Effects of Systolic Atrial Function on Plasma Renin Activity and Natriuretic Peptide Secretion after High Rate Atrial and Ventricular Pacing in Dogs

Rapid atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 ± 0.21 cm vs 2.41 ± 0.23 cm, P = 0.002). Compared with baseline, LAA-E velocities were significantly reduced (0.65 ± 0.12 m/s vs 0.26 ± 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 ± 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 ± 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 ± 252.21 fmol/L) with respect to baseline values (824.37 ± 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Is Atrial Sensing of Ventricular Far-Field Signals Important in Single-Lead VDD Pacing?

In single-lead VDD pacing the atrial sensitivity frequently is programmed to sensitive values. Atrial sensing of ventricular far-field signals should be reduced by differential atrial sensing. The aim of the study was to evaluate the effectiveness of this approach. Methods: The study included 10 patients with a single-lead VDD pacemaker (Thera 8948, Lead 5032). The atrial sensitivity was set to its most sensitive value of 0.18 mV and the telemetered intraatrial EGM was continuously recorded. After atrial tracked ventricular pacing, VVI pacing was performed with pacing rates from 100 to 160 beats/min in steps of 10 beats/min and up to 165 beats/min. The peak-to-peak amplitudes of P waves (P) and ventricular far-field signals (VFFS) were measured from the recordings. The ratio P/VFFS that defines the atrial signal-to-noise ratio was calculated, and the time from stimulus to maximum of the far-field signals amplitude (Tmax) was measured. Results: P measured 0.98 ± 0.76 mV. A VFFS was visible in the atrial channel in all patients with an amplitude of 0.45 ± 0.25 mV (range 0.01–1.0 mV), independent of the pacing rate. The ratio P/VFFS was 3.9 ± 4.2 (range 0.9–21.0). Tmax measured 99.4 ± 15.2 ms during sinus rhythm. A rate dependent shortening of Tmax to 92.7 ± 11.2 ms at 140 beats/min was observed (P = 0.001). At rates above 140 beats/min no further shortening occurred. Conclusion: Ventricular far-field signals are measurable in the atrial channel of VDD systems and may reach considerable amplitudes, which are not rate dependent. Although differential sensing provides favorable P waves to ventricular far-field signal ratios, refractory periods are needed to avoid far-field sensing. The rate dependent shortening of the ventricular signal can be detected in the atrial channel in VDD pacing.     

Atrial Electromechanical Sequence and Contraction Synchrony during Single- and Multisite Atrial Pacing in Patients with Brady-Tachycardia Syndrome

Objectives: Investigation of which atrial pacing modality provides atrial synchrony and the most physiological atrial contraction pattern in patients with brady-tachycardia syndrome.
Methods: Fifteen healthy subjects and 57 patients with sinus node dysfunction, atrial fibrillation recurrences, and prolonged P-wave on the electrocardiogram treated with multisite atrial (MSA) pacing were studied. One atrial lead was implanted in the coronary sinus (CS) ostium area, the other at the right atrial appendage (RAA): RAA+CS group (28 patients), or Bachmann's bundle (BB) region: BB+CS group (29). Sinus rhythm (SR) and CS, RAA, BB, RAA+CS, and BB+CS pacing modalities were evaluated. Electromechanical delay (EMD) in atrial walls was assessed by tissue Doppler echocardiography. Interatrial (ΔinterA), intra-right (ΔRA), and intra-left (ΔLA) atrial dyssynchrony were calculated.
Results: During SR, in the study group versus controls, important ΔinterA: 55 ± 23 versus 22 ± 11 ms (P < 0.01) and ΔLA: 47 ± 21 versus 21 ± 6 ms (P < 0.001) were present. Single-site BB and both MSA pacing modes restored ΔinterA and ΔLA (ΔinterA: 24 ± 16, 20 ± 13 and 14 ± 9 ms, ΔLA: 28 ± 18, 28 ± 13 and 20 ± 10 ms during BB, RAA+CS and BB+CS pacing, respectively). CS pacing prolonged lateral RA EMD, while RAA pacing LA walls EMD, which resulted in ΔinterA persistence. CS pacing induced ΔRA (50 ± 23 vs 16 ± 8 ms, P < 0.0001 vs controls). Atrial contraction sequence during BB pacing resembled that observed in controls.
Conclusions: (1) Single-site BB and both MSA pacing modes restored atrial synchrony. (2) Single-site RAA and CS ostium pacing retained interatrial dyssynchrony; moreover, CS pacing created RA dyssynchrony. (3) Single-site BB pacing provided physiological atrial contraction sequence.     

