Atrial Stimulus Research Articles

Right Ventricular Pressure Shows Greater Sensitivity Than Left Ventricular Pressure to Dual Chamber Coupled Pacing in Ischemic Heart Failure Dogs

Dual chamber coupled pacing (DCCP) has potential as a therapy for patients with heart failure by increasing atrial and ventricular contractility and reducing the mechanical heart rate (MHR). DCCP has global effects on the heart due to the propagated depolarization and, therefore, it is likely that the increase in contractility is similar in the left and right ventricle. The objective of this study was to evaluate the effects of DCCP on right ventricular and left ventricular hemodynamics. Methods: Eight dogs were given serial intracoronary injections of microspheres until their ejection fraction dropped to # 35% (biplane echocardiography). The animals were then anesthetized with isoflurane and fentanyl and instrumented with pressure sensors in the RV, LV and aorta during closed-chest surgery. Pacing leads were placed in the right atrial appendage and RV apex. DCCP was performed with stimuli that were delivered to the RV 10, 30, 50, 100 and 150 ms after the effective refractory period. The order of the different coupling intervals was randomized. An atrial premature stimulus was delivered 60 ms prior to the ventricular stimulus. Hemodynamic data during normal sinus rhythm (NSR) and DCCP were gathered for one minute. The median of the final 30 seconds of each period was used to calculate the following parameters for both the RV and LV: maximum change in pressure with respect to time (dPdtmax), maximum pressure (max), pulse pressure (pulse), mechanical heart rate (MHR), and mean arterial pressure (mABP). Results: Significant differences between the right and left ventricular responses to DCCP were seen when potentiation was greatest at the shortest coupling interval (10 ms). At this setting the percent change in RVPmax and RVPpulse was significantly greater than LVPmax and LVPpulse. As shown in the Figure below, dPdtmax was not significantly different. Discussion: DCCP has always been assumed to affect the left and right heart equally. These data suggest that there may be significant differences in the effects of DCCP on the left and right heart. These differences might be due to the site of delivery of the premature ventricular stimulus.

Utilization of the ics3000 programmer to measure interatrial conduction intervals and to optimize the av delay in patients with biventricular pace-makers and icds irrespective of make and model

The current Biotronik ICS3000 programmer software enables recording of a filtered esophageal left atrial electrogram (LAE) in addition to the surface ECG. It can be utilized to measure interatrial conduction intervals (IACT) in patients with DDD systems irrespective of make and model. Aims To study relations between interatrial conduction intervals and optimal Doppler AV delay (AVD) in biventricular paced congestive heart failure (CHF) patients and to test ICS3000 for simplified AVD optimization. Methods LAE and transmitral flow (TMF) were recorded simultaneously to measure determinants of the optimal AV delay (AVD) in 32 CHF patients (21 Medtronic, 11 Biotronik DDD or ICD systems: 20m, 12f, 65,3±10,4y, NYHA III, QRS150ms): Programming unphysiologically long AVD in VDD operation, 1. IACT was AVD minus interval between left atrial deflection (LA) and ventricular stimulus (Sv). 2. Duration of undisturbed left atrial electromechanical contribution (LA-EAClong) was measured between LA and end of atrial contribution (EAC) in TMF. During unpysiologically short AVD in DDD operation we measured 3. IACT between atrial stimulus and LA and 4. the latency of prematurely ending atrial contribution (Sv-EACshort) between Sv and EAC in TMF. In VDD and DDD operation, optimal AVD was calculated by the formula AVDoptimal = IACT + LA-EAClong - Sv-EACshort . Results Results are demonstrated in the table as mean±SD: View this table: Conclusions 1. Optimal AVD in CHF patients was found to be on average 45ms longer than individual interatrial conduction interval. Thus, 2. irrespective of make and model, the ICS3000 programmer based LEA can be used to approximate the optimal AVD in biventricular pacing by adjusting about 45ms between left atrial deflection and ventricular stimulus.

