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R B Krol

Publications and source records attributed to R B Krol.

At least 19 recordsLinked to original sources
PubMed2001

Right and left atrial activation during external direct-current cardioversion shocks delivered for termination of atrial fibrillation in humans.

We examined the regional electrophysiologic effects of successful and unsuccessful direct-current cardioversion shocks on different right and left atrial regions in patients with sustained atrial fibrillation (AF). Patients with sustained AF undergoing external cardioversion underwent simultaneous mapping of the right and left atria. Electrogram changes after shock delivery, regional atrial activation, and effects of shock intensity were analyzed. Twenty-two patients with sustained AF received 52 shocks (mean 2.4/patient, 22 successful and 30 unsuccessful). The efficacy of 50, 100, 200, and 300 J was 18%, 39%, 100%, and 100%, respectively. In all 22 successful shocks, there was virtually simultaneous termination of electrical activity in all right and left atrial regions mapped. Unsuccessful shocks resulted in a significant increase in mean atrial cycle length at lateral right atrium, superior left atrium, and proximal, mid, and distal coronary sinus (p = 0.01), but not at the interatrial septum (p >0.2), which often disappeared before the next shock. This cycle length prolongation was accompanied by reduction in fragmented and chaotic electrograms (p <0.03) and emergence of discrete electrograms at all right and left atrial regions that persisted until the next shock. The changes in electrogram morphology failed to alter the surface electrocardiographic appearance of AF. There was no correlation between the shock intensity and the magnitude of these effects. We conclude that termination of AF with external cardioversion shocks is associated with the widespread extinction of regional atrial wave fronts. Unsuccessful shocks are associated with a temporary slowing of atrial activation at all regions except at the interatrial septum and emergence of organized and/or rapidly propagating wave fronts.

Adult↗
PubMed2000

Catheter mapping of spontaneous and induced atrial fibrillation in man.

The clinical electrophysiologic study of atrial fibrillation [AF] has recently progressed from static characterization of the substrate to the dynamic investigation of both induced and spontaneous AF in man. Prior studies have demonstrated inhomogeneity and greater dispersion of atrial refractoriness in patients with AF, but recently atrial electrical remodeling with consequent abbreviation of atrial refractory periods has also been reported. Yet further experimental observations have suggested the existence of additional arrhythmogenic mechanisms for certain AF subsets. These include studies that have demonstrated a stable atrial flutter circuit in one atrium with fibrillatory conduction or a focal atrial tachyarrhythmia arising commonly in the left atrium. Efforts at catheter mapping of AF are now in progress. New mapping techniques and novel devices are currently being employed. We have performed catheter mapping simultaneously in right and left atrial sites at onset and during sustained pacing-induced and spontaneous AF in patients with ischemic and/or hypertensive heart disease. Atrial premature complexes that initiated spontaneous AF typically had coupling intervals ranging from 260 to 400 ms and most frequently arose in the crista terminalis, right atrioventricular junction or superior left atrium. AF at onset showed discrete electrograms at virtually all right and left atrial regions mapped and the region of earliest atrial activation during AF was in close proximity to the premature complexes in over 90% of patients. The regional atrial activation sequence for the first 10 AF beats demonstrated stable or unstable patterns in individual patients. In contrast to spontaneous AF, the initial arrhythmia of induced AF was seen to have a significantly different site of earliest atrial activation but similar discrete electrograms in different atrial regions. However, as with spontaneous AF, the site of extrastimulus delivery was in close proximity to the first induced beat. We conclude that regional catheter mapping of AF is feasible and safe in man and organized electrical activity is frequently observed at AF onset in patients with heart disease. Both right and left atrial regions can be the source of atrial premature complexes and at the onset of spontaneous AF. Induced AF may have differing activation patterns than spontaneous AF but both demonstrate earliest activation in proximity to the initiating atrial premature complex. These findings may help explain therapeutic benefits of right and left atrial interventions and pacing therapies in AF.

Atrial Fibrillation↗
PubMed1999

Regional endocardial mapping of spontaneous and induced atrial fibrillation in patients with heart disease and refractory atrial fibrillation.