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.     

Effects of Verapamil on Electrophysiological Properties in Paroxysmal Atrial Fibrillation

Verapamil is used to control ventricular response during atrial fibrillation (AF). Limited data is available on the effects of verapamil on atrial vuinerability in human AF. The effects of intravenous verapamil (0.15 mg/kg) on electrophysiological properties of the atrium were investigated in 12 patients with documented paroxysmal AF by electrophysiological studies. Sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly affected by verapamil. The intraatrial conduction delay zone was significantly increased (33 ± 20 msec before verapamil versus 50 ± 22 msec after verapamil, P < 0.01, and the maximal intraatrial conduction delay was also significantly prolonged by verapamil, both to the His bundle region (30 ±12 msec before verapamil versus 42 ± 15 msec after verapamil. P < 0.01) and to the coronary sinus (40 ± 15 msec before verapamil versus 53 ± 17 msec after verapamil, P < 0.01). The fragmented atrial activity zone was significantly increased (15 ± 14 msec before verapamil versus 25 ± 22 msec after verapamil, P < 0.02), and the percentile fragmented atrial activity was also significantiy increased by verapami] (149 ± 18 msec before verapamil versus 174 ± 44 msec after verapamil, P < 0.05). The repetitive atriaJ firing zone remained unchanged. Sustained AF spontaneousiy occurred in only one patient after the administration of verapamil. Thus, verapamil may modulate the abnormal atrial electrophysiology in paroxysmal AF, and wouid favor production of atrial reentry.     

Is Dual Site Better Than Single Site Atrial Pacing in the Prevention of Atrial Fibrillation?

Long-term prevention of atrial fibrillation is not constantly realized by single-site right atrial pacing, and the beneficial role of multisite atrial pacing is still being studied. Accordingly, we compared the effectiveness of dual site and single site atrial pacing in 83 patients (50 men, 33 women, aged 69 +/- 10 years), who received a DDD device for primary sinus node dysfunction or bradycardia with documented atrial fibrillation. Inclusion criteria for dual site pacing were a sinus P wave > or = 120 ms and at least two episodes of documented paroxysmal AF in the 6 months preceding implantation. Dual site atrial pacing (high right atrium-coronary sinus ostium) was performed in 30 cases, and was compared to 53 single site paced patients, 21 with a P wave > or = 120 ms and 32 with a P wave < 120 ms. The basic pacing rate was programmed at 68 +/- 4 beats/min (range 60-75 beats/min). Sinus P wave (133 +/- 20 vs 95 +/- 9 ms; P < 0.001), paced P wave (107 +/- 14 vs 99 +/- 15; P < 0.05), number of antiarrhythmic drugs used (2.4 +/- 1.2 vs 1.6 +/- 1.5, P < 0.05), and the duration of symptoms (8.1 +/- 4.5 vs 3.8 +/- 2.4 years; P < 0.001) were significantly higher in dual site patients. The other characteristics were similar. During the follow-up of 18 +/- 15 months (range 3-30 months), paroxysmal AF was documented in 33 patients. Among these patients, 13 developed permanent AF following at least one episode of paroxysmal AF. When comparing dual site patients and single site patients with a P wave duration > or = 120 ms, paroxysmal AF incidence was lower in the dual site group (9/30 patients vs 15/21 patients, P < 0.01), as well as permanent AF (1/30 patients vs 8/21 patients, P < 0.01). By contrast, comparison between dual site patients and the group of single site patients with a P wave duration < 120 ms did not evidence any significant differences in paroxysmal (9/30 patients vs 9/32 patients) and permanent (1/30 patients vs 4/32 patients) AF incidences. Dual site seems better able than single site atrial pacing to improve the natural history of patients with a prolonged P wave, reducing the incidence of paroxysmal and permanent AF. No benefit could be expected in patients with a normal P wave duration.     

Atrial Pressure and Experimental Atrial Fibrillation

SIDERIS, D.A., et al .: Atrial Pressure and Experimental Atrial Fibrillation . A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300–600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 ± 12.2 mmHg, mean ± SD) than maintenance of sinus rhythm (16.8 ± 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.     

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.     