Evaluation of the Atrial Evoked Response for Capture Detection with High‐Polarization Leads

AutoCapture based on the evoked response can be confounded by electrode polarization. In this study, polarization was measured in human subjects who had chronic atrial leads. The aim of the study was to determine whether electrode polarization can be measured using a time integral atrial evoked-response integral (AERI) of the negative portion of the atrial paced ER evoked-response signal and to determine whether high-polarization atrial leads unsuitable for AutoCapture can be identified a priori. Atrial intracardiac-electrogram (IEGM) signals from 39 patients with implanted pacemakers were recorded and analyzed. The signals were recorded during conventional atrial-threshold searches. A total of 221 atrial-capture thresholds were recorded, ranging from 0.25 to 2.75 V with a mean of 0.79 V. Each evoked response was evaluated using the AERI in a 36 ms window following the 0.4 ms atrial stimulus. The polarization was estimated as a linear function of stimulus voltage using the evoked-response signal integral of captured beats identified on the IEGM. The 221 threshold-search datasets were obtained using leads with eight different electrode materials. Polarization could be measured using AERI as a function of stimulus voltage. Furthermore, this polarization measure can be used to identify high-polarization leads, which are ill suited for the atrial AutoCapture algorithm.

Effects of a blocked atrial beat on the atrioventricular nodal recovery property in patients with dual nodal pathways.

Dual AVN physiology can be demonstrated by a variety of maneuvers. To determine whether AVN recovery times following a blocked extrastimulus facilitate or obscure detection of dual AVN physiology, 11 patients (9-17 years) were studied with dual AVN pathways by using single and double atrial extrastimuli. With a single atrial extrastimuli, the premature atrial stimulus (A2) was coupled to basic atrial beats (A1). The fast and slow AVN recovery curves were constructed with plots of the nodal conduction time against the recovery time (A1A2,A2H2). With double atrial extrastimuli, a fixed blocked A2 beat (A2B) was followed by a scanning atrial beat (A3). The nodal recovery property post-A2B was studied by plots of A2BA3,A3H3. In all patients the recovery curve of the fast pathway post-A2B had a leftward shift when compared to that of the pre-A2B curve (i.e., the AH was shortened at the same recovery time). The window of slow pathway conduction post-A2B disappeared totally in five patients and decreased significantly in six patients (post-A2B: 26 +/- 42 ms; pre-A2B: 80 +/- 65 ms, P < 0.05). In the six patients that still had slow pathway conduction post-A2B, the slow pathway effective refractory period post-A2B was significantly less than that of pre-A2B (215 +/- 38 vs 268 +/- 16 ms, P < 0.05). The fast pathway effective refractory period post-A2B was also diminished significantly (235 +/- 62 vs 357 +/- 76 ms, P < 0.0001). The authors conclude that blocked atrial beats decrease the visibility of the slow pathway conduction.

Paradoxical induction of cross-talk in a dual chamber pacemaker by increasing the ventricular output.

Cross-talk was induced in a unipolar DDD pacemaker by increasing the output of the ventricular channel. Oversensing by the ventricular channel was probably due to the detection of a relatively large summation signal consisting of the afterpotential and the superimposed activity from the atrial stimulus.

Case report: complex arrhythmia induced by noncompetitive atrial pacing algorithm of DDDR pacemaker.

This report describes the occurrence of a repetitive nonreentrant ventriculoatrial (VA) synchronous rhythm precipitated by the noncompetitive atrial pacing algorithm of a Medtronic DDDR pacemaker. This algorithm delivers an atrial stimulus 300 ms after the detection of an atrial signal in the postventricular atrial refractory period of the pacemaker. In our patient, the atrial stimulus released by the algorithm was ineffectual because it encountered prolonged refractoriness of the atrial myocardium. This situation produced a repetitive nonreentrant VAl synchronous rhythm in the setting of retrograde VA conduction.

Pacemaker repetitive nonreentrant ventriculoatrial synchronous rhythm. A review.

Ventriculoatrial (VA) synchrony during dual chamber pacing can occur in any patient who has the ability to sustain repeated retrograde conduction. If the retrograde P wave is sensed, the result will be an endless loop tachycardia or repetitive reentrant VA synchrony. VA synchrony can also occur when a dual chamber pacemaker does not sense a retrograde P wave within the postventricular atrial refractory period. In this situation if the normally suprathreshold atrial stimulus at the end of the atrial escape interval is continually delivered when the atrial myocardium is physiologically refractory, the result will be a repetitive nonreentrant VA synchronous rhythm. Repetitive nonreentrant VA synchrony may produce unfavorable hemodynamic consequences and the pacemaker syndrome. It represents an example of functional atrial undersensing combined with functional loss of atrial capture. Management requires modification of the programmed settings of the pacemaker and utilization of certain algorithms designed for other functions but nevertheless effective in this situation.

