Irakli Giorgberidze
Rutgers University
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Journal of the American College of Cardiology | 1997
Atul Prakash; Sanjeev Saksena; Michael D. Hill; Ryszard B. Krol; Anand N. Munsif; Irakli Giorgberidze; Philip Mathew; Rahul Mehra
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.
American Journal of Cardiology | 1999
Sanjeev Saksena; Irakli Giorgberidze; Rahul Mehra; Michael D. Hill; Atul Prakash; Ryszard B. Krol; Philip Mathew
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.
American Journal of Cardiology | 1995
Irakli Giorgberidze; Sanjeev Saksena; Ryszard B. Krol; Philip Mathew
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)
Journal of Interventional Cardiac Electrophysiology | 1997
Irakli Giorgberidze; Sanjeev Saksena; Luc R. Mongeon; Rahul Mehra; Ryszard B. Krol; Anand N. Munsif; Philip Mathew
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.
Journal of Interventional Cardiac Electrophysiology | 1999
Ryszard B. Krol; Sanjeev Saksena; Atul Prakash; Irakli Giorgberidze; Philip Mathew
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.
Journal of Interventional Cardiac Electrophysiology | 1997
John Neglia; Ryszard B. Krol; Irakli Giorgberidze; Philip Mathew; Carolyn Lewis; Anand N. Munsif; Sanjeev Saksena
The clinical efficacy of electrical algorithms for termination of slowventricular tachycardia (VT) and ventricular fibrillation (VF) inimplantable cardioverter-defibrillators (ICDs) is well established. Suchalgorithms have not been equally well defined for fast VT reversion. Wereport the testing of a prospectively designed algorithm for ICDs to treatfast VT that is inherently less responsive to antitachycardia pacing thanslow VT. Fourth-generation ICD devices were programmed to threeprospectively defined tachycardia detection zones as follows: cyclelengths≤ 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 biphasicshock (>15J), while a 3- or 5-J biphasic shock was usually administered forfast 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 heartdisease, with a mean age of 65 ± 9 years, received either a Medtronic7219D (23 patients), 7219C (2 patients), 7218SP1 (2 patients), or 7218C (1patient) ICD with a nonthoracotomy lead system. The defibrillation thresholdwas 10 ± 5 J. At predischarge electrophysiologic testing, a single 3-or 5-J shock terminated all episodes of fast VT tested. During a follow-upof 18 ± 9 months, there were four nonarrhythmic deaths. Fourteenpatients (50%) had a total of 21 VF, 44 fast VT, and 202 slow VTepisodes. Twenty-three of 24 (96%) VF, 33 of 39 (84%) fast VT,and 193 of 202 (95.5%) slow VT episodes were terminated with thefirst delivered therapy in each therapy algorithm (p=NS). The overallefficacy 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 thisstudy. We conclude that a third detection and therapy zone can besuccessfully programmed in ICDs to define a range of fast VT episodes thatcan be effectively terminated with lower energy cardioversion shocks withcomparable success and freedom from arrhythmic symptoms to electricaltherapies used for slow VT and VF..
American Journal of Cardiology | 1997
Theofilos M Kolettis; Sanjeev Saksena; Philip Mathew; Ryszard B. Krol; Irakli Giorgberidze; Ghanshyam Bhambhani
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.
Pacing and Clinical Electrophysiology | 1994
Sanjeev Saksena; Irakli Giorgberidze
In this issue of FACE, Conti et al.^ describe one of the technical problems associated with radiofrequency catheter ablation (RFCA) of leftsided accessory pathways (APs) using tbe retrograde left ventricular approacb. Tbey encountered entanglement of tbe contoured tip catbeter electrode in tbe subvalvular mitral apparatus and efforts to witbdraw tbe catbeter resulted in cbest discomfort and bypotension. Failure of valve leaflet approximation during systole witb acute mitral incompetence was ecbocardiograpbically documented. Tbe authors were able to disentangle the catbeter under ecbocardiograpbic guidance and tbis resolved the patients symptoms and tbe bemodynamic abnormality. This report raises important technical considerations vis-a-vis this specific complication of RFCA, incites reevaluation of patient safety issues during tbe ever expanding universe of RFCA applications, and sbowcases tbe regulatory dilemma in this physician improvised tberapy.
American Journal of Cardiology | 1998
Atul Prakash; Philippe Delfaut; Irakli Giorgberidze; Ryszard B. Krol; Philip Mathew; Sanjeev Saksena
This report illustrates the complexity of internal atrial defibrillation and implantable cardioverter-defibrillator therapy in patients with dual site atrial pacing systems.
Journal of Cardiovascular Pharmacology and Therapeutics | 1997
Sanjeev Saksena; Irakli Giorgberidze
For some time now, cardiologists have labored to identify coronary patients at high risk for arrhythmic death by noninvasive methods and develop effective protective pharmacologic therapies. This strategy has increasingly floundered on both fronts. Risk stratification using ventricular function in patients with and without congestive heart failure has had the greatest prognostic value in predicting overall survival but has had lesser impact with respect to sudden cardiac death survival (1,2). Signal-averaged electrocardiography and ambulatory electrocardiograph monitoring analyses have had a limited role to date as predictors of arrhythmic events largely due only to a modest specificity and predictive accuracy (3). Exercise testing has also had low sensitivity. Newer approaches such as heart rate variability, while promising, are yet to be