drug use for all classes declined from 4 +/- 1.9 drugs before implantation to 1.5 +/- 0.5 (p < 0.01) drugs after implantation. Twelve (80%) of 15 patients remained in atrial paced rhythm at 13 +/- 3 months. CONCLUSIONS We conclude that multisite right atrial pacing is feasible, effective and safe for long-term application. Atrial pacing significantly prolongs arrhythmia-free intervals in patients with drug-refractory paroxysmal AF. Dual-site right atrial pacing may offer additional benefits and should be considered either as the primary mode or in patients unresponsive to single-site pacing.

Acute Effects of Dual-Site Right Atrial Pacing in Patients With Spontaneous and Inducible Atrial Flutter and Fibrillation

OBJECTIVES We tested the ability of dual-site right atrial pacing to prevent atrial fibrillation (AF) or atrial flutter induced by single-site atrial pacing and correlated its efficacy with clinical patient characteristics, atrial activation times and refractory periods. BACKGROUND Prevention of recurrent AF with long-term dual-site right atrial pacing has been demonstrated in our previous studies. However, the mechanism of antiarrhythmic benefit is unclear. METHODS Using standard electrophysiologic methods, baseline electrocardiographic and electrophysiologic measurements (mean +/- SD) were obtained. Programmed atrial stimulation was performed for AF or atrial flutter induction. Atrial pacing was performed at two drive cycle lengths (600 and 400 ms) and followed by one to three atrial extrastimuli at one to four pacing sites in the right atrium. In patients with inducible AF or atrial flutter, reinduction was then attempted during a dual-site atrial pacing drive train. This was achieved by simultaneously pacing at the high right atrium and coronary sinus ostium at an identical rate to the baseline stimulation, with the atrial extrastimuli being delivered at the pacing site responsible for the initial AF episode initiation. RESULTS Twenty patients (10 men, 10 women, mean [+/- SD] age 64 +/- 16 years) with symptomatic AF (n = 10) or atrial flutter (n = 10) were studied. There was a significant abbreviation of the P wave duration to 103 +/- 17 ms with dual-site pacing compared with sinus rhythm (120 +/- 12 ms, p = 0.005) and high right atrial pacing (121 +/- 17 ms, p = 0.005). This was also associated with a characteristic change in P wave configuration with an inferior and leftward axis shift. The effective refractory period at the high right atrium remained unchanged with dual-site atrial pacing compared with single-site high right atrial pacing. Sixteen patients had inducible AF or atrial flutter and could be tested after dual-site atrial pacing. The induced atrial tachyarrhythmia was suppressed in nine patients (56%), who had either induced AF (n = 5) or atrial flutter (n = 4). The difference in the effective refractory period between the high right atrium and the coronary sinus ostium pacing sites was significantly greater (33 +/- 12 ms) in patients with suppression of atrial tachyarrhythmia with dual-site atrial pacing compared with patients without suppression (15 +/- 13 ms, p = 0.001). P wave abbreviation did not correlate with arrhythmia suppression. There was no correlation between suppression of inducible AF or atrial flutter and demographic or clinical patient characteristics. CONCLUSIONS Dual-site right atrial pacing from the high right atrium and coronary sinus ostium can suppress inducible AF or atrial flutter elicited after single-site high right atrial pacing in selected patients. Acute suppression is more likely in patients with greater dispersion of right atrial refractoriness between these two sites.

Clinical efficacy and safety of atrial defibrillation using biphasic shocks and current nonthoracotomy endocardial lead configurations

