Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

Prevention of chronic atrial fibrillation by pacing in the region of Bachmann's bundle: results of a multicenter randomized trial

INTRODUCTION: Atrial pacing locations that decrease atrial activation and recovery time may be preferable in patients with a history of atrial arrhythmias. This multicenter prospective randomized study compared the efficacy of Bachmann's bundle (BB) region pacing to right atrial appendage (RAA) pacing in patients with recurrent paroxysmal atrial fibrillation (AF). METHODS AND RESULTS: Patients with standard pacing indications (n = 120, 70+/-11 years) were randomized to atrial pacing in either the RAA (n = 57) or BB region (n = 63). Implantation time was similar between groups (88+/-36 min [n = 38] for BB vs 83+/-34 min [n = 34] for RAA). No differences in pacing threshold, impedance, or sensing between BB and RAA groups were observed at implantation or after the 6-week, 6-month, and 1-year follow-up periods. Average length of follow-up was 12.6+/-7.4 months for the BB group and 11.8+/-8.0 months for the RAA pacing group. The percentage of atrial pacing was similar between groups (61%+/-34% RAA vs 65%+/-31% BB at 2 weeks after implant). BB atrial pacing significantly (P < 0.05) shortened p wave duration compared with sinus rhythm (123+/-21 msec vs 132+/-21 msec, n = 50) 2 weeks after implant. In contrast, p wave duration was longer during atrial pacing from the RAA position compared with sinus rhythm (148+/-23 msec vs 123+/-23 msec, n = 37). Additionally, p wave duration was shorter during BB pacing than during RAA pacing. Patients with BB pacing had a higher (P < 0.05) rate of survival free from chronic AF (75%) compared with patients with RAA pacing (47%) at 1 year. CONCLUSION: BB region pacing is safe and effective for attenuating the progression of AF.     

Electrocardiographic features of atrial depolarization during pacing of right atrial appendage.

Identification of atrial capture during pacing from right atrial appendage is frequently difficult. Electrocardiograms of forty five patients implanted with AAI/DDD pacemakers (thirty unipolar, fifteen bipolar) were analysed to characterize the specific morphology of paced P waves. Compared to sinus P waves, atrial pacing resulted in atrial depolarization of lower amplitude (0.16 +/- 0.05 mv vs 0.11 +/- 0.032 mv, P less than 0.005) but increased duration (0.07 +/- 0.009 sec vs 0.08 +/- 0.017 sec, P less than 0.005). P wave morphology was similar in unipolar and bipolar pacing units. It was positive in lead I (80%), II (71.11%), III (80%) and aVF (75.55%). In lead aVL, paced P waves were usually diphasic with an initial negative deflection (35.55%). Precordial leads showed paced atrial depolarization of small amplitude and did not help in identification of atrial capture. In unipolar pacing P waves were best seen in lead III because of small pacing spike in this lead. Lead II was suitable for identification of paced P waves in bipolar pacing. Thus careful examination of standard ECG leads for paced P waves of low amplitude, prolonged duration and specific morphology can help in confirming atrial capture following pacing stimulus from right atrial appendage.     

Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.     

Acute short-term effect of VVI pacing mode on P wave dispersion in patients with dual chamber pacemakers

The acute or chronic effect of VVI pacing on P wave duration in the same patient with dual chamber pacemaker has not been studied before. Hence, with the purpose of determining whether VVI pacing increases dispersion of atrial refractoriness, we undertook a comparative study with the aid of a simple noninvasive approach, namely P wave dispersion (PWD) determined from surface electrocardiogram in the same patients who were implanted with dual chamber pacemakers. Pmax duration calculated in VVI paced mode was significantly higher than in VDD paced mode (121+/-21 vs. 111+/-17 ms, P=0.021). PWD (33+/-15 vs. 40+/-23 ms, P=0.062) did not demonstrate any significant difference between VDD and VVI paced modes, respectively. In conclusion, the findings of our study suggest that short-term VVI pacing itself does not have any direct effect on PWD in patients with dual chamber pacemakers. Different pacing modes in the long term might be responsible for altering PWD and the occurrence of atrial fibrillation while affecting the autonomic nervous system.     