Eccentricities of dual chamber implantable pacemakers.

The consequences of a short 160 ms postventricular atrial refractory period (PVARP) were studied in 27 patients with Medtronic Elite series of pacemakers (programmed to the unipolar mode) by using chest wall stimulation and myopotential interference. Because the ventricular refractory period is nonprogrammable at 230 ms, appropriately timed signals produced As-Vr combinations where As is an atrial sensed event and Vr is a ventricular event detected in the ventricular refractory period. The As-Vr combination inhibited the release of the atrial stimulus at the completion of the atrial escape interval in the DDI, DDIR, DDD, and DDDR modes. A paced ventricular beat (Vp) was documented to initiate automatic PVARP extension in circumstances where Vp was preceded by a Vr event and the pacemaker interpreted the Vr-Vp sequence as 2 ventricular events without an intervening atrial event and Vp as a ventricular premature beat. Knowledge of these eccentricities should facilitate the interpretation of complex pacemakers responses to interference.

Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli.

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.

Effects of procainamide and dl-sotalol on the changes of atrial electrophysiology induced by high current stimulation.

The relation between high current atrial stimulation and antiarrhythmic drugs was not clear. We evaluated the effects of procainamide and dl-sotalol on the electrophysiological changes induced by high current stimulation. Effects of high current atrial stimulation on effective refractory period, dispersion of refractoriness, conduction velocity, and wavelength of the earliest atrial premature beat were evaluated at baseline and after infusion of procainamide (10 patients) and dl-sotalol (10 patients). High current atrial stimulation shortened effective refractory period locally (-12% +/- 4.0%, -7.0% +/- 3.0%, -5.1 +/- 3.3%, and -3.0 +/- 2.0%, at 0, 7, 14, and 21 mm from the S1 stimulation site, respectively; P < 0.001); increased the dispersion of refractoriness (from 17.8 +/- 8.5 to 27.4 +/- 12.5 ms, P < 0.001); decreased conduction velocity of the earliest premature beat (from 0.58 +/- 0.10 to 0.52 +/- 0.09 ms, P = 0.01); and decreased wavelength of the earliest atrial premature beat (from 10.9 +/- 2.4 to 8.8 +/- 2.1 cm, P < 0.001). These effects of high current stimulation persisted after procainamide infusion. However, after dl-sotalol infusion, high current atrial stimuli did not change the dispersion of refractoriness (23.1 +/- 10 ms vs 26.4 +/- 10.4 ms; P > 0.05, twice diastolic threshold vs 10 mA); conduction velocity of the earliest premature beat (0.54 +/- 0.06 ms vs 0.50 +/- 0.06 ms, P > 0.05); or wavelength of the earliest premature atrial beat (11.5 +/- 1.6 m/s vs 10.1 +/- 1.7 cm; P > 0.05). Although high current atrial stimulation shortened effective refractory period locally, increased dispersion of refractoriness, and decreased the wavelength of the earliest premature atrial impulse, these effects were abolished by dl-sotalol but not procainamide.

Inappropriate sensing of atrial stimuli in patients with third-generation defibrillators and DDD pacemakers.

Although the problem of ICD sensing of paced ventricular stimuli has been resolved by incorporation of VVI pacing into current ICDs, many patients required separate DDD pacemakers. We report a problematic PM-ICD interaction: the inability to prevent sensing of paced atrial stimuli ("atrial sensing") leading to double-counting in DDD-PM-requiring patients with transvenous (TV) ICDs with aggressive autogain sensing (CPI Ventak PRxII or III). Four of eight patients receiving both transvenous DDD PMs and ICDs (CPI Endotak lead, at the RV apex), had atrial sensing, leading to double counting, despite intraoperative testing of multiple atrial locations with an active fixation lead. Five patients had a PRxII/III ICD, four with atrial sensing (80%), and three a PRx without atrial sensing. Patients with atrial sensing were not distinguished by any clinical or device related variable. In patients with atrial sensing (all with heart block), the PM was programmed to VDD mode. No patient has received inappropriate therapy or failed to sense VF in follow-up. In many patients with TV ICDs who required DDD pacing, no atrial position can be found without ICD sensing of atrial stimuli. While in patients with heart block this problem can be circumvented by programming to the VDD mode, in patients with sinus incompetence it may only be resolved by the combination ICD-DDD PM, currently in development.

