Effects of single-site versus biventricular epicardial pacing on myocardial performance in an immature animal model of atrioventricular block

INTRODUCTION: Single-site ventricular pacing results in dyssynchronous ventricular activation and may contribute to ventricular dysfunction. We evaluated epicardial biventricular (BiV) pacing as a means of maintaining synchronous ventricular activation in an acute piglet model of AV block with normal ventricular anatomy and function. METHODS AND RESULTS: We used left ventricular (LV) impedance catheters and tissue Doppler imaging to assess the cardiodynamics of immature piglets (n = 6, 33-78 days, 9.35 +/- 0.85 kg). Following catheter ablation of the AV node, a pacemaker was programmed 20 beats per minute above the intrinsic atrial rate. The animals were paced at 5-minute intervals via the following AV sequential configurations: Right atrial appendage (RA)-RV apex (RVA), RA-LV apex (LVA), and RA-biventricular (RVA/LVA). RA-RVA was the experimental control. LV systolic mechanics, measured by the slope of the end-systolic pressure-volume relationship (E(es)), increased with BiV pacing (12.8 +/- 3.4 mmHg/mL, P < 0.02) or single-site LVA pacing (10.6 +/- 3.4 mmHg/mL, P < 0.05) compared with single-site RVA pacing (8.3 +/- 1.4 mmHg/mL). QRS duration lengthened compared with sinus rhythm (42 +/- 8 msec) with either RVA (56 +/- 9 msec, P < 0.02) or LVA (54 +/- 7 msec, P < 0.03), but not with BiV (48 +/- 7 msec, P = 0.08) pacing. Tissue Doppler imaging showed LV dyssynchrony with RVA (septal-to-lateral delay 46.0 +/- 51.7 msec), with return toward normal with LVA (-9.6 +/- 33.6 msec, P < 0.04) or BiV (-4.1 +/- 33.8 msec, P < 0.04) pacing. CONCLUSIONS: In this acute immature piglet model of AV block, LV performance improved with single-site pacing from the LVA and BiV pacing (RVA/LVA), as compared with single-site pacing from the RVA. These changes correlated with tissue Doppler indices of mechanical synchrony, though not necessarily with QRS duration.     

Avoidance of right ventricular pacing in cardiac resynchronization therapy improves right ventricular hemodynamics in heart failure patients

Background: Cardiac resynchronization therapy (CRT) applied by pacing the left and right ventricles (BiV) has been shown to provide synchronous left ventricular (LV) contraction in heart failure patients. CRT may also be accomplished through synchronization of a properly timed LV pacing impulse with intrinsically conducted activation wave fronts. Elimination of right ventricular (RV) pacing may provide a more physiological RV contraction pattern and reduce device current drain. We evaluated the effects of LV and BiV pacing over a range of atrioventricular intervals on the performance of both ventricles.
Methods: Acute LV and RV hemodynamic data from 17 patients with heart failure (EF = 30 ± 1%) and a wide QRS (138 ± 25 msec) or mechanical dyssynchrony were acquired during intrinsic rhythm, BiV, and LV pacing.
Results: The highest LV dP/dt_max was achieved during LV pre- (LV paced prior to an RV sense) and BiV pacing, followed by that obtained during LV post-pacing (LV paced after an RV sense) and the lowest LV dP/dt_max was recorded during intrinsic rhythm. Compared with BiV pacing, LV pre-pacing significantly improved RV dP/dt_max (378 ± 136 mmHg/second vs 397 ± 136 mmHg/second, P < 0.05) and preserved RV cycle efficiency (61.6 ± 14.6% vs 68.6 ± 11.4%, P < 0.05) and stroke volume (6.6 ± 4.4 mL vs 9.0 ± 6.3 mL, P < 0.05). Based on LV dP/dt_max, the optimal atrioventricular interval could be estimated by subtracting 30 msec from the intrinsic atrial to sensed RV interval.
Conclusions: Synchronized LV pacing produces acute LV and systemic hemodynamic benefits similar to BiV pacing. LV pacing at an appropriate atrioventricular interval prior to the RV sensed impulse provides superior RV hemodynamics compared with BiV pacing.     