Difference between electrical remodelling after pulmonary veins and right atrium appendage pacing.

OBJECTIVE: Pulmonary veins (PVs) are important sources of paroxysmal atrial fibrillation (AF). Rapid atrial pacing changes atrial electrophysiology, and facilitates the induction and maintenance of AF. The purpose of our study was to evaluate the changes in atrial effective refractory period (AERP) proprieties and in ionic currents in PVs myocytes from dogs subjected to rapid atrial pacing in PVs and right atrial appendage (RAA) and to relate these changes to the ability to induce AF. METHODS: Twelve mongrel dogs in normal sinus rhythm were paced from the superior left PVs or RAA at 500 bpm for 4 h. Electrophysiological studies were conducted to determine the changes in AERP, dispersion, and rhythm. Ionic currents were evaluated using patch clamp technique in single PVs myocytes in sham-operated dogs, and the results were compared with those from PVs and RAA pacing groups. RESULTS: The presence of rapid atrial pacing was associated with a marked shortening in AERP in both PVs and RAA pacing group with a marked increase in AERP dispersion in PVs pacing. Both L-type calcium current (I(Ca,L)) and the transient outward current (I(to)) were reduced in both groups with an increased significance in PVs pacing group. The density of I(Ca,L) was decreased significantly from (-6.03 +/- 0.63) pA/pF in the control group to (-3.21 +/- 0.34) pA/pF in the PVs pacing group and (-4.75 +/- 0.41) pA/pF in the RAA pacing group (n = 6, P < 0.05), whereas the density of I(to) was decreased significantly from (8.45 +/- 0.71) pA/pF in the control group to (5.21 +/- 0.763) pA/pF in the PVs pacing group and (6.84 +/- 0.69) pA/pF in the RAA pacing group (n = 6, P < 0.05). CONCLUSION: Our findings provide likely ionic mechanisms of shortened repolarization in induced atrial tachycardia with a decrease in I(Ca,L) and I(to) densities, which is the likely mechanism for a decrease in action potential duration rate adaptation in the canine rapid pacing model more pronounced in the PVs pacing group underlying the crucial role of PVs in initiating AF.     

Simple electrocardiographic markers for the prediction of paroxysmal atrial fibrillation in hyperthyroidism

BACKGROUND: Hyperthyroidism is a major cause of paroxysmal atrial fibrillation (AF). The purpose of this study was to evaluate the predictors of AF in the patients with clinical and subclinical hyperthyroidism. METHODS AND RESULTS: The study population consisted of four groups: group I (57 euthyroid healthy persons), group II (33 patients with subclinical hyperthyroidism), group III (69 patients with overt hyperthyroidism) and group IV (31 patients with overt hyperthyroidism and documented paroxysmal AF). The maximum P wave duration (P maximum) in group IV (114 +/- 8 ms) was significantly higher than group I (102 +/- 7 ms, p < 0.001), group II (106 +/- 7 ms, p < 0.001) and group III (108 +/- 9 ms, p0.005). The P wave dispersion (PWD) was measured as 46 +/- 9 ms in group IV and this was significantly higher than group I (29 +/- 8 ms, p < 0.001), group II (36 +/- 9 ms, p < 0.001) and grup III (38 +/- 8 ms, p = 0.001). The P maximum and PWD were higher in the patients with subclinical hyperthyroidism compared to healthy individuals. Univariate regression analysis revealed that age, P maximum and PWD, multivariate analysis showed that P maximum and PWD were significant predictors of paroxysmal AF. A PWD value of 37.5 ms separated group IV from others with a sensitivity of 90%, specificity of 85%, and positive predictive accuracy of 77%. CONCLUSION: Simply measuring P maximum and PWD values, we could identify the patients with high risk for the development of AF and these simple ECG parameters may help in clinical judgement to determine the requirement for treatment in the patients with subclinical hyperthyroidism.     