We undertook a prospective randomized clinical trial evaluating efficacy and safety of internal atrial defibrillation in patients with drug-refractory atrial fibrillation (AF). Consecutive patients with paroxysmal or chronic AF were randomly tested with 3 internal atrial defibrillation lead configurations and biphasic shocks. Patients with implanted cardiac pacemakers were tested with the right atrium (RA) and left pulmonary artery or coronary sinus (CS) configuration. Shocks were initially delivered without anesthesia to assess patient tolerance. The need for backup ventricular defibrillation and pacing support was evaluated. Eighteen patients with (n = 15) or without (n = 3) structural heart disease, mean left ventricular ejection fraction 36 +/- 14%, and mean left atrial diameter 4.5 +/- 0.6 cm were studied. The mean defibrillation threshold in the best randomized lead configuration was 9.9 +/- 7.7 J. Mean defibrillation threshold for the right ventricle (RV) and superior vena cava configuration was 13.3 +/- 5 J, which was significantly lower than the RA and axilla configuration (20.1 +/- 7.4 J, p < 0.04) but not the RV to RA configuration (16.5 +/- 11 J, p > 0.2). The mean defibrillation threshold using the RA-left pulmonary artery/CS configuration was 8.9 +/- 9 J (p > 0.2 vs RV-superior vena cava). There was a bimodal distribution of defibrillation thresholds. Low atrial defibrillation thresholds correlated with absence of heart disease, higher ejection fraction, and smaller left ventricular end-diastolic diameter. Shocks were hemodynamically well tolerated, but 2 of 18 patients (11%) had nonsustained ventricular tachycardia after shock delivery. Six of 18 patients (33%) had postshock bradyarrhythmias. Fourteen of 16 patients perceived shocks > or = 3 J as intolerable.(ABSTRACT TRUNCATED AT 250 WORDS) [corrected]

INTERACTION BETWEEN ELECTRONIC ARTICLE SURVEILLANCE SYSTEMS AND IMPLANTABLE DEFIBRILLATORS : INSIGHTS FROM A FOURTH GENERATION ICD

We present a case report of an inappropriate discharge from a fourth generation implantable cardioverter defibrillator (ICD) as a result of exposure to electromagnetic interference. A 60‐year‐old man implanted with a Medtronic 7219D defibrillator experienced shocks without preceding symptoms while walking through an electronic surveillance system in a store. Though this has been reported, the mechanism of the interaction remains unexplained. The electrogram storage capabilities of this particular device enabled us to establish that this resulted from inappropriate sensing of the electromagnetic interference.

Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation

We analyzed the patterns of atrial activation and characterized the electrophysiologic properties of regional atrial sites in the, right atrium and left atrium at the onset of atrial fibrillation (AF) induced with programmed right atrial (RA) stimulation. Intraatrial conduction, atrial electrogram return cycle lengths for the first AF cycle, RA and left atrial (LA) activation maps during AF, and the stability and reproducibility of atrial activation sequences at AF onset and maintenance were analyzed in 23 patients with AF. Correlation of intracardiac electrograms with surface electrocardiographic morphology was attempted. Maximum intraatrial conduction delay for high RA premature beats was observed at the coronary sinus ostium (n = 15), His bundle region (n = 13) or interatrial septum (n = 15). The return cycle lengths for the first AF cycle showed increasing conduction delay with increasing prematurity of the last extrastimulus in most patients. Suprisingly, discrete atrial electrograms with regular or irregular cycle lengths were present at the onset of electrocardiographic documented coarse AF in 13 of 15 patients (87%). Fragmented or chaotic atrial activity were present in 2 of 15 patients (13%) in coarse AF but observed at > or = 1 atrial sites in 7 of 8 patients (88%) with fine AF (p = 0.001). The atrial activation sequence at the onset of the induced AF elicited by high RA extrastimuli usually showed the earliest activation site at the crista terminalis (9 patients) or interatrial septum (9 patients). In contrast, induced AF elicited from other RA sites usually showed earliest atrial activation at the septum (3 patients) or coronary sinus ostium (3 patients). Atrial activation sequences for the first induced AF cycle were usually reproducible in most patients. Atrial activation patterns during the first 10 cycles for AF were stable in RA and LA regions in 6 of 23 patients (260%) but demonstrated significant change(s) at > or = 1 region in 17 of 23 patients (74%) (p <0.05). We conclude that pacing induced AF elicited by RA premature beats commences as a regular or irregular rapid atrial tachycardia consistent with a transitional, but often organized, arrhythmia. The activation sequence and electrophysiologic behavior of the first induced AF cycle is consistent with intraatrial reentry and reproducible in most patients. More than 1 atrial activation sequence can sometimes be observed, emphasizing the dynamic nature of the initial RA reentrant circuits.