Comparison of echocardiography and device based algorithm for atrio-ventricular delay optimization in heart block patients

AIM: To compare the atrio-ventricular (AV/PV) delay optimization by echocardiography and intra-cardiac electrocardiogram (IEGM) based QuickOpt algorithm in complete heart block (CHB) patients, implanted with a dual chamber pacemaker. METHODS: We prospectively enrolled 20 patients (age 59.45 ± 18.1 years; male: 65%) with CHB, who were implanted with a dual chamber pacemaker. The left ventricular outflow tract velocity time-integral was measured after AV/PV delay optimization by both echocardiography and QuickOpt algorithm method. Bland-Altman analysis was used for agreement between the two techniques. RESULTS: The optimal AV and PV delay determined by echocardiography was 155.5 ± 14.68 ms and 122.5 ± 17.73 ms (P < 0.0001), respectively and by QuickOpt method was 167.5 ± 16.73 and 117.5 ms ± 9.10 ms (P < 0.0001), respectively. A good agreement was observed between optimal AV and PV delay as measured by two methods. However, the correlation of the optimal AV (r = 0.0689, P = 0.77) and PV (r = 0.2689, P = 0.25) intervals measured by the two techniques was poor. The time required for AV/PV optimization was 45.26 ± 1.73 min by echocardiography and 0.44 ± 0.08 min by QuickOpt method (P < 0.0001). CONCLUSION: The programmer based IEGM method is an automated, quick, easier and reliable alternative to echocardiography for the optimization of AV/PV delay in CHB patients, implanted with a dual chamber pacemaker.     

Impact of catheter ablation of the coronary sinus on paroxysmal or persistent atrial fibrillation

Objectives: This study evaluated the impact of catheter ablation of the coronary sinus (CS) region during paroxysmal and persistent atrial fibrillation (AF).
Background: The CS musculature and connections have been implicated in the genesis of atrial arrhythmias.
Methods: Forty-five patients undergoing catheter ablation of AF were studied. The CS was targeted if AF persisted after ablation of pulmonary veins and selected left atrial tissue. CS ablation was commenced endocardially by dragging along the inferior paramitral left atrium. Ablation was continued from within the vessel (epicardial) if CS electrograms had cycle lengths shorter than that of the left atrial appendage.
RF energy was limited to 35 W endocardially and 25 W epicardially. The impact of ablation was evaluated on CS electrogram cycle length (CSCL) and activation sequence, atrial fibrillatory cycle length measured in the left atrial appendage (AFCL) and on perpetuation of AF.
Results: Endocardial ablation significantly prolonged CSCL by 17 ± 5 msec and organized the CS activation sequence (from 13% of patients before to 51% after ablation); subsequent epicardial ablation further increased local CSCL by 32 ± 27 msec (P < 0.001). AFCL prolonged significantly both during endocardial and epicardial ablation (median: 152 to 167 msec P = 0.03) and was associated with AF termination in 16 (35%) patients (46% of paroxysmal and 30% of persistent AF). AFCL prolongation ≥5 msec and/or AF termination was associated with more rapid activity in the CS region originally: P ≤ 0.04.
Conclusion: Catheter ablation targeting both the endocardial and epicardial aspects of the CS region significantly prolongs fibrillatory cycle length and terminates AF persisting after PV isolation in 35% of patients.     

Nonuniform Anisotropy is Responsible for Age-Related Slowing of Atrioventricular Nodal Reentrant Tachycardia

Age-Related Slowing of AVNRT. Introduction : AV nodal reentrant tachycardia cycle length has been shown to he longer in the elderly population. Microfibrosis associated with aging producing nonuniform anisotropic conduction or changes in membrane ionic properties could explain this finding.
Methods and Results : Forty-five patients (33 women and 12 men) with typical AV nodal reentrant tachycardia were studied to analyze the effects of age on electrophysiologic characteristics of the tachycardia using high-density catheter mapping of the triangle of Koch. We classified patients into group A (age ≤ 45 years, mean [± SD] 32.7 ± 8.8, n = 27) and group B (age > 45 years, mean [± SD] 61.1 ± 10.2, n =18). Retrograde atrial activation was recorded during tachycardia by means of a 2-mm decapolar catheter at the His bundle, a quadripolar catheter at the high right atrium, a multipolar catheter (6 to 10 poles) in the coronary sinus, and a deflectable quadripolar catheter at the posterior triangle of Koch. The AH interval at the AV junction as well as HA intervals at several atrial sites were measured during tachycardia. HA intervals at all atrial recording sites except in the posterior triangle of Koch were significantly longer in group B, as well as the tachycardia cycle length (362 vs 329 msec, P = 0.01). The mean AH interval was prolonged by 24 msec in group B, but this difference did not reach statistical significance. A sequential pattern of retrograde atrial activation during tachycardia was more frequently recorded in group B.
Conclusions : Since the delayed activation to the atrium was heterogeneous, transverse nonuniform anisotropic conduction is a likely explanation of these age-related modifications of AV nodal reentrant tachycardia characteristics.     