Effects of simultaneous atrioventricular pacing on atrial refractoriness and atrial fibrillation inducibility: role of atrial mechanoelectrical feedback

INTRODUCTION: The purpose of this study was to evaluate the effects of an acute increase in atrial pressure on refractoriness (mechanoelectrical feedback) and the vulnerability to atrial fibrillation (AF) and to investigate the effects of autonomic blockade and verapamil on mechanoelectrical feedback in humans. METHODS AND RESULTS: Right atrial pressure and effective refractory period (ERP) at the right atrial appendage (RAA) and high right atrial septum were measured during sinus rhythm, and during atrial and simultaneous AV pacing at a cycle length of 300 msec, either in the absence (n = 25) or presence (n = 22) of pharmacologic autonomic blockade. In another 15 patients, the protocol was performed before and after infusion of verapamil 0.15 mg/kg. In the absence of autonomic blockade, AV pacing resulted in a higher mean right atrial pressure (11.7 +/- 3.3 vs 4.3 +/- 3.0 mmHg, P < 0.001) and a shorter atrial RAA ERP (144 +/- 23 msec vs 161 +/- 21 msec; P < 0.001) compared with atrial pacing; AF was induced more often during AV pacing (87%) than during atrial pacing (20%) and was related directly to the right atrial pressure (r = 0.39, P = 0.004) and indirectly to the RAA ERP (r = -0.42, P < 0.001). The susceptibility to sustained AF was greatly enhanced by autonomic blockade. Verapamil markedly attenuated the shortening of ERP and the propensity for AF that occurred during simultaneous AV pacing. CONCLUSION: An acute increase in atrial pressure during tachycardia is associated with shortening of atrial refractoriness and a propensity for AF, i.e., atrial mechanoelectrical feedback, which may be enhanced by autonomic blockade and attenuated by calcium channel blockade.     

Two-dimensional echocardiographic determination of right atrial emptying volume: a noninvasive index in quantifying the degree of tricuspid regurgitation

Contrast echocardiography and inferior vena cava ultrasonography are useful techniques in diagnosing tricuspid regurgitation (TR) but are not helpful in estimating the severity. Using a computerized light-pen method for tracing the right atrial (RA) border during systole and diastole in the apical 4-chamber view, single-plane volume determinations were calculated in 10 normal subjects (Group I), 18 patients with atrial fibrillation (AF) and no TR (Group II), 14 patients with mitral stenosis and mild TR (Group IIIa), and 8 patients with mitral stenosis and severe TR (Group IIIb). TR was quantitated as absent, mild or severe by contrast right ventriculography. The RA end-systolic volume was 36.4 +/- 13.1 ml in Group I patients, 59.1 +/- 16.8 ml in Group II patients, 76.9 +/- 55.4 ml in Group IIIa patients, and 154.6 +/- 57.3 ml in Group IIIb patients (all Groups versus Group I, p less than 0.001). The mean RA emptying volume, which equals RA end-systolic volume--RA end-diastolic volume, was 15.3 +/- 5.0 for Group I, 17.7 +/- 3.0 for Group II, 30.4 +/- 8.0 for Group IIIa, and 71.6 +/- 25.4 for Group IIIb. All 8 patients with severe TR but none of the 14 patients with mild TR had an RA emptying volume greater than 40 ml (p less than 0.001). In addition, all 28 patients in Groups I and II but only 4 of 14 patients in Group III had an RA emptying volume less than 26 ml (p less than 0.01). The mean RA pressure measured at cardiac catheterization correlated with RA emptying volume (r = 0.71, p less than 0.001). Thus, RA emptying volume is useful for separating severe TR from mild TR in patients with mitral stenosis.     

Suppression of atrial fibrillation by atrial pacing.