Effects of Septal Pacing on P Wave Characteristics: The Value of Three-Dimensional Echocardiography

SZILI-TOROK, T., et al .: Effects of Septal Pacing on P Wave Characteristics: The Value of Three-Dimensional Echocardiography. Interatrial septum (IAS) pacing has been proposed for the prevention of paroxysmal atrial fibrillation. IAS pacing is usually guided by fluoroscopy and P wave analysis. The authors have developed a new approach for IAS pacing using intracardiac echocardiography (ICE), and examined its effects on P wave characteristics. Cross-sectional images are acquired during pullback of the ICE transducer from the superior vena cava into the inferior vena cava by an electrocardiogram- and respiration-gated technique. The right atrium and IAS are then three-dimensionally reconstructed, and the desired pacing site is selected. After lead placement and electrical testing, another three-dimensional reconstruction is performed to verify the final lead position. The study included 14 patients. IAS pacing was achieved at seven suprafossal (SF) and seven infrafossal (IF) lead locations, all confirmed by three-dimensional imaging. IAS pacing resulted in a significant reduction of P wave duration as compared to sinus rhythm (   99.7 ± 18.7   vs   140.4 ± 8.8  ms; P < 0.01   ). SF pacing was associated with a greater reduction of P wave duration than IF pacing (   56.1 ± 9.9   vs   30.2 ± 13.6  ms; P < 0.01   ). P wave dispersion remained unchanged during septal pacing as compared to sinus rhythm (   21.4 ± 16.1   vs   13.5 ± 13.9  ms; NS   ). Three-dimensional intracardiac echocardiography can be used to guide IAS pacing. SF pacing was associated with a greater decrease in P wave duration, suggesting that it is a preferable location to decrease interatrial conduction delay. (PACE 2003; 26[Pt. II]:253–256)     

The Effects of Atrial Electrical Remodeling on Atrial Defibrillation Thresholds

EVERETT, T.H. et al. : The Effects of Atrial Electrical Remodeling on Atrial Defibrillation Thresholds. Electrical remodeling of atrial fibrillation may account for the increase in atrial defibrillation thresholds over time. The aim of this study was to examine the time course of electrical remodeling and the benefit of early defibrillation on the defibrillation threshold. Twenty‐six mongrel dogs weighing 27.6 ± 3.3 kg were induced into AF by repeated high output burst atrial pacing. Eight dogs were paced for multiple time periods of 5, 20, 40, and 60 minutes. Five dogs each had burst pacing for 4 hours and 8 hours, and eight dogs were paced at a high rate (640 beats/min ) for 48 hours. Biphasic atrial defibrillation shocks with a pulse width of 3/3 ms synchronized to the left apical electrogram were delivered to coil electrode catheters positioned in the lateral left and right atria. Defibrillation voltage was increased from 50 V in 20‐ to 30‐V steps until defibrillation was successful. As the pacing period increased, a decrease in atrial fibrillation cycle lengths and atrial effective refractory period was not observed before 8 hours. Similarly, the defibrillation threshold did not change significantly until the 8‐hour pacing period was reached. The defibrillation thresholds were 69 ± 28 V for 5 minutes, 64 ± 20 V for 20 minutes , 99 ± 85 V for 40 minutes , 78 ± 51 V for 60 minutes , 78 ± 38 V for 4 hours , 124 ± 33 V for 8 hours , and 133 ± 32 V for 48 hours (mean ± SD ) (P < 0.05 ). Atrial electrical remodeling in a rapid atrial pacing canine model is not observed until after 4 hours of burst atrail pacing. The atrial defibrillation threshold increases with increasing duration of burst atrial pacing, and follows a similar time course to other parameters of electrical remodeling.     

Mechanism of Atrial Fibrillation:

