Relationship Between Interatrial Conduction Times and Left Atrial Dimension in Patients Undergoing Atrioventricular Stimulation

Interatrial conduction time (IACT) and left atrial dimension (LAD) were determined in 75 patients (41 males, 34 females, mean age 78.2 ± 7,9 years) undergoing atrioventricular (AV) stimulation. The LAD was measured by M mode echocardiography as the distance between the posterior aortic wall and the posterior left atrial wall. The IACT was determined during a transvenous dual chamber pacemaker implant done under local anesthesia (lidocaine). The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the right atrium recorded in a unipolar mode (unipolar J-shaped had positioned in the right appendage) to the ID of the left atrium (bipolar esophageal lead, left atrial positive deflection equal to the negative one) during sinus rhythm. The right atrium then was paced at a rate slightly greater than the spontaneous one. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID. The PIACT was also measured during incremental right atrial pacing (10 beats/min step increase to 180 beats/min) and, from these measurements, the maximum increase of PIACT (MIPIACT) was deduced. The LAD was measured at 39.5 ± 8.7 mm, SIACT at 70.3 ± 24.8 msec, PIACT at 118.8 ± 27.9 msec, and MIPIACT at 16.5 ± 16.4 msec. We found highly significant relationships between SIACT and LAD(P = 0.0006, r - 0.39), PIACT and LAD (P = 0.0001, r = 0.45), and MIPIACT and LAD (P = 0.0006, r = 0.38). We also noted that the LAD was greater in patients in whom MIPIACT was >10 msec than in patients in whom the MIPIACT was negligible (P < 0.002). However, the “r” values indicate that IACT is probably determined by multiple factors, and LAD appears to be one of the most important. Thus, we demonstrated the existence of highly significant relationships between the LAD determined by M mode echocardiography and the IACT when sensing and pacing the right atrium. We also demonstrated that the LAD was greater in patients in whom PIACT increased by an appreciable duration during fast atrial pacing. These results must be kept in mind when choosing a mode of stimulation and determining the AV delay (dual chamber pacemaker), particularly in patients with left atrial enlargement in whom the contribution of the atrial contraction and its timing are hemodynamically determinant.     

Atrial Septal Pacing to Synchronize Atrial Depolarization in Patients with Delayed Interatrial Conduction

The current method of pacing the right atrium from the appendage or free wall is often the source of delayed intraatrial conduction and discoordinate left and right atrial mechanical function. Simultaneous activation of both atria with pacing techniques involving multisite and multilead systems is associated with suppression of supraventricular tachyarrhythmias and improved hemodynamics. In the present study we tested the hypothesis that pacing from a single site of the atrial septum can synchronize atrial depolarization. Five males and two females (mean age 58 ± 6 years) with drug refractory paroxysmal atrial fibrillation (AF) were studied who were candidates for AV junctional ablation. All patients had broad P waves (118 ± 10 ms) on the surface ECG. Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle, and distal coronary sinus (CS) were recorded. The atrial septum was paced from multiple sites. The site of atrial septum where the timing between HRA and distal CS (d-CS) was ≤ 10 ms was considered the most suitable for simultaneous atrial activation. An active fixation atrial lead was positioned at this site and a standard lead was placed in the ventricle. The interatrial conduction time during sinus rhythm and AAT pacing and the conduction time from the pacing site to the HRA and d-CS during septal pacing were measured. Atrial septal pacing was successful in all patients at sites superior to the CS os near the fossa ovalis. During septal pacing the P waves were inverted in the inferior leads with shortened duration from 118 ± 10 ms to 93 ± 7 ms (P < 0.001), and the conduction time from the pacing site to the HRA and d-CS was 54.3 ± 6.8 ms and 52.8 ± 2.5 ms, respectively. The interatrial conduction time during AAT pacing was shortened in comparison to sinus rhythm (115 ± 18.9 ms vs 97.8 ± 10.3 ms, P < 0.05). In conclusion, simultaneous activation of both atria in patients with prolonged interatrial conduction time can be accomplished by pacing a single site in the atrial septum using a standard active fixation lead placed under electrophysiological study guidance. Such a pacing system allows proper left AV timing and may prove efficacious in preventing various supraventricular tachyarrhythmias.     