BACKGROUND: Atrial fibrillation (AF) is a common arrhythmia in patients with an implanted pacemaker, but the role of atrial pacing in preventing AF is still unclear. METHODS AND RESULTS: Sixty-six patients (67.8+/-12.1 years) were enrolled: 54 with sick sinus syndrome (SSS), 11 with atrioventricular blocks (AVB), and 1 with SSS and AVB. The prevalence of AF was investigated. In 22 patients with AF, the AF burden was estimated under "back-up pacing" (40-50 beats/min), then under "atrial pacing" (60-85 beats/min). The prevalence of AF in the SSS group tended to be higher than that in the AVB group (48.1% vs 18.2%, p=0.06). The AF burden in patients with a percentage of atrial pacing (% atrial pacing) <50% was significantly greater than that in patients with % atrial pacing >or=50% (12.5+/-21.1% vs 4.2+/-10.3%, p<0.05). AF disappeared immediately after "atrial pacing" in 4 patients (18.2%). In 9 patients (40.9%), the AF burden decreased gradually, and AF disappeared in 6 patients (27.3%) after 207.9+/-130.2 days. CONCLUSION: The prevalence of AF may be higher in patients with SSS than in those with AVB. Atrial pacing has a preventive effect on AF, and the effect of atrial pacing is not always immediate but is progressive in some patients.     

Prevention of paroxysmal atrial fibrillation in patients with sinus bradycardia: role of right atrial linear ablation and pacing site

INTRODUCTION: Right atrial linear lesions (RALL), either alone or in combination with antiarrhythmic drug therapy, may modify the substrate for maintenance of atrial fibrillation (AF). The aim of this prospective randomized study was to determine whether RALL provides additional benefit to right atrial appendage pacing (RAAP) and/or interatrial septum pacing (IASP) and drug therapy in patients with symptomatic paroxysmal AF and sinus bradycardia requiring permanent atrial pacing. METHODS AND RESULTS: Sixty-four patients (33 men and 31 women, mean age 73 +/- 10 years) completed the 6-month follow-up. Patients were randomized to either RALL (n = 33) or non-right atrial linear lesions (NRALL), and then to either IASP (n = 32) or RAAP (n = 32). Fifteen RALL patients were paced at the IAS and 18 at the RAA. Seventeen NRALL patients were paced at the IAS and 14 at the RAA. No statistical difference was observed with regard to the mean atrial tachyarrhythmia (AT) burden between NRALL (84 +/- 169 min/day) and RALL patients (202 +/- 219 min/day). Mean AT burden was significantly lower in the IASP group (70 +/- 150 min/day) than in RAAP group (219 +/- 317 min/day; P < 0.016). In the RALL group, the mean AT burden was 99 +/- 180 min/day in the IASP patients and 288 +/- 372 min/day in the RAAP patients (P < 0.046). In the NRALL group, no statistical difference in the mean AT burden was observed between IASP patients (46 +/- 117 min/day) and RAAP patients (130 +/- 211 min/day). CONCLUSION: The results of the present study indicate that RALL did not provide any additional therapeutic benefit to combined antiarrhythmic drug therapy and septal or nonseptal atrial pacing in patients with sinus bradycardia and paroxysmal AF.     

Inducibility of atrial fibrillation during atrioventricular pacing with varying intervals: role of atrial electrophysiology and the autonomic nervous system