We performed simultaneous catheter mapping of right and left atrial regions at onset and during sustenance of spontaneous atrial fibrillation (AF) in patients with ischemic and/or hypertensive heart disease. Seventeen patients with structural heart disease had spontaneous and electrically induced AF episodes mapped from their onset simultaneously in multiple right and left atrial regions. Atrial premature complexes (APCs) that initiated spontaneous AF had coupling intervals ranging from 260 to 400 ms (mean 332 +/- 61), most commonly arising from the lateral right atrium (31%), right atrioventricular junction (13%), atrial septum (6%), superior left atrium (25%), or inferior left atrium (25%). APC morphology on surface electrocardiograms did not correlate with origin in specific atrial regions. The earliest regions of atrial activation for the first AF cycle were the lateral right atrium (n = 5), superior left atrium (n = 4), distal or mid coronary sinus (n = 4), atrial septum (n = 2), and right atrioventricular junction at the His bundle location (n = 2). Spontaneous AF at onset usually showed discrete but irregular electrograms at virtually all right and left atrial sites mapped, with a reproducible region of AF initiation in all 8 patients with multiple events. The region of earliest atrial activation at spontaneous AF onset was in close proximity to the APC origin in 15 of 16 patients (94%), and 39 of 40 episodes (97%) mapped. Stable patterns of right and left atrial activation were observed at AF onset in 14 patients. Induced AF elicited with right atrial stimulation demonstrated different sites of earliest regional atrial activation at onset compared with spontaneous AF events in 4 of 8 patients. However, discrete intracardiac electrograms were also present in induced AF in all of the mapped atrial regions. Furthermore, the site of extrastimulus delivery in induced AF was also found to be in close proximity to the earliest region of atrial activation for the first AF beat. We conclude that spontaneous AF is initiated by APCs arising in different right or left atrial regions in patients with structural heart disease and the initial region of atrial activation in AF is in proximity to the region of APC origin. Organized and repetitive electrical activation is frequently observed in both right and left atria at AF onset. Although electrically induced AF may have different activation patterns than spontaneous AF at onset in many patients, both types of AF demonstrate organization and earliest atrial activation in proximity to the initiating APC.

Aged↗
PubMed1999

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.

Aged↗
PubMed1999

Interactions of antiarrhythmic drugs with implantable defibrillator therapy for atrial and ventricular tachyarrhythmias.

Implantable cardioverter defibrillators (ICDs) have proven highly successful in the treatment of recurrent ventricular and atrial arrhythmias. Despite their high efficacy in terminating arrhythmias, concomitant therapy with antiarrhythmic drugs in ICD recipients remains common. Antiarrhythmic drugs are employed in an attempt to to limit patient exposure to high-energy shocks, primarily by reducing the number of arrhythmia reccurrences, suppressing coexisting arrhythmias, affecting rate and organization of tachycardias, and increasing efficacy of painless pacing therapies. Data regarding interaction of antiarrhythmic drugs with ICDs are incomplete and mostly based on animal models; however, it is clear that antiarrhythmic drugs affect all aspects of function of devices such as defibrillation threshold, pacing threshold, and sensing of both atrial and and ventricular arrhythmias. Because significant change in any of these functions may result in a nonfunctional device, and magnitude of drug effect in an individual patient is unpredictable, careful assessment of ICD function after an institution of therapy with antiarrhythmic drugs is mandatory.

Anti-Arrhythmia Agents↗
PubMed1999

Prospective clinical evaluation of a programmed atrial stimulation protocol for induction of sustained atrial fibrillation and flutter.

UNLABELLED: 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 a 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 extrastimuli in 9 (20%) patients, double extrastimuli 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 the 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.

Aged↗
PubMed1998

Regional right and left atrial activation patterns during single- and dual-site atrial pacing in patients with atrial fibrillation.