Atrial fibrillation (AF) has been associated with premature beats and decreased atrial conduction velocity. This study examined a new index of dynamic inter-atrial conduction time (iaCT) in patients with paroxysmal AF (PAF). We compared 42 consecutive patients with paroxysmal AF (mean age = 52 ± 16 years) without structural heart disease with 39 age-matched patients (mean age = 49 ± 15 years) who underwent ablation of junctional tachycardias. Prior to investigation, all antiarrhythmic drugs were discontinued for an appropriate period of time. The following measurements were made: baseline iaCT (iaCTb) between high right atrium (HRA) and distal coronary sinus, iaCT during HRA pacing S1S1 600 ms (iaCTS1), maximum prolongation of iaCT during S2 and S3 delivery (iaCTS2, iaCTS3). We then derived the decremental index (DI), the maximum percent prolongation of iaCT = iaCT S3-iaCTS1/iaCTS1%. In patients with PAF, iaCTb was 81.3 ± 24 ms versus 59.5 ± 14 ms in controls (P = 0.0001). Atrial fibrillation was reproducibly and easily induced with a prominent increase in iaCT in 11 patients with AF. In this subgroup DI was 92 ± 17%, compared to 45 ± 21% in the other patients with AF (P = 0.0001) and 21 ± 15% in the control group (P = 0.0001). Spontaneous isolated or repetitive ectopic activity was observed in 11 patients with AF (26%), and decremental atrial conduction was observed in 76% of patients with AF. This study supports the role of dynamic inter-atrial conduction disturbances in patients with lone PAF. The DI may be a new index of vulnerability to paroxysmal AF.     

Clinical Utility of Intraatrial Pacemaker Stored Electrograms to Diagnose Atrial Fibrillation and Flutter

POLLAK, W.M., et al. : Clinical Utility of Intraatrial Pacemaker Stored Electrograms to Diagnose Atrial Fibrillation and Flutter. The purpose of this study was to determine if intraatrial electrograms (EGMs) are required to diagnose specific types of atrial tachyarrhythmias detected by pacemaker diagnostics. DDD pacemakers in 56 patients were programmed to store episodes of atrial tachyarrhythmias. Some episodes had a stored atrial EGM snapshot of the atrial tachyarrhythmia. The EGMs were analyzed to confirm whether the stored episodes were true atrial tachyarrhythmias or other pacemaker-sensed events. EGM confirmation of atrial tachyarrhythmias correlated with increasing duration and rate of episodes. In particular, using EGMs, 8 (18%) of 44 episodes < 10 seconds in duration confirmed atrial tachyarrhythmias compared to 16 (89%) of 18 episodes > 5 minutes in duration (  P < 0.001  ). Only 10 (18%) of 56 detected atrial arrhythmia episodes at rates < 250 complexes per minute were confirmed by the atrial EGM as true arrhythmias compared to 33 (57%) of 58 detected episodes at rates > 250/min (  P < 0.001  ) Twenty-nine (91%) of 32 EGM confirmed episodes of atrial fibrillation/flutter had an atrial rate > 250 complexes per minute and were a minimum of 10 seconds in duration. Fifteen (88%) of 17 episodes meeting the combined stored data criteria of > 250 complexes per minute and duration > 5 minutes were confirmed as atrial fibrillation or flutter by stored EGMs. Atrial EGMs identified that 71 (62%) of 114 stored high atrial rate (HAR) episodes were events other than true atrial tachyarrhythmias. Pacemaker diagnostic data with intraatrial EGMs can diagnose specific atrial tachyarrhythmias and identify other pacemaker-sensed events. Stored episodes > 250 complexes per minute and > 5 minutes in duration had a high correlation with atrial fibrillation and flutter.     

Effects of Left Atrial Dilatation on the Endocardial Atrial Defibrillation Threshold: A Study in an Ovine Model of Pacing Induced Dilated Cardiomyopathy

Left atrial (LA) dilatation is a common finding in patients with chronic atrial fibrillation (AF). Progressive dilatation may alter the atrial defibrillation threshold (ADFT). In our study, epicardial electrodes were implanted on the LA free wall and right ventricular apex of eight adult sheep. Large surface area, coiled endocardial electrodes were positioned in the coronary sinus and right atrium (RA). LA dilatation was induced by rapid ventricular pacing (190 beats/min) for 6 weeks and echocardiographically assessed weekly along with the ADFT (under propofol anesthesia). LA effective refractory period (ERP) was measured every 2–3 days using a standard extra stimulus technique and 400 ms drive. The AF cycle length (AFCL) was assessed from LA electrograms. During the 6 weeks of pacing the mean LA area increased from 6.1 ± 1.5 to 21.3 ± 2.4 cm². There were no significant changes in the mean ADFT (122 ± 15 V), circuit impedance (46 ± 5 Ω), or LA AFCL (136 ± 23 ms). There was a significant increase in the mean LA ERP (106 ± 10 ms at day 0, and 120 ± 13 ms at day 42 of pacing). In this study, using chronically implanted defibrillation leads, the minimal energy requirements for successful AF were not significantly altered by ongoing left atrial dilatation. This finding is a further endorsement of the efficiency of the coronary sinus/RA shock vector. Furthermore, the apparent stability of the AF present may be a further indication of a link between the type of AF and the ADFT.     