INTRODUCTION: Patients receiving VVI pacemakers have a higher incidence of paroxysmal atrial fibrillation (AF) than those receiving DDD pacemakers. However, the mechanism behind the difference is not clear. The purpose of this study was to investigate whether atrial electrophysiology and the autonomic nervous system play a role in the occurrence of AF during AV pacing. METHODS AND RESULTS: The study population consisted of 28 patients who had (group I, n = 15) or did not have (group II, n = 13) AF induced by a single extrastimulus during pacing with different AV intervals. Atrial pressure, atrial size, atrial effective refractory periods, and atrial dispersion were evaluated during pacing with different AV intervals. Twenty-four-hour heart rate variability and baroreflex sensitivity also were examined. Atrial pressure, atrial size, effective refractory periods in the right posterolateral atrium and distal coronary sinus, and atrial dispersion increased as the AV interval shortened from 160 to 0 msec. During AV pacing, group I patients had greater minimal (52+/-17 vs 25+/-7 msec; P < 0.005) and maximal (76+/-16 vs 36+/-9 msec; P < 0.005) atrial dispersion than group II patients. The differences in atrial size and atrial dispersion among different AV intervals were greater in patients with AF than in those without AF. Baroreflex sensitivity (6.6+/-1.7 vs 3.9+/-1.0; P < 0.00005), but not heart rate variability, was higher in patients with AF than in those without AF. CONCLUSION: Abnormal atrial electrophysiology and higher vagal reflex activity can play important roles in the genesis of AF in patients receiving pacemakers.     

Electrocardiographic characteristics in low atrial septum pacing

AIM: The aim of the study was to compare P-wave morphology and duration in pacing from the low right atrial septal wall and the high right atrial appendage (RAA). METHODS: The electrocardiogram (ECG) of 50 patients with low atrial septum (LAS) pacing and that of 50 patients with RAA pacing were compared with their electrocardiogram during sinus rhythm. RESULTS: In the frontal plane, patients with LAS pacing showed a superior P-wave axis between -60 degrees and -90 degrees . In all patients with RAA pacing, a P-wave axis between 0 degrees and +90 degrees was observed as in sinus rhythm. In the horizontal plane, all patients with LAS pacing had an anterior P-wave axis between +90 degrees and +210 degrees , whereas all patients with RAA pacing had a posterior P-wave axis between -30 degrees and -90 degrees . The terminal part of biphasic P waves in lead V 1 in LAS pacing was always positive, a pattern that was never observed in P waves of sinus origin or in RAA pacing. P-wave duration was longer with RAA pacing compared with LAS pacing (115 +/- 19 vs 80 +/- 14 milliseconds [ P < .01]). CONCLUSION: The total atrial activation time during LAS pacing is shorter than that during RAA pacing. The electrical atrial activation sequences in LAS pacing and RAA pacing are significantly different. The morphology of biphasic P waves in lead V1 during LAS pacing suggests that the initial part of activation occurs in the left atrium and the terminal part in the right atrium.     

Effect of flestolol on ventricular rate during atrial fibrillation in Wolff-Parkinson-White syndrome

The ultrashort-acting beta blocker flestolol was studied during atrial pacing and atrial fibrillation (AF) in 10 patients with Wolff-Parkinson-White syndrome. Flestolol was given as a 100-micrograms/kg bolus followed by a 10-micrograms/kg/min infusion for 15 minutes. The drug did not alter the antegrade effective refractory period of the accessory pathway or the atrial paced cycle length at which block occurred in the accessory pathway. After flestolol, the percent of preexcited QRS complexes during AF increased (60 +/- 10 vs 87 +/- 5%, p = 0.01). Despite this, the ventricular rate slowed, with increases in mean RR interval (382 +/- 20 vs 416 +/- 22 ms, p = 0.02) and in the shortest interval between preexcited QRS complexes (251 +/- 18 vs 270 +/- 17 ms, p less than 0.01). The effect of isoproterenol 3 to 5 micrograms/min was studied in 5 patients. During atrial pacing, isoproterenol decreased the antegrade refractory period and the atrial paced cycle length of block in the accessory pathway (p less than or equal to 0.05). During AF, it decreased the percent of preexcited QRS complexes, mean RR interval and shortest interval between preexcited QRS complexes (p less than 0.05). Flestolol reversed the effects of isoproterenol both during atrial pacing and AF. Thus, flestolol does not alter conduction over the accessory pathway during atrial pacing, but during AF it slows conduction over the accessory pathway and prevents isoproterenol-mediated increases in ventricular rate. This suggests that in patients with Wolff-Parkinson-White syndrome sympathetic stimulation after the onset of AF enhances conduction over the accessory pathway and is an important determinant of ventricular rate.     