We examined the activation of the right atrium and left atrium by pacing from different atrial sites using several single- and dual-site atrial pacing modes in patients with atrial fibrillation or flutter. We also analyzed the effect of these pacing modes on fixed coupled extrastimuli in this population. Patients underwent detailed mapping of regional right atrial (RA) and left atrial (LA) sites. Bipolar pacing was performed individually from the high right atrium, coronary sinus ostium, and the distal coronary sinus, and simultaneously from the high right atrium and coronary sinus ostium (dual-site RA pacing) or high right atrium and distal coronary sinus (biatrial pacing). Extrastimuli were delivered from the high right atrium at fixed coupling intervals of 350 and 250 ms. Twenty patients with atrial fibrillation were studied. P-wave duration during pacing was significantly abbreviated by both dual-site RA and biatrial pacing (p <0.001 vs high RA pacing, respectively) but not by any other single-site atrial pacing method. Both dual-site atrial pacing modes also significantly abbreviated P wave durations for closely coupled high RA premature beats (p <0.001) in contrast to high RA pacing. During the basic pacing drive and for high RA extrastimuli, RA activation at the crista terminalis and atrial septum was comparable in sinus rhythm, high RA pacing, and in both dual-site atrial pacing methods, but was significantly delayed by coronary sinus ostial and distal coronary sinus pacing. In contrast, proximal coronary sinus activation was delayed with high RA pacing compared with all other pacing modes, and high RA extrastimuli encountered reduced conduction delay at this location with dual-site atrial pacing modes. LA activation was advanced superiorly by both single-site coronary sinus pacing methods and both dual-site atrial pacing techniques. Inferior and lateral LA activation was advanced by all pacing modes using a coronary sinus pacing site. However, earlier activation of LA sites occurred for high RA premature beats after both dual-site pacing methods (p <0.05) compared with single-site pacing modes. Incremental conduction delay at different atrial regions for closely coupled high RA extrastimuli ranged from 33% to 120% during high RA pacing and was significantly attenuated at multiple RA and LA sites by dual-site RA and biatrial pacing. Distinct global, as well as regional electrophysiologic effects, may mediate the variable antiarrhythmic effects of different and novel atrial pacing methods.

Aged↗
PubMed1998

Long-term outcome of patients with drug-refractory atrial flutter and fibrillation after single- and dual-site right atrial pacing for arrhythmia prevention.

OBJECTIVES: An initial crossover study comparing dual- and single-site right atrial pacing was performed followed by a long-term efficacy and safety evaluation of dual-site right atrial pacing in patients with drug-refractory atrial fibrillation (AF). Also examined was the efficacy of two single-site right atrial pacing modes (high right atrium and coronary sinus ostium) and the long-term need for cardioversion, antithrombotic and antiarrhythmic drug therapies during dual-site atrial pacing. METHODS: Thirty consecutive patients with drug-refractory symptomatic AF and documented primary or drug-induced bradycardia were implanted with a dual chamber rate-responsive pacemaker and two atrial leads. Single-site atrial pacing was performed at the high right atrium or the coronary sinus ostium. Continuous atrial pacing was maintained. RESULTS: Mean arrhythmia-free intervals increased from 9+/-10 days in the control period preceding implant to 143+/-110 days (p < 0.0001) in single-site right atrial pacing and 195+/-96 days in dual-site right atrial pacing (p < 0.005 versus single-site pacing and p < 0.0001 versus control). Dual-site right atrial pacing significantly increased the proportion of patients free of AF recurrence (89%) as compared to single-site right atrial pacing (62%, p = 0.02). High right atrial pacing and coronary sinus ostial pacing had similar efficacy for AF prevention. Effective rhythm control was achieved in 86% of patients during dual right atrial pacing. Seventy-eight percent of patients at 1 year and 56% at 3 years remained free of symptomatic AF. The need for cardioversion was reduced after pacemaker implant (p < 0.05) and antithrombotic therapy was reduced (p < 0.06) without any thromboembolic event. Coronary sinus ostial lead dislodgement was not observed after discharge. CONCLUSIONS: Atrial pacing in combination with antiarrhythmic drugs eliminates or markedly reduces recurrent AF. Prevention of AF is enhanced by dual-site right atrial pacing. High right atrial and coronary sinus ostial pacing do not differ in efficacy. Dual-site right atrial pacing is safe, achieves long-term rhythm control in most patients, decreases the need for cardioversion, and antithrombotic therapy can be selectively reduced.

Aged↗
PubMed1998

Multisite electrode pacing for prevention of atrial fibrillation.