The effect of variable retrograde penetration on dual AV nodal pathways: observations before and after slow pathway ablation LDD.

Retrograde VA conduction is usually over the fast pathway and rarely over the slow pathway in patients with dual AV nodal pathways. It is unknown whether this apparent unidirectional conduction of the slow pathway is due to the lack of its retrograde conducting ability or the result of concealment. The effect of variable retrograde AV nodal penetration on antegrade AV nodal conduction was determined in patients with typical AV nodal reentrant tachycardia before and after the slow pathway ablation. Variable retrograde penetration was produced by delivering a ventricular extrastimulus simultaneously with (VE-0), 50 ms after (VE-50), or 100 ms after (VE-100) the last basic atrial stimulus, while atrial extrastimuli were used to determine changes of anterograde AV nodal effective refractory period (ERP) and A-H interval. The AV nodal functions measured without the ventricular extrastimuli served as the baseline. Although the mean slow pathway ERP was not significantly different among the different stimulation protocols, a significant shortening of the slow pathway conduction time (A-H from 348 +/- 60 to 324 +/- 119 ms, P < 0.05) was observed with upper level retrograde penetration of the AV node (VE-0). This facilitating effect became a prolonging effect when the retrograde penetration level moved to the lower level (VE-100, A-H from 324 +/- 119 to 366 +/- 122 ms, P < 0.05). The fast pathway ERP shortened with an upper level penetration (VE-0) but tended to prolong with a lower level retrograde-penetration (VE-100) both before and after the slow pathway ablation (preablation, from 348 +/- 143 of the baseline to 302 +/- 114 to 360 +/- 143 ms, P < 0.05; postablation, from 314 +/- 101 of the baseline to 274 +/- 118 to 361 +/- 143 ms, P < 0.05). The mean A2-H2 interval of the slow pathway was significantly shorter than the baseline (350 +/- 44 ms) with VE-0 (249 +/- 48 ms, P < 0.05) and VE-50 stimulation (285 +/- 82 ms, P < 0.05) but not with VE-100 stimulation (330 +/- 83 ms, P = NS). Before slow pathway ablation, the A2-H2 interval of the fast pathway at equal coupling intervals was shorter than the baseline (165 +/- 53 ms) with VE-0 (144 +/- 47 ms, P < 0.01) and VE-50 stimulation (152 +/- 43 ms, P < 0.05) but tended to be longer with VE-100 stimulation (175 +/- 47 ms, P = NS). After slow pathway ablation, the mean A2-H2 interval at the same coupling interval was shorter than the baseline (173 +/- 39 ms) with VE-0 (139 +/- 35 ms, P < 0.05), VE-50 (153 +/- 32 ms, P = 0.05) but tended to be longer with VE-100 stimulation (178 +/- 49 ms, P = NS). We conclude that: (1) concealed retrograde conduction can be demonstrated in both the slow and the fast AV nodal pathways; and (2) concealed retrograde conduction may either shorten or prolong anterograde refractoriness and conduction time, depending on the level of retrograde penetration.

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and...

Analysis of atrial sensed far-field ventricular signals: a reassessment.

Accurate detection of the spontaneous far-field ventricular signal may be used to determine the ventricular activation, and hence, the interval from atrial stimulus to the ventricular R wave (AR interval) using a standard atrial pacing lead. This can be useful in developing a physiological atrial rate responsive (AAIR) pacemaker and in further improving DDD(R) pacing algorithms. In order to better characterize the atrial sensed far-field ventricular signal, 200 consecutive patients undergoing pacemaker implantation were studied. The amplitude of the far-field ventricular signal was significantly smaller than that of the atrial deflection. In all recordings, the slew rate of the atrial deflection was larger than that of the far-field ventricular signal. Subdivision of the recordings by electrode position, pocket location, or QRS duration on the surface ECG resulted in significantly different signal characteristics. The amplitude and slew rate of the far-field ventricular signal were significantly smaller in bipolar versus unipolar sensing. Atrial sensed far-field ventricular recordings could also be obtained in the case of ventricular pacing. Our results indicate that accurate sensing of the far-field ventricular signal from an atrial pacing lead is conceivable in most patients. The different signal characteristics in relation to parameters, such as electrode position, sensing mode, and pocket location, may be useful in determining the optimal conditions for signal sensing.

Exercise induced sympathetic influences do not change interatrial conduction times in VDD and DDD pacing.