Low-energy endocardial defibrillation using an axillary or a pectoral thoracic electrode location.

BackgroundA significant proportion of patients receiving endocardial defibrillation lead systems must accept either high defibrillation thresholds (DFTs) with lower safety margins or lead implantation by thoracotomy. We examined the feasibility of achieving universal application of endocardial leads and lower defibrillation energy requirements by optimizing the lead system location in conjunction with biphasic shocks. Methods and ResultsTwo defibrillation catheter electrodes were positioned in the right ventricle and superior vena cava. Thoracic patch electrodes were placed at three sites (apical, pectoral, and axillary). Fifteen-joule, 10-J, and 5-J bidirectional simultaneous biphasic shocks were delivered across three different triple electrode configurations (right ventricle, superior vena cava, and patch) after inducing ventricular fibrillation (VF), and DFT was determined. All patients in whom VF was reproducibly inducible (14 patients) could be reproducibly defibrillated at 15 J at one or more patch electrode locations. Fifteen-joule shocks were effective at three thoracic electrode locations in 12 patients and at two electrode locations in 6 patients. The lowest mean single-shock DFI was 8.1±3.8 J. In 4 patients, ventricular flutter was reproducibly induced and reverted at 15 J in all patients. Mean DFT for the axillary location was 83±3.5 J and was significantly lower than apical (12.8±5.6 J, P=.008) and pectoral (11.6±4.1 J, p>.04) patch locations. The probability of success was significantly higher at 10 J with axillary location (78% of patients, p>.03 compared with both other sites) and at 15 J (P<.05 compared with the apical location). Low-energy endocardial defibrillation (s10 J) was feasible in 10 of 14 tested patients at more than 1 thoracic electrode location at 10 J, whereas only 1 of 7 successful patients could be reverted at more than 1 electrode location at 5 J (P<.02). ConclusionsThe use of axillary or pectoral patch lead location can allow endocardial defibrillation with biphasic shocks at energies s15 J in this lead configuration. Virtually universal application of endocardial defibrillation lead systems can be predicted from these data. Reduction in maximum pulse generator output to 525 J using these two thoracic electrode locations with bidirectional shocks can be feasible and maintain an adequate safety margin and permit thoracic pulse generator implantation. Lowering endocardial defibrillation energy <10 J requires increasing specificity of thoracic electrode location.

Efficacy and safely of radiofrequency catheter ablation of left-sided accessory pathways through the coronary sinus

Radiofrequency catheter ablation of left-sided accessory pathways (APs) with the use of an endocardial technique carries all potential risks of left heart catheterization. We analyzed the determinants of success, efficacy, and safety of radiofrequency catheter ablation from the coronary sinus (CS), as a potential alternative to the endocardial technique in these patients. Thirteen patients (mean age 40 +/- 20 years) with 15 left-sided APs and a history of symptomatic supraventricular tachycardia were included in the study. Nine APs were localized in the left posteroseptal region, and the remaining 6 in the left free wall. Ablation from CS was attempted in 12 patients with 14 APs. In 1 patient ablation within the CS was not deemed safe because of a small venous lumen. All 14 APs were successfully ablated using either CS ablation alone or combined with the endocardial technique. Efficacy of the CS ablation as a primary technique was 56% (5 of 9 APs). In 5 additional APs, ablation in the CS eliminated pathway conduction after failed endocardial attempts. CS ablation either as a primary or a secondary technique eliminated conduction in 10 of 14 APs (71.4%) (group 1). In the remaining 4 APs (group 2), the primary CS attempt was unsuccessful and APs were ablated with a subsequent endocardial approach. Determinants of success for the CS method were local AP to atrial and/or ventricular electrogram amplitude ratios > or = 1 (p < 0.05). The success rate of CS ablation was 83% in the left posteroseptal APs adjoining the branching point of the middle cardiac vein or a CS anomaly.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.