Left atrial appendage function in patients with different pacing modes

Many studies suggest that patients who receive a ventricular pacemaker have a higher incidence of systemic thromboembolism compared to patients receiving a physiological pacemaker. However, the exact mechanism regarding the etiology of thromboembolism remains unclear. We evaluated the left atrial appendage (LAA) functions, using multiplane transesophageal echocardiography (TEE), in patients with different pacing modes. In order to evaluate the ejection fraction (EF), peak emptying (V(E)) and filling (V(F)) flow velocities of the LAA by TEE, we studied 31 patients (mean age 63+/-18.5 years) who had been paced for 5.0+/-2.9 years. Patients with atrial fibrillation, left ventricular dysfunction and mitral valve disease were excluded. The pacing indications were complete atrioventricular block (AVB) in 19 patients (9 VVI, 10 VDD or DDD) and sick sinus syndrome (SSS) in 12 patients (5 VVI, 7 DDD). Mean EF, V(E) and V(F) of the LAA were significantly lower in all patients with ventricular pacing (25.5+/-15.6%, 30.4+/-15.6 cm/s and 29. 1+/-19.2 cm/s, respectively) compared to those with physiologic pacing (48.5+/-16.9%, 59.6+/-16.3 cm/s, 57.9+/-18.5 cm/s, respectively) (P<0.01 in all). When patients were further classified with respect to underlying heart disease whether they had SSS or AVB, all measurements of the LAA (EF, V(E) and V(F)) in both subgroup of patients with SSS and AVB were found significantly lower in those with ventricular pacing than in those with physiologic pacing (Tables 3 and 4). This decrease, especially in LAA flow, was much greater in those with SSS (Mean V(E) and V(F) <20 cm/s). In a patient paced with VVI for SSS, a thrombus was detected within the LAA cavity. In conclusion, these results suggest that the pacing modality appeared to influence the LAA functions in paced patients. Patients with asynchronous ventricular pacing modes had a significantly higher incidence of depressed LAA functions than did patients with physiological pacing, especially more marked in patients with sick sinus syndrome. This may be a factor responsible for increased risk of thrombus formation and thromboembolic events in this patient population.     

The effects of class IA antiarrhythmic drug on the common type of atrial flutter in combination with pacing therapy

In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10 ms. In 10 patients before the drug administration, common AF was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patients, and common AF was converted into sinus rhythm in only 1 patient. After the drug administration common AF was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 +/- 12 ms vs. 298 +/- 37 ms, p less than 0.005) and widened the entrainment zone (64 +/- 7 ms vs. 90 +/- 20 ms, p less than 0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common AF at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.     

Electrophysiological determinants of atrial fibrillation in sinus node dysfunction despite atrial pacing.