The Effects of Reverse Atrial Electrical Remodeling on Atrial Defibrillation Thresholds

MANGRUM, J.M., et al. : The Effects of Reverse Atrial Electrical Remodeling on Atrial Defibrillation Thresholds. The implantable atrial defibrillator is a developing therapeutic option for paroxysmal atrial fibrillation, but shock related discomfort continues to be a limiting factor. To further characterize successful defibrillation, the relationship between reverse atrial electrical remodeling and internal atrial defibrillation thresholds in canines with chronic atrial fibrillation was examined. Testing was performed in 21 dogs. Chronic atrial fibrillation was induced in eight dogs by creating moderate mitral regurgitation and rapidly pacing the right atrium for ≥ 6 weeks. The atrial fibrillation cycle length, atrial effective refractory period, refractory period dispersion, and internal atrial defibrillation thresholds were determined after establishment of chronic atrial fibrillation after 4 hours of sinus rhythm postcardioversion and 7 days of sinus rhythm postcardioversion. These measurements were then compared to a normal population of 13 dogs. The atrial defibrillation thresholds were 6.6 J (1.9–10.1 J) initially, 2.9 J (1.5–3.7 J) after 4 hours of sinus rhythm, and 0.9 J (0.4 – 1.3 J) after 7 days of sinus rhythm (  P = 0.04  ). This decrease was associated inversely with the atrial effective refractory period (  P < 0.03  ), and atrial fibrillation cycle length (  P < 0.05  ), and with a decrease in atrial refractory period dispersion after 7 days of sinus rhythm (  P = 0.04  ). These electrophysiological measurements reached normal population levels by 7 days. Atrial defibrillation thresholds decrease as atrial reverse electrical remodeling occurs and this reduction corresponds to increased atrial fibrillation cycle length, increased atrial refractoriness, and decreased refractory period dispersion.     

Electrical Atrial Remodeling Assessed by Monophasic Action Potential and Atrial Refractoriness in Patients with Structural Heart Disease

The present study was performed to assess the effect of induced atrial fibrillation (AF) on atrial monophasic action potentials (MAPs) and atrial refractory period (ERP) in patients with structural heart disease. An electrode MAP catheter was placed in the right atrium to continuously measure atrial potential duration (APD₉₀) in 13 patients (coronary artery disease, 10 patients; dilated cardiomyopathy, 2 patients; hypertrophic cardiomyopathy, 1 patient) without spontaneous AF episodes. AF was induced by rapid atrial stimulation (300–1500/min). If sinus rhythm returned within 10 minutes, AF was reinduced. The atrial ERP was measured during atrial pacing at a basic cycle length of 550 ms before AF induction and after its conversion. Results: The mean atrial ERP and the atrial APD₉₀ before AF was 242 ± 34 ms and 256 ± 23 ms, respectively. ERP and APD_go shortening was observed after 3 minutes of AF. After 11 ± 0.5 min (10 min 20 s-13 min 10 s) of AF, ERP and APD₉₀ reached their minimal values of 72%± 13% and 71%± 10% of baseline, respectively. ERP and APD₉₀ returned to their initial values within 10 minutes after conversion of AF. A tendency toward longer duration of consecutive AF episodes and facilitation of their induction was observed. Conclusion: The present study confirms that short episodes of AF modify the electrophysiological properties of the atria in humans. In patients with structural heart disease, induced atrial fibrillation shortens the atrial ERP as well as the atrial APD₉₀. The changes were reversible within 10 minutes after arrhythmia termination.     

Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

Type II Atrial Flutter Interruption with Transesophageal Pacing: Use of Propafenone and Possible Change of the Substrate