Evidence for Multiple Atrio-AV Nodal Inputs in the Normal Dog Heart

Multiple Atrio-AVN Inputs in Dog Heart. Introduction : Complete AV block after combined fast pathway (FP) and slow pathway (SP) ablation is uncommon. The purpose of this study was to interrupt activation of these and additional inputs by placing a radiofrequency lesion across the interatrial septum between the FP and SP ablation sites.
Methods and Results : In eight anesthetized open chest dogs, FP ablation induced significant A-H prolongation (δA-H: 51±14 msec; P < 0.001) and a shift of earliest retrograde atrial activation from the anterior septum to the region of the coronary sinus (CS) os. Subsequently, ablation of the interatrial septum across the fossa ovalis was successful in 5 of 8 dogs, changing the sequence of atrial activation (A) so that A at the His-bundle electrogram, which initially preceded A at the CS os (18 ± 4 msec vs 46 ± 7 msec, P < 0.01), now followed CS os A (81 ± 31 msec vs 59 ± 20 msec, P < 0.05). Additional ablation of the SP caused a type II Mobitz AV block or complete AV block in 5 of 8 dogs. The four dogs with complete AV block sbowed a stable, high junctional escape rhytbm at a rate of 64 ± 16 beats/min. Pacing between the ablation lesions and the AV node in one dog showed 1:1 AV conduction and Wenckebach-type AV block indicating preserved AV nodal function. Histology showed necrotic changes in the FP and SP transitional cell zones and in the atrial tissue of the interatrial septum. However, the compact AV node. His bundle, and adjacent atria and transitional cells were undamaged.
Conclusion : There are additional AV nodal inputs in the interatrial septum in addition to the anterior FP and posterior SP inputs. Ablation of all of these may be required, if the aim is production of complete AV block proximal to the AV node with a high Junctional escape rhythm.     

Normal atrial activation and voltage during sinus rhythm in the human heart: an endocardial and epicardial mapping study in patients with a history of atrial fibrillation

Background: The three-dimensional contributions to human atrial activation in sinus rhythm have not been specifically characterized. We evaluated the sequence of endocardial and epicardial activation and voltage of the atria during normal sinus rhythm.
Methods and Results: The study group includes 35 patients with history of symptomatic atrial fibrillation. Prior to catheter ablation of atrial fibrillation, we performed multielectrode electroanatomic mapping during sinus rhythm, endocardially of the RA, LA, and coronary sinus (CS) and, in 10 patients, epicardially of the transverse sinus and oblique sinus. Following activation of the atrial region of the sinus node, the epicardial transverse sinus was activated 11 ± 18 msec later, while the earliest endocardial LA activation occurred in the region of Bachmann's bundle at 31 ± 13 msec, significantly earlier than the earliest epicardial LA activation of the oblique sinus at 54 ± 10 msec (P < 0.002). The posterior LA revealed complex types of activation in 66% of patients analyzed, due to the convergence of wavefront propagation from the CS, oblique sinus, and endocardial LA. Bipolar voltage measurements revealed significantly higher values for the epicardium (mean 3.05 ± 1.31 mv) than for the endocardium (mean 1.65 ± 0.75 mv), P < 0.0001 between both groups.
Conclusions: In sinus rhythm, we have characterized endocardial and epicardial atrial activation and voltage, and provide an analysis and understanding of the genesis of the P wave complex in humans.     

Slowing of the Ventricular Rate During Atrial Fibrillation by Ablation of the Slow Pathway of AV Nodal Reentrant Tachycardia

Influence of Slow Pathway Ablation on Atrial Fibrillation. Introduction : The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.     