Atrioventricular Interval Optimization in the Right Atrial Appendage and Interatrial Septum Pacing: A Comparison Between Echo and Peak Endocardial Acceleration Measurements

PADELETTI, et al. : Atrioventricular Interval Optimization in the Right Atrial Appendage and Interatrial Septum Pacing: A Comparison Between ECHC and Peak Endocardial Acceleration. Interatrial septum pacing (IASP) reduces interatrial conduction time and consequently may interfere with atrioventricular delay (AVD) optimization. We studied 14 patients with an implanted BEST Living system device able to measure peak endocardial acceleration (PEA) signal. The aims of our study were to compare the (1) optimal AVD (OAVD) in right atrial appendage pacing (RAAP) and IASP, and (2) OAVD derived by the PEA signal versus OAVD derived by Echo/Doppler evaluation of the left ventricular filling time (LVFT) and cardiac output (CO). Measurements were performed in DDD VDD modes Eight patients (group A) had RAAP and six patients (group B) had IASP. In group A, OAVD measured by LVFT, CO, and PEA was 185 ± 23 ms , 177 ± 19 ms , and 192 ± 23 ms in DDD and 147 ± 19 ms , 135 ± 27 ms , and 146 ± 20 ms in VDD, respectively. OAVD measured by LVFT, CO, and PEA was significantly longer in DDD mode than in VDD (P < 0.01, P < 0.01, P < 0.001 ). In group B, OAVD measured by LVFT, CO, and PEA was 116 ± 19 ms , 113 ± 10 ms , and 130 ± 30ms in DDD and 106 ± 16 ms , 96 ± 15 ms , and 108 ± 26 ms in VDD, respectively. No statistical differences were observed between DDD and VDD. Significant correlations between OAVDs PEA derived and OAVDs LVFT and CO derived were observed (r = 0.71, r = 0.69, respectively ). When new techniques of atrial stimulation, as IASP, are used an OAVD shorter and similar in VDD and DDD has to be considered. The BEST Living system could provide a valid method to ensure, in every moment, the exact required OAVD to maximize atrial contribution to CO.     

Transvenous Left Atrial and Left Ventricular Pacing in Ebstein's Anomaly with Severe Interatrial Conduction Block

The implantation of permanent pacemakers in patients with congenital heart disease can be challenging. This report describes the complexity of pacemaker implantation in a patient with Ebstein's disease, tricuspid valve replacement, and right atrial abnormalities like severe intra- and interatrial conduction block that prevented dual chamber pacing from conventional sites. This case illustrates the promising possibility to circumvent the interatrial conduction block with single left atrial pacing instead of biatrial pacing which was not suitable here.     

Interatrial Conduction During Cardiac Pacing

DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 ± 18 ms during sinus rhythm to 122 ± 30 ms during right atrial pacing (p < 0.001). In 16 patients with P wave duration < 110 ms interatrial conduction prolonged from 85 ± 10 ms during sinus rhythm to 111 ± 9 ms during right atrial pacing (p < 0.01) compared to 114 ± 20 ms prolonging to 111 ± 19 ms (p < 0.01] in 9 patients with P wave duration > 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60–160 heats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p < 0.0001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.     

DDD pacing and interatrial conduction block: importance of optimal AV interval setting

The case of a 83-year-old patient undergoing DDD pacemaker implantation for sick sinus syndrome with postimplant detection of advanced interatrial conduction block is described. At nominal AV interval programming values (175 ms), absence of P wave following an atrial spike was observed, and the presence of an interatrial conduction disturbance was demonstrated by a Doppler transmitral flow pattern analysis and transesophageal ECG recording. AV interval lengthening up to 300 ms resulted in proper timing of atrial and ventricular contractions. Awaiting for conclusive data about biatrial pacing, interatrial conduction blocks can be managed in some cases by proper programming of conventional DDD systems.     

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 (M_A) 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 M_A-LA conduction times measured in the presence of atrial sensing (VDD) as well as the conduction time S_A-LA from atrial stimulus (S_A) to LA, determined during atrial pacing (DDD) were found to be individual constants independent of exercise induced sympathetic influences. Thus, having determined an optima! 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 (S_A-LA, respectively M_A-LA) and the (LA-LV)_mech/opt interval. Due to the constant S_A-LA and M_A-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 electrophysiologica] measurements need to be considered.     