Using telemetry, right atrial electrogram (RA), and marker channel of atrial sense events (MA) in combination with the left atrial electrogram (LA), recorded by a filtered bipolar esophageal lead, interatrial conduction during submaximal exercise and at rest was examined in 46 DDD pacemaker patients. The RA-LA and MA-LA conduction times measured in the presence of atrial sensing (VDD) as well as the conduction time SA-LA from atrial stimulus (SA) to LA, determined during atrial pacing (DDD) were found to be individual constants independent of exercise induced sympathetic influences. Thus, having determined an optimal mechanical interval (LA-LV)mech/opt from left atrium to ventricle by other methods, the optimal AV delay for DDD as well as for VDD operation can be calculated by the sum of the appropriate interatrial conduction time (SA-LA, respectively MA-LA) and the (LA-LV)mech/opt interval. Due to the constant SA-LA and MA-LA, the difference between these two values (AV delay correction interval) is a constant as well, which remains unchanged during exercise. Therefore, in selecting the rate responsive AV delay, only hemodynamic and not electrophysiological measurements need to be considered.

Effect of continuous vagal enhancement on concealed conduction and refractoriness within the atrioventricular node

This study examined the complex interaction between vagal enhancement and how a concealed atrial impulse alters atrioventricular (AV) nodal function. In theory, vagal augmentation could increase or decrease the effect that a premature atrial beat has on the subsequent beat. In 10 patients we established the AV nodal effective refractory period (ERP) without and with a conditioning atrial stimulus(S c); the stimulation protocol was then repeated after enhancing reflex vagal tone with a continuous phenylephrine infusion. During phenylephrine infusion, the sinus cycle length prolonged from 827 ± 99 to 1,029 ± 223 ms (p < 0.001) and AV nodal ERP increased from 331 ± 51 to 425 ± 64 ms (p < 0.005). At control, AV nodal ERP in the presence of S c prolonged to 536 ± 69 ms (p < 0.001), and during phenylephrine infusion increased to 579 ± 57 ms (p < 0.01), a change significantly less than during control (58 ± 14% vs 31 ± 14%, respectively, p < 0.01). Further experiments suggest that the effect of Sc was reduced because it occurred earlier relative to the vagally prolonged AV nodal ERP. In conclusion, this study demonstrates a complex relation between the timing of a premature atrial beat causing concealed conduction and the degree of vagal tone. The concealed beat, as related to the AV node ERP, has a substantial effect on subsequent AV nodal conduction. These data give insights into clinical AV nodal function.

Inappropriate sensing of atrial stimuli in patients with a third generation defibrillator and DDD pacemaker

Inappropriate sensing of atrial stimuli in patients with a third generation defibrillator and DDD pacemaker

724-6 Resetting Responses During Atrioventricular Nodal Reentrant Tachycardia Suggest an Anisotropic Mechanism

We hypothesized that an anatomically determined circuit should have an identical excitable gap regardless of the site of stimulation, while a functional anisotropic circuit could show differences depending on stimulation site. In order to explore the nature of the reentrant circuit, and to characterize the excitable gap during atrioventricular nodal reentrant tachycardia (AVNRT), we determined the resetting response patterns in eight patients with typical AVNRT (meantachycardia cycle length (TCl) 346 ± 18 msec). Premature atrial stimuli were delivered during tachycardia from the area of the slow pathway (SPI in 7 patients, the fast pathway (FP) in 6 patients, and the ventricle (V) in 7 patients and the subsequent return cycles (As-Ar) were analyzed. In all patients, two or more sites were stimulated. Ventricular extrastimulation employed double extrastimuli such that the first extrastimulus did not interact with the circuit and acted as a conditioning stimulus. The excitable gap was defined as the range of coupling intervals from first reset to tachycardia termination. Duration of Excitable Gap (msec) by Stimulation Site Patient 1 2 3 4 5 6 7 8 Mean %TCL FP 10 * 65 20 30 20 10 * 26 ± 21 7 SP 35 80 90 40 * 20 20 20 43 ± 30 12 V 35 75 45 * 50 50 10 20 42 ± 19 12 AVNRT could be reset from the atrium and from the ventricle at all sites studied. In all cases, when the coupling intervals of premature extrastimuli were plotted against the return cycle (As-Ar), an increasing resetting response pattern was obtained. There was no decremental conduction over the retrograde FP with V stimulation. 1) The reentrant circuit of AVNRT can be reset from multiple sites. 2) The circuit as a whole demonstrates partial excitability with heterogenicityof conduction over individual pathways. 3) A difference in the measured excitable gap of &gt; 20 msec dependent on stimulation site was seen in 5/8 patients and suggests a functionally determined circuit and anisotropic reentry.