Optimal Atrioventricular Delay in CRT Patients Can Be Approximated Using Surface Electrocardiography and Device Electrograms

Electrocardiographic AV Delay Adjustment . Background: Optimization of the atrioventricular (AV) delay (AVD) may result in an improvement in cardiac resynchronization therapy (CRT) outcome. Previous studies have shown positive correlation between interatrial conduction time measured invasively during the implant procedure and optimal AVD determined postimplant using Doppler echocardiography. We hypothesized that the optimal AVD can be predicted noninvasively from surface electrocardiogram (ECG). Methods: The optimal sensed (SAV) and paced (PAV) AVDs were determined for CRT patients (n = 63) by programming different AVDs (in 20 ms steps, in random sequence) and evaluating Doppler images of the mitral flow (iterative method). The time intervals between atrial sensing (As) and pacing (Ap) to the end of the P‐wave (Pend) and to the right ventricular sensing (RVs) were measured from 5 ECG leads (limb, V1, and V3) and device telemetry during sinus rhythm and atrial pacing. Results: Optimal SAV was 120 ± 30 ms and correlated with As‐Pend (R = 0.69, P < 0.0001) and As‐RVs (R = 0.45, P = 0.0003). Optimal PAV was 172 ± 38 ms and correlated with Ap‐Pend (R = 0.65, P < 0.0001) and Ap‐RVs (R = 0.60, P < 0.0001). Regression analysis suggested a simple method of AVD adjustment by pacing the ventricles 40 ms after the end of the sensed P‐wave or 30 ms after the end of the paced P‐wave but not at the expense of biventricular capture. Such a method would have resulted in significantly lower deviation from echo‐optimal AVDs compared with programming fixed values. Conclusion: A simple method of providing 30–40 ms separation between the end of the P‐wave and ventricular pacing pulse can be used to approximate echocardiographically optimal AV delays. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1226‐1232, November 2010)     

The hemodynamic benefit of differential atrioventricular delay intervals for sensed and paced atrial events during physiologic pacing

The ability to program different atrioventricular (AV) delay intervals for paced and sensed atrial events is incorporated in the design of some newer dual chamber pacemakers. However, little is known regarding the hemodynamic benefit of differential AV delay intervals or the magnitude of difference between optimal AV delay intervals for paced and sensed P waves in individual patients. In this study, Doppler-derived cardiac output was used to examine the optimal timing of paced and sensed atrial events in 24 patients with a permanent dual chamber pacemaker. The hemodynamic effect of utilizing separate optimal delay intervals for sensed and paced events compared with utilizing the same fixed AV delay interval for both was determined. The optimal delay interval during DVI (AV sequential) pacing and VDD (atrial triggered, ventricular inhibited) pacing at similar heart rates was 176 +/- 44 and 144 +/- 48 ms (p less than 0.002), respectively. The mean difference between the optimal AV delay intervals for sensed (VDD) and paced (DVI) P waves was 32 ms and was up to 100 ms in some individuals. The difference between optimal AV delay intervals for sensed and paced atrial events was similar in patients with complete heart block and those with intact AV node conduction. At the respective optimal AV delay intervals for sensed and paced P waves, there was no significant difference in the cardiac output during VDD compared with DVI pacing. However, cardiac output significant declined during VDD pacing at the optimal AV delay interval for a paced event and during DVI pacing at the optimal interval for a sensed event.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pacing techniques in the management of supraventricular tachycardias. Part 2. An implanted atrial synchronous pacemaker with a short atrioventricular delay for the prevention of paroxysmal supraventricular tachycardias.

An implanted atrial synchronous pacemaker with an atrioventricular delay of 30 msec is described. This pacemaker was implanted into a patient with paroxysmal supraventricular tachycardia due to an intra AV nodal reciprocal mechanism. The pacemaker was able to trigger from atrial potentials following atrial premature beats down to a coupling time of 300 msec. Following each triggering atrial potential, a ventricular stimulus was applied 30 msec later thereby producing a ventricular premature beat in response to each sinus beat or each atrial premature beat. Retrograde conduction from this atrial premature beat blocked the re-entry mechanism within the AV node and prevented the initiation of tachycardia. A detailed discussion on all parameters of function of this pacemaker is presented.     

Conduction Properties of the Inferior Vena Cava-Tricuspid Annular Isthmus in Patients with Typical Atrial Flutter

Conduction Properties of the Annular Isthmus. Introduction : A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter.
Methods and Results : Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 ± 23 msec), inferolateral tricuspid annulus pacing (71 ± 23 msec), or entrainment of flutter (72 ± 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 ± 22 msec), proximal coronary sinus pacing (73 ± 21 msec), or entrainment of flutter (64 ± 15 msec).
Conclusion : Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.     