Type II atrial flutter (AFII) is an arrhythmia which usually cannot be interrupted by atrial pacing: the underlying mechanism is considered to be a leading circle without an excitable gap. We investigated whether the administration of propafenone, an antiarrhythmic drug, which primarily decreases conduction velocity, has a beneficial effect on AFII interruption using transesophageal pacing. Twelve patients with an AFII were randomized into 2 groups in which pacing was performed without treatment (group A) or two hours after the administration of 600 mg of oral propafenone (group B). Sinus rhythm was attained in 0 of 6 patients in group A and in 4 of 6 patients in group B (P < 0.05). The baseline mean cycle length was the same in both groups (175 ± 7 (A) vs 168 ± 8 ms (B); it lengthened significantly after the administration of propafenone (219 ± 33 vs 168 ± 8 ms; P < 0.05). Propafenone did not significantly lengthen the cycle in the two patients in whom interruption of the arrhythmia was impossible. Our data show that propafenone has a facilitating effect on atrial pacing only when it significantly prolongs the cycle length of the arrhythmia, possible expression of a conversion of AFII into type I, with an anatomical substrate and an excitable gap allowing arrhythmia capture and interruption. In the two patients in whom sinus rhythm was not restored, the absence of a direct dependence of the cycle length on the change in conduction velocity induced by propafenone may be explained by the persistence of a functionally determined circuit, resistant to atrial pacing.     

Efficacy of Ventricular Rate Stabilization by Right Ventricular Pacing During Atrial Fibrillation

To assess the effect of right ventricular pacing on rate regularity during exercise and daily life activities, 16 patients with sinoatrial disease and chronic atrial fibrillation (AF) were studied. Incremental ventricular pacing was commenced at 40 beats/min until > 95% of ventricular pacing were achieved during supine, sitting, and standing. Thirteen patients also underwent randomized paired submaximal exercise tests in either a fixed rate mode (VVI) or a ventricular rate stabilization (VRS) mode in which the pacingrate was set manually at 10 beats/min above the average AF rate duringthe last minute of each exercise stage. The pacing interval for rate regularization was shortest during standing (692 ± 26 ms) compared with either supine or sitting (757 ± 30 and 705 ± 26 ms, respectively, P < 0.05). During exercise, VRS pacing significantly increased the maximum rate (119 ± 5.2 vs 106 ± 4.2 ms, P < 0.05), percent of ventricular pacing (85%± 5% vs 23%± 7%, P < 0.05), rate regularity index (5.8%± 1.6% vs 13.4%± 1.9%, P < 0.05), and maximum level of oxygen consumption (12.4 ± 0.5 vs 11.3 ± 0.5 ml/kg, P < 0.05) compared with VVI pacing. There was no change in oxygen pulse or difference in symptom scores in this acute study between the two pacing modes. It is concluded that right ventricular pacing may significantly improve rate regularity and cardiopulmonary performance in patients with chronic AF. This may be incorporated in a pacing device for rate regularization of AF using an algorithm that is rate adaptive to postural and exercise stresses.     

Differentiating the Ligament of Marshall from the Pulmonary Vein Musculature Potentials in Patients with Paroxysmal Atrial Fibrillation: Electrophysiological Characteristics and Results of Radiofrequency Ablation

TAI, C.-T., et al. : Differentiating the Ligament of Marshall from the Pulmonary Vein Musculature Potentials in Patients with Paroxysmal Atrial Fibrillation: Electrophysiological Characteristics and Results of Radiofrequency Ablation. It was reported that paroxysmal atrial fibrillation (PAF) can be initiated by ectopic atrial beats originating from the pulmonary vein (PV) or left atrial tract (LAT) within the ligament of Marshall (LOM). The aim of this study was to differentiate the LAT from the PV potentials, and to investigate the results of radiofrequency ablation guided by these potentials. Ten patients (  age 60 ± 12 years  ) with PAF who had a recording of double potentials (DPs) in or around the left PV were included. Group I had five patients with the second deflection of DPs (D2) due to activation of the LAT, and Group II had five patients with D2 due to activation of the PV musculature. There were no significant difference in the isoelectric interval between DPs, the activation time, and amplitude of D2 between Groups I and II. During distal coronary sinus (CS) pacing, the CS ostium (CSO) to D2 interval was shorter compared with that during sinus rhythm in Group I (  39 ± 19 vs 71 ± 25 ms, P = 0.04  ), but was longer in Group II (  96 ± 16 vs 44 ± 19 ms, P = 0.04  ). During ectopic activation, three patients in Group I, but no Group II patients, had transformation of recorded DPs into triple potentials. Radiofrequency ablation guided by the earliest activation of the LAT potential was performed with transient suppression of PAF, but ablation guided by the earliest activation of the PV potentials had a high success rate in eliminating PAF. In conclusion, differentiating the LAT from the PV potentials for initiation of PAF is feasible by an electrophysiological approach, and may be important for radiofrequency ablation of PAF.