Atrial and Ventricular Stimulation Threshold Development: A Comparative Study in Patients with a DDD Pacemaker and Two Identical Carbon-Tip Leads

The atrial and ventricular pacing threshold development during the first postoperative year was studied in a group of patients receiving DDD pacemakers. Identical carbon-tip endocardial leads were implanted in atrium and ventricle. Atrial and ventricular voltage stimulation thresholds were measured at implantation, and noninvasively at 1 and 12 months thereafter. The atrial amplifier sensitivity required for adequate P wave sensing during follow-up was also determined. The possible influence of a number of factors upon atrial and ventricular threshold evolution was statistically assessed. The threshold data were complete in 57 patients (mean age +/- SD, 65.2 +/- 12.4 years). Thirteen patients had a diagnosis of sinus node disease, whereas 44 had not. Patient age and diagnosis did not significantly influence atrial or ventricular stimulation threshold development. Atrial sensing thresholds were not related to atrial stimulation thresholds during follow-up. Atrial pacing thresholds were higher than ventricular thresholds at pacemaker implantation (P less than 0.00005), but the postoperative threshold rise and thresholds at 1 and 12 months postoperatively did not differ significantly between the atrium and ventricle. The ratio of chronic to acute stimulation thresholds was higher on the ventricular than on the atrial level (0.001 greater than P greater than 0.0005). The chronic atrial threshold showed a logarithmic relation to the threshold at implantation (P = 0.0006); postoperative threshold rise was not a significant determinant of the chronic atrial threshold (P = NS). On the ventricular level, the reverse was seen: The chronic threshold was related to the postoperative threshold rise (P = 0.0015, logarithmic relation), but not to the implantation threshold (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship Between Atrial Conduction Defects and Fractionated Atrial Endocardial Electrograms in Patients with Sick Sinus Syndrome

The relationship between abnormal atrial electrograms (AAE) recorded during sinus rhythm by endocardial calheter mapping of the right atrium and the afrial conduction defects of sinus impulses or single atrial extrastimuli was investigated in 44 patients with sick sinus syndrome. The patients were divided into two groups on the basis of the presence (n = 29) or absence (n = 15) of AAE recorded during sinus rhythm. The P wave duration in the AAE (+) Group patients was 137 ± 14 msec, and 125 ± 15 msec in (he AAE (−) Group; P < 0.02. The intraatrial conduction time of sinus impulses in the AAE (+) Group was 54 ± 12 msec, and 39 ± 9 msec in the AAE (−) Group; P < 0.001. The interatrial conduction time in the AAE (+) Group was 101 + 14 msec, and 78 ± 16 msec in the AAE (−) Group; P < 0.001. In the AAE (+) Group, H (38%) patients ha d a sinus node recovery time > 4 seconds, whereas in the AAE (−) Group there was only one (6%) patient; P < 0.03. AAE showed a specificity of 93% and a positive predictive accuracy of 91% in predicting inducibility of atrial fibrillation. The sensitivity was 35% and the negative predictive accuracy was 42%. Sustained atrial fibrillation was induced in ten (35%) patients of the AAE (+) Group, and in one (7%) patient of the AAE (−) Group; P < 0.05. These data suggest that in patients with sick sinus syndrome who possess abnormal endocardial eJectrograms in sinus rhythm within the right atrium have: (1) a significantly longer P wave duration: (2) a significantly longer intraatrial and interafrial conduction time of sinus impulses; and (3) a significantly greater sinus node dysfunction and higher incidence of induction of sustained atriai fibrillation. It is concluded that there are significantly greater atrial conduction defects in patients with sick sinus syndrome who possess AAE within the right atrium during sinus rhythm.     

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid-right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120-ms cycle length was performed five times at each pacing site to evaluate the in-ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200-ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.     