AIMS: The effectiveness of atrial pacing in reducing the incidence of atrial fibrillation in patients with sinus node dysfunction is incomplete, and the correlation between electrophysiological atrial properties and the effect of permanent atrial pacing has been poorly investigated. Accordingly, the aim of the present study was to correlate electrophysiological data, in terms of atrial refractoriness, conduction parameters, and propensity to atrial fibrillation induction, and the likelihood of atrial fibrillation after DDD device implantation. METHODS AND RESULTS: The authors reviewed electrophysiological data of 41 patients with sinus node dysfunction (mean age 70 +/- 8 years, who were investigated free of anti-arrhythmic treatments before pacemaker implantation. At a drive cycle length of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and latent vulnerability index (effective refractory period [ERP] A2), were measured. Atrial fibrillation induction was tested with up to three extrastimuli in 34 patients. Induction of sustained atrial fibrillation (> 1 min) was considered as the end-point. P-wave duration on the surface ECG in lead II/V1 was also measured. Minimal atrial rate was programmed between 60 and 75 bpm (mean: 64 +/- 4 bpm). After implantation, the patients were followed-up for 28 +/- 17 months, and ECG-documented occurrence of atrial fibrillation was determined. Electrophysiological characteristics of patients with (n = 12) or without (n = 29) paroxysmal atrial fibrillation before implantation were similar. When comparing patients with (n = 11) or without (n = 30) post-pacing atrial fibrillation occurrence, no differences were found in age, underlying heart disease, left atrial size, minimal pacing rate, and follow-up duration. Additionally, between the two former groups, there was no significant difference in terms of effective refractory periods (233 +/- 47 ms vs 239 +/- 25 ms), functional refractory periods (280 +/- 48 ms vs 272 +/- 21 ms), S1-A1 (44 +/- 20 ms vs 37 +/- 13 ms) and S2-A2 latency (77 +/- 28 ms vs 66 +/- 22 ms), and A1 duration (60 +/- 23 ms vs 53 +/- 16 ms). In contrast, in patients with post-pacing atrial fibrillation occurrence, the P wave was more prolonged (116 +/- 22 ms vs 98 +/- 13 ms; P < 0.01), A2 was longer (116 +/- 41 ms vs 87 +/- 27 ms; P < 0.01), effective refractory periods/A2 was lower (2.1 +/- 0.4 cm vs 3.1 +/- 1.4 cm; P < 0.05), and rate of atrial fibrillation induction was higher (8/11 patients vs 8/23 patients; P < 0.05). Electrophysiological characteristics of patients free of post-pacing atrial fibrillation with associated (n = 6) or unassociated (n = 24) paroxysmal atrial fibrillation history before implantation were quite similar. In patients with post-pacing atrial fibrillation with associated (n = 6) or unassociated atrial fibrillation history (n = 5) before implantation, effective refractory periods was statistically different (207 +/- 23 ms vs 264 +/- 46 ms; P < 0.05). Values of effective refractory periods < 220 ms were significantly more frequent in patients with post-pacing atrial fibrillation than in patients without (4/11 patients vs 2/30 patients; P < 0.05). When comparing patients with post-pacing atrial fibrillation with effective refractory periods > or = 220 ms (n = 7) and < 220 ms (n = 4), A2 duration was remarkably prolonged (145 +/- 42 ms vs 90 +/- 11 ms; P < 0.05) in those with effective refractory periods > or = 220 ms. By contrast, between the two groups, effective refractory periods/A2 were identical (2.08 +/- 0.6 cm vs 2.15 +/- 0.3 cm; P = n.s.). CONCLUSION: Prolonged atrial refractoriness, lesser degrees of conduction disturbance and a lower rate of atrial fibrillation induction seem to be predictive of stable sinus rhythm. In contrast, patients with persistence of atrial fibrillation despite pacing have a more abnormal and inhomogeneous atrial substrate, as well as a higher rate of atrial fibrillation induction. Prolonged P wave, shortened refractoriness, or remarkably abnormal conduction disturbances in the presence of prolonged refractoriness limit the effectiveness of standard atrial pacing in atrial fibrillation prevention. Identification of predictive criteria of failure of single-site atrial pacing may be used to consider dual-site atrial pacing in such patients with sinus node dysfunction.     