Site of accessory pathway block after radiofrequency catheter ablation in patients with the Wolff-Parkinson-White syndrome.

Recent studies have demonstrated that the most common site of accessory pathway conduction block following the introduction of a premature atrial stimulus during atrial pacing is between the accessory pathway potential and the ventricular electrogram, consistent with block at the ventricular insertion of the accessory pathway. However, no prior study has evaluated the site of conduction block during radiofrequency catheter ablation procedures. Therefore, the objective of this study was to determine the site of conduction block after catheter ablation of accessory pathways by analyzing and comparing the local electrograms recorded before and after radiofrequency energy delivery at successful ablation sites. The electrograms evaluated in this study were obtained from 85 consecutive patients who underwent successful radiofrequency catheter ablation of a manifest accessory pathway. The 50 left free-wall accessory pathways were ablated using a ventricular approach and the 35 right free-wall or posteroseptal accessory pathways were ablated using an atrial approach. The characteristics of local electrograms recorded immediately before and immediately after successful ablation of the accessory pathway were determined in each patient. The site of accessory pathway block was determined by comparing the amplitude, timing, and morphology of the local electrograms at successful sites of radiofrequency catheter ablation before and after delivery of radiofrequency energy. A putative accessory pathway potential was present at the successful target site in 74 of the 85 patients (87%). Conduction block occurred between the atrial electrogram and the accessory pathway potential in 66 patients (78%) and between the accessory pathway potential and the ventricular electrogram in eight patients (9%). The site of block could not be determined in 11 patients (13%) in whom an accessory pathway potential was absent. Conduction block occurred most frequently between the atrial electrogram and the accessory pathway potential regardless of accessory pathway location. No electrogram parameter or accessory pathway characteristic was predictive of the site of conduction block. The results of this study demonstrate that conduction block occurs most frequently between the local atrial electrogram and the accessory pathway potential during radiofrequency catheter ablation of accessory pathways. This is true regardless of whether the accessory pathway is ablated from the atrial or ventricular aspect of the mitral or tricuspid annulus.

Measurements of cardiac output by impedance cardiography in pacemaker patients at rest: Effects of various atrioventricular delays

Objectives. The purpose of this study was to evaluate the ability of impedance cardiography to determine the change in cardiac output caused by modifications in the atrioventricular (AV) delay in DDD (dual-chamber) pacing mode while pacing the atrium and ventricle at different programmed rates.Background. Impedance cardiography permits continuous noninvasive monitoring of hemodynamic variables on a beat to beat basis.Methods. Eleven patients with a DDD pacemaker were evaluated by impedance cardiography. Stroke volume, cardiac output and total peripheral resistance were assessed in the supine rest position during both DDD and ventricular (VVI) pacing. Hemodynamic variables were measured during DDD pacing at rates ranging from 60 to 110 beats/min in 10-beats/min increments with programmed AV delay varying from 50 to 250 ms in 50-ms increments. When the pacemaker was reprogrammed to the VVI pacing mode, these measurements were repeated at the same pacing rates.Results. Cardiac output measurements during programmed conditions were found to be highly reproducible. The mean coefficient of variation was 3% during DDD pacing; it was 6% in the VVI pacing mode. A large decrease in cardiac output (≈30%) was found when i pacemaker was reprogrammed from the DDD to the VVI pacing mode. At DDD pacing rates between 70 to 110 beats/min, the highest cardiac output occurred at an average AV delay of < 120 ms from atrial stimulus to ventricular stimulus. At an average AV delay of ≥200 ms, the cardiac output in the DDD and VVI pacing modes was similar.Conclusions. 1) Impedance cardiography allows highly reproducible noninvasive assessments of cardiac output in pacemaker patients; 2) inappropriate programming of the AV interval in patients with atrial and ventricular pacing can decrease cardiac output significantly, and the extent of the decrease is similar to or less than that observed in ventricular pacing; 3) hemodynamic measurements obtained with impedance cardiography can facilitate optimal programming of pacemaker variables.