Cardiac resynchronization therapy with sequential biventricular pacing: impact of echocardiography guided VV delay optimization on acute results.

BACKGROUND: Cardiac resynchronization therapy (CRT) improves left ventricular synchrony as evaluated by tissue Doppler imaging (TDI), leading to improved left ventricular performance and reverse remodeling. New CRT devices enable programming of left and right VV delay. The aim of this study was to determine whether sequential biventricular (BiV) pacing by echo-guided programming of VV delay would enhance the response to CRT. METHODS: 15 consecutive patients with severe heart failure and left bundle branch block underwent CRT by BiV device implantation. They were studied with conventional and TDI echo the day before implantation. Left ventricular ejection fraction (LVEF) was determined, and the electromechanical delay (QS), defined as the time interval from the beginning of the QRS to the S wave in pulsed TDI, was assessed in each of the four left ventricular basal segments. The dyssynchrony index was calculated as the difference between the longest and shortest electromechanical delay (QS(max-min)). The parameters were re-evaluated the day after implantation during simultaneous BiV pacing and with seven different VV delays. The optimal VV delay was determined by finding the VV interval corresponding to the maximum aortic velocity time interval (VTI). RESULTS: QS(max-min) decreased from 85.3 +/- 27.0 msec to 46.7 +/- 23.0 msec (p = 0.0002), LVEF increased from 21.7 +/- 7.3% to 30.0 +/- 7.7% (p = 0.0001) and aortic VTI increased from 12.7 +/- 3.6 cm to 15.2 +/- 4.0 cm (p < 0.0001), with simultaneous BiV pacing. The VV intervals were programmed as follows: LV pre-excitation by 10 msec in five patients, 20 msec in three, 30 msec in two, and 40 msec in three; and RV pre-excitation by 10 msec in one and by 20 msec in one. The maximal aortic VTI obtained with VV delay programming increased from 15.2 +/- 4.0 cm to 17.7 +/- 4.0 cm (p = 0.0005). During optimized sequential BiV pacing, QS(max-min) further decreased from 46.7 +/- 23.0 msec to 30.6 +/- 21.0 msec (p = 0.02) and LVEF further increased from 30.0 +/- 7.7% to 35.0 +/- 7.7% (p = 0.0003). CONCLUSIONS: Sequential BiV pacing with VV delay optimized by evaluation of aortic VTI enhanced the response to CRT with additional improvements in left ventricular synchrony and left ventricular function compared to simultaneous CRT.     

A prospective comparison of AV delay programming methods for hemodynamic optimization during cardiac resynchronization therapy

Introduction: There are several methods for programming the optimal AV delay (AVD) during cardiac resynchronization therapy (CRT). These include Doppler echocardiographic measurements of mitral inflow or aortic outflow velocities, an arbitrarily fixed AVD, and calculations based on intracardiac electrogram (EGM) intervals. The present study was designed to compare the acute effects of AVD programming methods during CRT.
Methods and Results: We studied 28 patients at CRT implant with invasive measurements of LV dP/dt to determine the effect of AVD during atrial sensed (AS) and atrial paced (AP) modes. The optimal AVD, defined as that resulting in the maximal LV dP/dt, was then compared with that predicted by several noninvasive methods. CRT increased LV dP/dt 11%± 11% during AS (heart rate: 73 ± 14 bpm) and 17%± 12% during AP (heart rate: 86 ± 12 bpm) (P < 0.001 vs AS). There was an excellent correlation between the EGM method and the maximum achievable LV dP/dt (AS: R²= 0.99, P < 0.0001, AP: R²= 0.96, P < 0.0001) and this method performed better than other techniques.
Conclusions: An electrogram-based optimization method accurately predicts the optimal AVD among patients over a wide range of QRS intervals during CRT in both AS and AP modes. This simple technique may obviate the need for echocardiography for AVD programming.     