Single Lead DDD System: A Comparative Evaluation of Unipolar, Bipolar, and Overlapping Biphasic Stimulation and the Effects of Right Atrial Floating Electrode Location on Atrial Pacing and Sensing Thresholds

Single lead DDD pacing using unipolar or bipolar stimulation is limited by high atrial threshold. Overlapping biphasic (OLBI) waveform stimulation via atrial floating ring electrodes may preferentially enhance atrial pacing and avoid diaphragmatic pacing. Single lead DDD pacing with OLBI atrial pacing was studied in 12 patients (6 men and 6 women; mean age 74 ± 7 years) with complete heart block. At implantation, atrial bipolar rings (area 27 mm², separation 10 mm) were positioned at radiological defined high, mid, and low right atrial (RA) levels, and P wave amplitude and atrial and diaphragmatic pacing thresholds were determined in each position using unipolar, bipolar, and OLBI stimulation in random order. Although statistically insignificant, both the maximum and minimum sensed P wave amplitudes tended to be lower in the low RA position. Independent of the stimulation modes, minimum atrial pacing threshold occurred in the mid-RA. At mid-RA. the atrial pacing threshold was significantly lower with OLBI pacing compared with either unipolar or bipolar mode (3.9 ± 2.2 V vs 6.7 ± 3.5 V and 6.9 ± 3.5 V, P < 0.05). Although the diaphragmatic thresholds were similar, OLBI pacing modes in the mid-RA and final location significantly improved the Safety margin for avoidance of diaphragmatic pacing compared with unipolar mode. There was no correlation between atrial pacing and sensing threshold. At predischarge testing, all but one patient who developed atrial fibrillation had satisfactory atrial capture and a stable atrial pacing threshold (day 0: 2.6 ± 1.1 V vs day 2: 3.2 ± 1.3V, P = NS). However, diaphragmatic pacing occurred in four of 11 (36%) patients, especially in the upright position (sitting and standing). Our preliminary clinical results suggest that OLBI pacing via atrial floating ring electrodes can reduce the atrial pacing threshold. To optimize atrial pacing and sensing, the bipolar electrodes should be located at the mid-RA level first, although the high RA is an alternative. Despite significant improvements in the safety margin for diaphragmatic pacing with OLBI pacing, diaphragmatic stimulation remains a clinical problem.     

Atrial Natriuretic Factor Release During Exercise in Patients Successively Paced in DDD and Rate Matched Ventricular Pacing

Dual chamber pacemakers were implanted in nine patients with permanent second or third degree AV block feight had complete retrograde block). Two identical exercise tests were performed after at least 1 month after implantation. During the first test (T₁) the pacemaker was programmed to the DDD mode and heart rates were recorded every 15 to 30 seconds during exercise and 30 minutes after exercise. Following 30 minutes of rest, the implanted pacemaker was programmed to the VVT mode and driven by an external pacemaker via a skin electrode. The second exercise test (T₂) was then performed and the rate of the external pacemaker was progressively changed to reproduce exactly the rate observed during T₁ at the same exercise stress. Atrial natriuretic factor (ANF) levels were determined at rest, at regular intervals during exercise, and 30 minutes after exercise. ANF levels and release were statistically higher during rate matched ventricular, than DDD pacing. It is concluded that preservation of AV synchrony reduces ANF release induced by heart rate acceleration during exercise.     

An Optimized AV Delay Algorithm for Patients with Intermittent Atrioventricular Conduction

Detection and promotion of an intermittent atrioventricular (A V) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDDj pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

Ventriculoatrial Conduction: A Cause of Atrial Malpacing in AV Universal Pacemakers. A Report of Two Cases

Retrograde atrial activation during ventricular pacing has often been a cause of intermittent or persistent arrhythmias (pacemaker-mediated tachycardia) in AV universal pacemakers. We recently encountered two cases in which VA conduction was responsible for atrial malpacing in patients with an implanted AV universal pacemaker, one programmed in DDD and one in DVI mode. Atrial malpacing was induced by the atrial refractoriness due to retrograde activation. In the first patient, it was observed when the pacemaker was programmed to a rate of 110 ppm (lower rate) and an AV interval of 200 ms in order to check crosstalk. In the second patient, it was observed after ventricular premature contractions.     