There is increasing evidence that single site atrial pacing is beneficial for atrial fibrillation (AF) prevention in sick sinus syndrome. Multisite atrial pacing methods such as dual site right atrial pacing and biatrial synchronous pacing are currently under active evaluation for AF and atrial flutter prevention in patients with or without bradyarrhythmias. Clinical studies have demonstrated that multisite atrial pacing has an incremental benefit as compared with single site right and left atrial pacing. The electrophysiologic rationale for the efficacy of multisite atrial pacing is based on the reduction of global and local atrial activation times during pacing and for closely coupled atrial premature beats. This results in earlier recovery of excitability and decreased conduction delay. Dual site right atrial pacing consisting of simultaneous pacing from the high right atrium and the coronary sinus ostium reduces the activation times in virtually all left and right atrial regions, especially in areas of conduction delay. Multisite pacing methods reduce the ability to initiate AF with atrial premature beats by reducing the window for AF induction and minimizing the dispersion of atrial refractoriness. In our long-term clinical experience including 30 patients with paroxysmal and chronic drug-refractory AF, 78% of the patients were free of AF recurrence at 1 year, 63% at 2 years, and 56% at 3 years. Rhythm control was achieved in 86% of patients during a follow-up period of 3 years. Concomitantly, we observed a marked reduction in need for anticoagulation, type I antiarrhythmic drugs, and cardioversion therapies. There were no coronary sinus lead-related complications during follow-up. After the initial favorable clinical experiences, two major prospective randomized trials (DAPPAF and SYNBIAPACE) are under way in North America and Europe to evaluate quantitatively the beneficial impact of multisite atrial pacing for AF prevention.

Atrial Fibrillation↗
PubMed1997

Risk stratification and clinical outcome of minimally symptomatic and asymptomatic patients with nonsustained ventricular tachycardia and coronary disease: a prospective single-center study.

The Multicenter Automatic Defibrillator Implantation Trial (MADIT) showed improved survival with defibrillator therapy but was restricted to coronary artery disease patients with nonsustained ventricular tachycardia (NSVT) and inducible nonsupressible VT. The outcome of patients without inducible VT or inducible but suppressed VT still remains unclear. We performed risk stratification at electrophysiologic (EP) study in 111 consecutive unselected patients with nonsustained VT and coronary artery disease and randomized them to drug or device therapy. Follow-up on selected therapy was 1-71 (mean 27 +/- 20) months. Of 111 patients, 39 patients (35%) had inducible sustained VT at baseline EP study and were stratified to a "higher" risk group (group 1) for sudden death. In 9 of these patients (group 1A), sustained VT was suppressed with class IA antiarrhythmic drugs; in the remaining 30 patients (group 1B) sustained VT was not suppressed with class IA antiarrhythmic drugs. The other 72 of 111 patients (65%) had no inducible sustained VT at EP study and were stratified to a "lower"-risk group (group 2) for sudden death. Mean LVEF in group 1 was 30 +/- 10% versus 37 +/- 9% in group 2 (p = 0.001). Selected therapy in group 1 was an implantable cardioverter defibrillator (16 patients) or guided drug therapy (electrophysiologically guided class I antiarrhythmic drugs = 7 patients; Holter-guided class III antiarrhythmic drugs = 16 patients). In group 2, empiric drug therapy included beta blockers in 29 patients or Holter-guided class III antiarrhythmic drugs in 17 patients, with no antiarrhythmic drug therapy being administered in 26 patients. Mean LVEF tended to be lower in patients receiving class III antiarrhythmic drug therapy (34 +/- 12%) than in patients receiving beta blockers (40 +/- 10%, p = 0.06). Three-year total survival was comparable in group 1 (70%) and in group 2 (81%), but sudden cardiac death mortality tended to be lower in group 1 versus group 2 (0 vs 9%, p = 0.09). Patients receiving class III antiarrhythmic therapy had significantly higher 3-year all cause (40%, p = 0.04) and sudden death (25%, p = 0.06) mortality than patients receiving beta blockers (17% and 8% respectively) or no antiarrhythmic drug therapy (4% and 0%, respectively). The following conclusions can be drawn from this analysis: (1) Electrophysiologically guided drug therapy and implantable defibrillators can minimize the risk of sudden cardiac death in patients with coronary artery disease and inducible sustained VT stratified to higher risk of sudden death. A comparable outcome with respect to sudden death prevention in drug-suppressed or drug-refractory patients suggests limited prognostic benefit of class IA drug testing. (2) Lower-risk patients with severely depressed LVEF and minimal or no symptoms do not have a favorable outcome with respect to sudden and all-cause mortality on Holter-guided class III drug therapy. However, asymptomatic patients with mildly depressed left ventricular function have low sudden death event rates on beta blocker or no antiarrhythmic drug therapy.