Frequency mapping of the pulmonary veins in paroxysmal versus permanent atrial fibrillation

Introduction: The pulmonary veins (PVs) are a dominant source of triggers initiating atrial fibrillation (AF). While recent evidence implicates these structures in the maintenance of paroxysmal AF, their role in permanent AF is not known. The current study aims to compare the contribution of PV activity to the maintenance of paroxysmal and permanent AF.
Methods and Results: Thirty-four patients with paroxysmal AF (n = 20) or permanent AF (n = 14) undergoing ablation were studied. Prior to ablation, 32 seconds of electrograms were acquired from each PV and the coronary sinus (CS). The frequency of activity of each PV and CS was defined as the highest amplitude frequency on spectral analysis. The effects of ablation on the AF cycle length (AFCL) and frequency and on AF termination were determined. Significant differences were observed between paroxysmal and permanent AF. Paroxysmal AF demonstrates higher frequency PV activity (11.0 ± 3.1 vs 8.8 ± 3.0 Hz; P = 0.0003) but lower CS frequency (5.8 ± 1.2 vs 6.9 ± 1.4 Hz; P = 0.01) and longer AFCL (182 ± 17 vs 158 ± 21 msec; P = 0.002), resulting in greater PV to atrial frequency gradient (7.2 ± 2.2 vs 4.2 ± 2.9 Hz; P = 0.006). PV isolation in paroxysmal AF resulted in a greater decrease in atrial frequency (1.0 ± 0.7 vs −0.05 ± 0.4 Hz; P < 0.0001), greater prolongation of the AFCL (49 ± 35 vs 5 ± 6 msec; P < 0.0001), and more frequent AF termination (11/20 vs 0/14; P = 0.0007) compared to permanent AF.
Conclusion: Paroxysmal AF is associated with higher frequency PV activity and lesser CS frequency compared to permanent AF. Isolation of the PVs had a greater impact on the fibrillatory process in paroxysmal AF compared to permanent AF, suggesting that while the PVs have a role in maintaining paroxysmal AF, these structures independently contribute less to the maintenance of permanent AF.     

Critical Atrial Site for Ablation of Pacing-Induced Atrial Fibrillation in the Normal Dog Heart

Site for Ablation of AF in Dogs. Introduction: Radiofrequency catheter ablation (RFA) has been used recently to treat atrial fibrillation (AF). The purpose of this study was to investigate a new approach to preventing AF by RFA.
Methods and Results: In open chest, anesthetized dogs, AF (lasting > 30 sec) was induced after burst stimulation, and electrophysiologic parameters were recorded before and after RFA. In group 1 (9 dogs) we performed selective and combined slow and fast pathway RFA, whereas in group 2(11 dogs) RFA was applied as a linear lesion at the mid-atrial septum between the inferior vena cava and the fossa ovalis. After ablation, the Wenckebach cycle length was significantly prolonged only in group 1 (194 ± 23 vs 282 ± 35 msec, P = 0.002). whereas the interval between the stimulus (S) artifact applied at the high right atrium to the His hundle (H) (SH interval) prolonged to the same extent in both groups (162 ± 14 vs 146 ± 45 msec. P = NS); group 1 due to an A-H prolongation whereas in group 2 it was due to an intra-atrial conduction delay. In group 1 AF still remained inducible, although with a longer mean R-R interval (215 ± 16 vs 433 ± 88 msec, P < 0.05). No instance of complete AV block developed. In group 2, sustained AF was noninducible in 10 dogs and its duration was markedly shorter in the remaining one (8 sec). Gross anatomy and histology did not reveal any damage inside of Koch's triangle, and particularly to the compact AV node.
Conclusion: These findings suggest that RFA at the mid-atrial septum prevents AF in the normal dog heart. This approach might also be successful in those clinical settings in which the atrial septum plays a critical role in the maintenance of sustained AF.     

Cardiac Parasympathetic Stimulation via QRS-Synchronous Low-Energy Shocks In Humans

Parasympathetic Stimulation via Intracardiac Shocks. Introduction: In patients receiving test shocks to verify lead connections at implantation, we anecdotally have observed postshock delay. The purpose of this study was to determine whether QRS-synchronous low-energy shocks delivered by implantable defibrillators result in postshock cycle length prolongation, and to determine the mechanism of this phenomenon.
Methods and Results: Twenty-five patients undergoing defibrillator testing were studied, three with epicardial patches and 22 with transvenous leads. Each patient received QRSsynchronous shocks of 0.2, 0.4, 0.6, and 2.0 J in random order. Patients were further randomized to receive either saline or 2.0 mg atropine intravenously, and then given a second sequence of shocks. At baseline, the postshock cycle length (1, 035 ± 245 msec) was significantly longer than the preshock cycle length (968 ± 177 msec, P = 0.01). In patients with a coronary sinus (CS) or superior vena cava (SVC) lead, the mean prolongation was 91 ± 160 msec, compared with 12 ± 106 msec for patients without such a lead (P < 0.0001). All energy levels resulted in significant postshock prolongation compared with preshock cycle lengths (P < 0.05). Postshock prolongation before atropine was 76 ± 162 msec, compared with −13 ± 52 msec afterward (P < 0.00001). Biphasic shocks resulted in greater postshock prolongation than monophasic shocks of equal energy.
Conclusion: Low-energy shocks delivered during the QRS complex cause postshock cycle length prolongation in man. This effect required the presence of a CS or SVC lead. Atropine inhibited this effect, suggesting the phenomenon was mediated by direct cardiac parasympathetic nerve stimulation by the intracardiac shock.     