Internal Atrial Defibrillation: Effect on Sinus and Atrioventricular Nodal Function and Implanted Cardiac Pacemakers

Internal atrial defibrillation (IAD) has been extensively evaluated for clinical efficacy but the need for concomitant demand pacing and the effect of IAD shocks on pacemaker function is not well studied. We prospectively evaluated: (l) the incidence of bradycardia as a result of IAD shocks; and (2) effect of these shocks on functioning of implanted cardiac pacemakers. Consecutive consenting patients with atrial fibrillation (AF) requiring cardioversion or undergoing electrophysiologi‐col study were selected for IAD. IAD shocks were delivered using the right ventricle to right atrium (RV‐RA), right ventricle to superior vena cava (RV‐SVC), right atrium to axillary patch (RA‐AX), and right atrium to left pulmonary artery or coronary sinus (RA‐LPA/CS) lead configurations. Mean RR interval before and after the shocks and the time interval from shock delivery to first QRS complex were analyzed for unsuccessful and successful shocks. Pacing and sensing function was analyzed in patients with previously implanted pacemakers. Twenty‐five patients, 18 men, mean age 67.9 ± 10 years were included in the study. A total of 305 shocks (264 unsuccessful, 41 successful) were analyzed. For unsuccessful shocks the mean post‐IAD shock RR interval (795 ± 205 ms) and the time to first post‐IAD shock QRS complex (970 ± 438 ms) were both significantly greater than the pre‐IAD shock RR interval (685 ±131 ms, P < 0.001). The increase in post‐IAD shock RB interval and time to first post‐IAD shock QRS complex was seen with all four lead configurations used. With successful shocks the mean post‐IAD shock sinus cycle length (1.105 ± 450 ms) and time to first post‐IAD shock QRS complex (1,126 ± 443 ms) were both also significantly greater than the pre‐IAD shock RR interval (766 ±172 ms). Nine patients (36%) had episodes of significant bradycardia after shock delivery. Shocks of up to 20 J using the RA‐LPA/CS lead configuration did not affect pacemaker function. IAD can result in transient bradycardia related to sinus and atrioventricular nodal effects requiring backup ventricular pacing. Shocks can be safely delivered using RA‐LPA or RA‐CS lead configurations in patients with implanted bipolar cardiac pacemakers.

Prospective Clinical Evaluation of a Programmed Atrial Stimulation Protocol for Induction of Sustained Atrial Fibrillation and Flutter

We sought to define a minimum standardized protocol for induction of atrial fibrillation [AF] and/or atrial flutter. In contrast to ventricular stimulation protocols, a stimulation protocol for induction of AF or atrial flutter has not been critically evaluated. Since suppression of inducible AF or atrial flutter is used as one of the endpoints of success of pharmacologic and ablation therapies, there is an obvious need to define minimally appropriate electrical stimulation protocol for induction of AF or atrial flutter. We prospectively evaluated 70 patients, 44 with spontaneous atrial flutter or AF and 26 controls without documented atrial arrhythmias. A standardized programmed stimulation protocol, which employed up to three atrial extrastimuli delivered at two atrial sites at two atrial drive pacing lengths, was used in attempt to reproduce sustained AF and atrial flutter. The study endpoint was induction of sustained (>30 s) AF or atrial flutter. Sustained AF or atrial flutter was induced in 39/44 (89%) patients and 2/26 (7%) of controls (p <0.01). The arrhythmia induced was atrial flutter in 19/21 (91%) of atrial flutter patients, AF in 17/18 (94%) AF patients, both atrial flutter and AF in 5 AF/atrial flutter patients (100%). Two patients with atrial flutter had both AF/atrial flutter and 1 patient with AF had atrial flutter induced. The arrhythmia was induced from first stimulation site in 37 patients (85%) using a single in 9 (20%) patients, double 18 (41%) patients and triple extrastimuli in 10 (23%) patients. Two patients (5%) required stimulation from second site with two and three extrastimuli, respectively. The overall sensitivity and specificity of this stimulation protocol were 89% and 92%, respectively with a positive predictive accuracy of 95%.Conclusions. 1. Up to three atrial extrastimuli and two atrial sites are needed to increase yield of AF/atrial flutter induction at electrophysiologic study. 2. Induction of either AF or atrial flutter correlates well with presence of a similar spontaneous arrhythmia. 3. A baseline determination of the induction mode may be desirable prior to evaluation of interventions directed at AF or atrial flutter.