持续快速心房起搏对犬肺静脉及心房组织连接蛋白43和Ⅲ型胶原的影响

目的　探讨持续快速心房起搏对犬肺静脉和心房组织连接蛋白 43(Cx43)和Ⅲ型胶原的影响。方法　16只杂种犬,随机分为持续快速心房起搏组(8只)和正常对照组 (8只 ),前者以 400次 /min的频率持续起搏 10周,建立心房颤动(房颤)动物模型。分别取两组犬的左上肺静脉、左房游离壁和右心耳等部位的心肌组织进行Cx43的免疫荧光半定量分析和Ⅲ型胶原纤维定量分析。结果10周后快速心房起搏组所有犬均可诱发出持续性房颤。快速心房起搏组犬肺静脉、左房游离壁和右心耳部位的Cx43水平显著高于正常对照组犬各相应的部位 (肺静脉: 3370 .91±275. 11与1405 .82±90. 38, P<0. 05;左房游离壁: 2448. 68±272 .10与 1467. 12±147 .93,P<0. 05;右心耳: 2331 .96±199 .61与 1288. 27±216 .22, P<0 .05)。快速心房起搏组犬肺静脉Cx43的水平显著高于左心房游离壁和右心耳(P<0. 05),而左心房和右心耳部位的Cx43水平差异无统计学意义 (P>0. 05)。持续快速心房起搏组犬肺静脉、左房游离壁和右心耳等部位的Ⅲ型胶原含量显著高于正常对照组犬各相应部位(肺静脉: 3301 97±309 70与 1404 56±178 02, P<0 05;左房游离壁: 2477 86±190. 43与1479. 20±187 .17, P<0 .05;右心耳: 2045 .92±139 .43与 1417. 07±139. 43,P<0 .05 )     

Maturational changes in ventriculoatrial conduction in the intact canine heart

This study reports on the changes in ventriculoatrial (VA) conduction that occur with maturation. Programmed atrial and ventricular premature extra-stimulation (coupled to a fixed paced cycle length) and rapid atrial pacing were performed in three groups of dogs: Group I = 8 neonates aged 5 to 14 days, Group II = 9 young dogs aged 6 to 9 weeks and Group III = 10 adult dogs. High right atrial, His bundle and right ventricular electrograms were recorded. There were no differences in the AH intervals at rest. In all but five animals, atrioventricular conduction was limited by the atrial functional refractory period (Group I, 109 +/- 12 ms; Group II, 152 +/- 22 ms; Group III, 167 +/- 19 ms). As expected, with rapid atrial pacing, Wenckebach conduction developed at a shorter cycle length in the younger animals (Group I, 145 +/- 20 ms; Group II, 153 +/- 15 ms; Group III, 200 +/- 25 ms, p less than 0.01). Ventriculoatrial conduction was documented in 87% of Group I puppies and 100% of Group II, but only 40% of Group III dogs. The effective and functional refractory periods of the VA conduction system were significantly shorter in the more immature groups of dogs (effective/functional: Group I, 124 +/- 27/168 +/- 22 ms; Group II, 139 +/- 23/202 +/- 13 ms; Group III, 270 +/- 28/326 +/- 25 ms; p less than 0.01). Relative to the adult dog, the immature heart showed a greater incidence of VA conduction and shorter VA refractory periods. This enhanced VA conduction may be of physiologic importance in the initiation and perpetuation of certain supraventricular arrhythmias.     

Increased AAI mode pacing threshold after termination of atrial fibrillation by acute administration of disopyramide phosphate.

AIMS: We studied changes in atrial pacing threshold after termination of atrial fibrillation (AF) by acute administration of disopyramide phosphate (DP) to elucidate the suitable setting for atrial pacing output before AF termination. METHODS AND RESULTS: Four patients with sick sinus syndrome implanted with AAI mode pacemakers were examined. Disopyramide phosphate (2 mg/kg body weight) was injected intravenously for termination of a total of eight AF episodes. The maximal pacing threshold after AF termination (5.2+/-0.8 V at 0.45 ms) was significantly higher than that at baseline (1.3+/-0.2 V at 0.45 ms; P<0.01) and the average increment was 433+/-68%. During a period free from AF, an acute administration of DP did not increase the atrial pacing threshold and serum disopyramide levels were not toxic. CONCLUSION: The increased atrial pacing threshold observed after AF termination cannot be explained by the action of DP alone. However, our results suggest that atrial pacing output should be set at the maximum value before DP is administered to induce AF termination in patients with AAI pacemaker-dependent bradyarrhythmias.