Aged↗
PubMed1997

Low-energy endocardial defibrillation using dual, triple, and quadruple electrode systems.

The feasibility of achieving both universal application of nonthoracotomy leads and low (< or = 15 J) defibrillation energy requirements by optimizing lead system configuration for use with low-output (<30 J) biphasic shock pulse generators was examined. Sixteen patients (mean age 62 +/- 8 years and mean left ventricular ejection fraction of 38 +/- 15%) were included in the study. All patients had either experienced syncope with induced ventricular tachycardia (n = 4) or had documented sustained ventricular tachycardia (n = 7) or ventricular fibrillation (n = 5). Defibrillation threshold testing was performed in 2 stages on different days in these patients. In the first stage, 2 defibrillation catheter electrodes were positioned in the right ventricle and superior vena cava with an axillary cutaneous patch. Fifteen-joule, 10- and 5-J biphasic shocks were delivered across 3 different electrode configurations-right ventricle to superior vena cava, right ventricle to axillary patch, right ventricle to a combination of superior vena cava and axillary patch. In the second stage, an 80-ml can electrode was added subcutaneously in a pectoral location to the previous leads. Configurations compared were the right ventricle to pectoral can, and right ventricle to an "array"-combining superior vena cava, can, and axillary patch leads. The defibrillation threshold was determined using a step-down method. In stage 1, mean defibrillation threshold for the right ventricle to axillary patch (12.7 +/- 5.9 J) and right ventricle to superior vena cava plus axillary patch (9.8 +/- 5.2 J) configurations was lower than the right ventricle to superior vena cava configuration (14.2 +/- 6.4 J, p <0.05). In stage 2, the defibrillation was higher for the right ventricle to pectoral can (9.2 +/- 5.1 J) configuration compared with the right ventricle to the array (5.6 +/- 3.6 J, p < or =0.05). The right ventricle to array had the lowest defibrillation threshold, whereas the right ventricle to pectoral can was the best dual electrode system. Low-energy endocardial defibrillation (< or =10 J) was feasible in 72% of tested patients with > 1 electrode configuration at 10 J, whereas only 53% of successful patients could be reverted at >1 electrode configuration at 5 J (p <0.05). Reduction in maximum pulse generator output to < or =25 J using these electrode configurations with bidirectional shocks is feasible and maintains an adequate safety margin.

Aged↗
PubMed1997

Right and left ventricular hemodynamic performance during sustained ventricular tachycardia.

Several factors may influence hemodynamic tolerance of a ventricular tachycardia (VT) episode but, to date, only VT rate has been used as a major detection criterion in selecting implantable cardioverter-defibrillator therapy algorithms. We examined hemodynamic changes during VT in humans and a possible correlation between left and right ventricular hemodynamic indexes. Right ventricular hemodynamic indexes could reflect systemic hemodynamics but previous studies have been inconclusive. Patients with coronary artery disease and a history of recurrent, sustained VT were studied. Aortic pressure and right and left ventricular pressures were simultaneously recorded with 2 dual micromanometer-tipped high-fidelity pressure catheters during sinus rhythm and during induced sustained monomorphic VT. Beat-to-beat analysis was performed using custom-made software. Nine patients (7 men, mean age 60 +/- 8 years, mean ejection fraction 24 +/- 8%) with 11 VT episodes (mean cycle length 283 +/- 48 ms) were studied. During VT, left and right ventricular systolic pressures showed a mean decrease of 57% and 26%, respectively, with weak correlation (r = 0.67, p = 0.06) between both values. There was also an increase in mean left and right ventricular end-diastolic pressures of 26% and 74%, respectively, and no correlation was seen (r = -0.2, p = 0.6). A significant correlation was found between changes in left and right ventricular maximal positive dP/dt (55% and 28% decrease, respectively (r = 0.69, p = 0.03) and between changes in left and right ventricular maximal negative dP/dt (64% vs 39% decrease, r = 0.71, p = 0.02). Most ventricular time parameters in both ventricles differed significantly during VT compared with sinus rhythm; however, only the decrease in right ventricular time to end-diastolic pressure correlated with the decrease in left ventricular systolic pressure, at the 10th VT beat (r = 0.8, p = 0.01). We conclude that left and right ventricles are hemodynamically unequally affected during rapid VT. Although right ventricular pressures cannot be reliably used to assess changes in the hemodynamic status of the left ventricle, additional parameters, such as dP/dt or changes in ventricular time intervals, should be further evaluated for inclusion in implantable cardioverter-defibrillator algorithms.