Atrial Electrophysiological Features in Patients with Wolff-Parkinson-White and Atrial Fibrillation: Absence of Rate Adaptation of Intraatrial Conduction Time Parameters

Clinical electrophysiology has not yet clearly defined atrial features that can predict spontaneous occurrence of atrial fibrillation (AF). The aim of this work was to identify atrial electrophysiological features that can distinguish Wolff-Parkinson-White patients with spontaneous AF from those without this arrhythmia. Sixty-nine patients with Wolff-Parkinson-White were divided into three groups: group I (16 patients) with spontaneous AF; group II (35 patients) with reciprocating tachycardia but not AF; and group III (18 patients) asymptomatic without documented arrhythmias. Atrial effective refractory periods (ERPs) and intraatrial conduction times in response to premature extrastimuli were analyzed. The latter were evaluated as the A₁A₂ interval minus the correspondent S₁S₂ interval (A₁A₂-S₁S₂), S₂A₂ and the interval A₁A₂ following the shortest S₁S₂ producing atrial activation (FRP'). All the parameters have been evaluated in two atrial sites and at two atrial pacing cycle lengths (600 and 400 ms). For all the parameters, the difference (“gradient”) was calculated between the values of the same parameter measured at the atrial pacing cycle length of 600 ms and that found at the atrial pacing cycle length of 400 ms in the same recording site in each patient was calculated. Atrial FRP did not differ significantly in the three groups. Intraatrial conduction parameters, evaluated in the high right atrium (HRA), were longer when measured at an atrial pacing of 400 ms and showed a lack of rate adaptation in patients with spontaneous AF. In group I patients in particular, FRP’became longer with the increase of atrial rate, while in groups 2 and 3, it usually shortened. The mean gradient of HRA FRP’was -15.0 ± 19 ms in group I as compared to 5.7 ±13 ms in group II and 6.4± 13 ms in group III (P < 0.001); sensitivity. specificity, and negative predictive value of a negative gradient in the identification of patients with spontaneous AF, were, respectively, 83%, 75%, and 93%. Patients from groups 2 and 3 did not differ in any of the analyzed parameters. Patients with Wolff-Parkinson-White and spontaneous AF showed prolonged intraatrial conduction times and a different behavior in response to modification of heart rate. (PACE 1997;20[Pt. I]:1318-1327)     

Accelerated AV Nodal Conduction with Use of Procainamide in Atrial Fibrillation

Background: Atrial fibrillation is a common dysrhythmia seen in the emergency department (ED). Chemical or electrical cardioversion may be performed on patients who have had atrial fibrillation for < 48 h duration and who are at low risk for thromboembolic events. Multiple studies suggest that intravenous procainamide is an appropriate agent in the treatment of acute atrial fibrillation due to its relatively low risk profile and high conversion rate. Objectives: A case is presented that demonstrates an adverse reaction to the use of intravenous procainamide for chemical cardioversion of atrial fibrillation in an otherwise hemodynamically stable patient. Case Report: We report a case of lone paroxysmal atrial fibrillation in a patient with a structurally normal heart who suffered paradoxical accelerated atrioventricular nodal conduction and secondary hypotension in response to procainamide administration. Conclusion: When administering procainamide for chemical cardioversion of atrial fibrillation, a low threshold should be maintained for administration of a complementary rate-controlling agent, and facilities for immediate electrical cardioversion always must be available.     

Sinus Node Dysfunction and Impairment of Global Atrial Conduction Time After High Rate Atrial and Ventricular Pacing in Dogs

ZUPAN, I., et al .: Sinus Node Dysfunction and Impairment of Global Atrial Conduction Time After High Rate Atrial and Ventricular Pacing in Dogs. It has been shown in animals and humans that AF shortens the atrial refractory period and impairs its rate adaptation. The aim of the study was to evaluate the effects of high rate pacing on sinus node function and intraatrial conduction. Eight dogs were subjected to rapid atrial pacing (AP) at a rate of 400 beats/min for 16 days. After a complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Sinus node recovery time (SNRT) was measured after pacing at 150, 160, and 170 beats/min. P wave duration was measured on a surface ECG recorded at a paper speed of 200 mm/s. Measurements were performed at baseline, immediately after AP or VP, and four weeks after termination of AP or VP. SNRT immediately after AP and VP was significantly prolonged at all three pacing rates   (P < 0.03)   . P wave duration increased significantly after either type of pacing   (AP: 74.3 ± 6.4 ms, VP: 70.0 ± 3.8 ms)   compared with baseline values   (60.6 ± 6.2 ms, P < 0.05)   . Rapid AP and VP induces sinus node dysfunction and prolongs intraatrial conduction time. The effects of sustained AP and VP on sinus node function and atrial myocardium returned toward control values 4 weeks after cessation of pacing. The authors hypothesize that reversible electrical remodeling occurs both in the sinus node and in the atrial myocardium. (PACE 2003; 26[Pt. II]:507–510)