Electrophysiologic spectrum of concealed intranodal conduction during atrial rate acceleration in a model of 2:1 atrioventricular block

Concealed anterograde penetration of the atrioventricular (AV) node has been used to explain a wide variety of electrocardiographic findings. The effects of atrial rate acceleration on this phenomenon remain undefined. To examine the dynamic interrelations between conducted and nonconducted beats at different atrial rates, a unique atrial pacing protocol of functional 2:1 AV block was used in 10 patients. The pacing protocol involved abrupt transitions from 2:1 to 1:1 AV conduction and enabled quantification of conduction delay produced by nonpropagated impulses over extremes of atrial rate. Stable 2:1 AV conduction was maintained over a mean range of atrial paced cycle lengths of 289 +/- 29.6 to 223 +/- 33.0 msec, respectively. The mean AV conduction time during 2:1 and corresponding 1:1 drives at the longest atrial paced rates were 169 +/- 33.5 and 136.5 +/- 26.9 msec, respectively--revealing a significant effect of nonpropagated impulses on subsequent conduction. Surprisingly, at the shortest atrial paced rates, the mean AV conduction times were 191.5 +/- 31.8 and 161.0 +/- 23.3 msec, respectively. The lack of significant changes in conduction time between 2:1 and 1:1 drives at the extremes of atrial rate (32.5 vs. 30 msec, p = NS) suggests that the effect of concealed conduction is "fixed" and independent of rate. Clinical implications and postulated electrophysiologic mechanisms are discussed.     

Do Population Studies Confirm the Benefit of Oral Anticoagulation in Atrial Fibrillation Demonstrated in Clinical Trials?

OBJECTIVES OF STUDY: We developed a method to record extracellular A-V nodal potentials in the beating dog heart, in vivo. METHODS: In eleven Na-pentobarbital anesthetized, open-chest dogs, an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted through a purse-string suture in the coronary sinus (CS) distal to the ostium and positioned electrographically so that the tip electrode recorded a His bundle (Hb) potential. RESULTS: Stable recordings of A-V nodal potentials (amplitude, 178 +/- 94 microV; duration 78 +/- 26 msec) were consistently made during sinus rhythm from the second and/or third bipolar pairs of electrodes. Programmed atrial stimulation and vagal stimulation resulted in loss of amplitude and increased duration of the A-V nodal potentials associated with A-H prolongation. In another series of experiments, crushing the sinus node in 6 dogs resulted in AV nodal rhythms with AV nodal potentials of varying amplitudes (132 to 840 microV) and durations (range 25 to 71 msec) as the earliest activation which preceded the Hb, atrial and ventricular deflections. One dog, showing dual AV nodal physiology as documented from the AV nodal function curve, had two distinctly different AV nodal potentials. The low-level, longer duration potentials were associated with longer (slow pathway) A-H intervals; whereas the shorter higher amplitude potentials (fast pathway) showed shorter A-H intervals, each occurring at a critical paced cycle length. CONCLUSION: We conclude that consistent extracellular AV nodal electrograms can be recorded in vivo although the configuration of these potentials varies depending on heart rate, autonomic stimulation and different arrhythmic conditions such as AV nodal escape rhythms and dual AV nodal physiology.     

Biventricular pacing and QT interval prolongation

Introduction: The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB).
Methods and Results: One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 ± 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 ± 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 ± 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 ± 9 ms during BiV pacing vs 178 ± 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 ± 34 ms with BiV pacing versus 445 ± 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 ± 9 ms vs 320 ± 20 ms, P < 0.0001). During a mean follow-up of 24 ± 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued.
Conclusion: Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.