Aged↗
PubMed1997

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.

Adult↗
PubMed1997

Evaluation of a programming algorithm for the third tachycardia zone in a fourth-generation implantable cardioverter-defibrillator.

The clinical efficacy of electrical algorithms for termination of slow ventricular tachycardia (VT) and ventricular fibrillation (VF) in implantable cardioverter-defibrillators (ICDs) is well established. Such algorithms have not been equally well defined for fast VT reversion. We report the testing of a prospectively designed algorithm for ICDs to treat fast VT that is inherently less responsive to antitachycardia pacing than slow VT. Fourth-generation ICD devices were programmed to three prospectively defined tachycardia detection zones as follows: cycle lengths < or = 260 ms for VF, 270-330 ms for fast VT, and > 330 ms for slow VT. The initial selected therapy for the VF zone was a high-energy biphasic shock (> 15 J), while a 3- or 5-J biphasic shock was usually administered for fast VT, and antitachycardia pacing was initially attempted for slow VT. Initial therapy was followed by backup therapy with high-energy shocks. Twenty-eight patients, 24 of whom were males, all with organic heart disease, with a mean age of 65 +/- 9 years, received either a Medtronic 7219D (23 patients), 7219C (2 patients), 7218SP1 (2 patients), or 7218C (1 patient) ICD with a nonthoracotomy lead system. The defibrillation threshold was 10 +/- 5 J. At predischarge electrophysiologic testing, a single 3- or 5-J shock terminated all episodes of fast VT tested. During a follow-up of 18 +/- 9 months, there were four nonarrhythmic deaths. Fourteen patients (50%) had a total of 21 VF, 44 fast VT, and 202 slow VT episodes. Twenty-three of 24 (96%) VF, 33 of 39 (84%) fast VT, and 193 of 202 (95.5%) slow VT episodes were terminated with the first delivered therapy in each therapy algorithm (p = NS). The overall efficacy of the entire electrical therapy algorithm was 100% for VF, 100% for fast VT, and 98% for slow VT episodes (p = NS). No patient experienced syncope or presyncope during fast VT or VF in this study. We conclude that a third detection and therapy zone can be successfully programmed in ICDs to define a range of fast VT episodes that can be effectively terminated with lower energy cardioversion shocks with comparable success and freedom from arrhythmic symptoms to electrical therapies used for slow VT and VF.

Aged↗
PubMed1997

Effects of high-frequency atrial pacing in atypical atrial flutter and atrial fibrillation.

Atypical atrial flutter has, hitherto, been relatively refractory to termination by rapid atrial pacing. High-frequency pacing (HFP) in the atrium, for termination of atrial flutter or atrial fibrillation (AF), and the electrophysiologic effects related to it have not been examined. We examined the clinical efficacy, safety, and electrophysiologic mechanisms of HFP using 50-Hz bursts at 10 mA applied at the high right atrium in patients with atypical atrial flutter (group 1) or AF (group 2), using a prospective randomized study protocol. Four burst durations (500, 1000, 2000, and 4000 ms) were applied at the high right atrium repetitively in random sequence in 22 patients with spontaneous atrial flutter or AF. Local and distant right and left atrial electrogram recordings were analyzed during and after HFP. HFP resulted in local and distant right and left atrial electrogram acceleration in 8 of 10 patients (80%) in group 1 but caused less frequent local atrial electrogram acceleration (6 of 12 patients) and no distant atrial electrogram effects in group 2 (p < .05 versus group 1). The HFP protocol was effective in arrhythmia termination in 6 of 10 patients in group 1 but in no patient in group 2 (p < .05 versus group 1). Standard HFP protocol applied at the high right atrium can frequently alter atrial activation in both atria and can terminate atypical atrial flutter. Efficacy in AF is limited, probably due to limited electrophysiologic actions beyond the local pacing site.

Adult↗
PubMed1997

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.

Defibrillators, Implantable↗