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Notes: 1. Rapid ventricular rate (VR) and rhythm irregularity during atrial fibrillation (AF) impair cardiac performance. Although digoxin has been widely used in patients with AF, its efficacy for the control of VR and rhythm irregularity is unsatisfactory. Whether low-dose amiodarone is more effective remains unclear.2. We randomized 16 patients (13 male, three female; mean (±SD) age 63 ± 9 years) with chronic AF to receive either digoxin or amiodarone for 24 weeks. At baseline and at 12 and 24 weeks follow up, Holter monitor recording and cardiopulmonary exercise test were performed to assess VR and rhythm irregularity control and exercise capacity.3. Seven and nine patients received digoxin and amiodarone, respectively. After 12 and 24 weeks treatment, both digoxin and amiodarone significantly decreased the mean ambulatory VR and the VR during peak exercise compared with baseline (all P 〈 0.05). At 24 weeks, there were no significant differences between digoxin and amiodarone in the percentage reduction in VR during ambulatory (27 ± 13 vs 25 ± 12%, respectively; P = 0.8) and peak exercise (13 ± 12 vs 12 ± 10%%, respectively; P = 0.6).4. The rhythm irregularity, as measured by SD of RR intervals and the root mean square of the SD of RR intervals, and the exercise capacity, as measured by exercise workload, maximal oxygen consumption (VO2), minute ventilation, ventilatory equivalent and oxygen pulse, were not significantly changed after treatment with digoxin or amiodarone (all P 〉 0.05).5. Quality of life, determined by SF-36 questionnaire, and AF symptomatology, as measured by the AF Symptom Checklist, were also not significantly changed after treatment with digoxin or amiodarone (all P 〉 0.05).6. In conclusion, digoxin and low-dose amiodarone had similar efficacy in the control of VR during ambulatory activity and exercise. However, both were less efficacious during exercise and did not significantly affect rhythm irregularity, exercise capacity, quality of life and AF symptomatology in patients with chronic AF.

Notes: 1. Atrial fibrillation (AF) is the most commonly occurring cardiac dysrhythmia and remains a challenge to medical therapy. Although the disorder has been recognized for over 100 years, surprisingly very little is understood about its pathophysiology. Over the past decade, a variety of experimental and animal models of AF have been developed and these have provided insights into the mechanism of AF.2. The pathophysiology of AF is complex. Atrial fibrillation can be caused either by a single source of very rapid impulses or, in the majority of cases, by multiple random re-entering wavelets. The notion that AF may be initiated by a single rapid firing focus and the perpetuation of AF may be partly dependent on macro re-entry around the natural atrial orifices provides a new potential curative therapy for AF by radiofrequency ablation.3. Shortening of atrial wavelength, either by slow atrial conduction velocities, short atrial refractory periods or both, seems to predispose to development of intra-atrial re-entry and, thus, AF. The functional mechanism by which anti-arrhythmic drugs terminate AF appears to be by prolonging the wavelength and decreasing the number of re-entry wavelets. These understandings are important for the future development of effective anti-arrhythmic agents against AF.4. The presence of a short and variable excitable gap during AF may be potentially important for termination of AF by pacing.5. New insights are being gained into the potential role and mechanism of electrical remodelling of the atrium due to AF. Repeated induction of AF by rapid atrial pacing leads to a shortening of atrial refractoriness with loss of rate adaptation, which favours the induction and maintenance of AF. These electrophysiological changes were assumed to occur during repeated AF and to facilitate the generation of multiple re-entrant wavelets. These data suggest that prompt restoration of sinus rhythm and new novel therapy that prevents or diminishes electrical remodelling may promote maintenance of sinus rhythm after successful cardioversion.

Notes: 1. It is now recognized that atrial fibrillation (AF) is not a benign condition, as it is associated with a 40% increase in mortality and a doubling of the risk of stroke.2. The development of AF leads to mechanical, electrophysiological and cellular changes in the atria that tend to sustain AF. This process is known as atrial remodelling.3. The three electrophysiological elements in the atria that initiate and sustain AF are: (i) shortening of the refractory period and an increase in dispersion; (ii) slowing of conduction velocity; and (iii) the presence of triggerin. foci.4. As AF is a heterogeneous disorder, therapeutic strategies include the use of devices (pacemakers and atrial defibrillators), radiofrequency ablation (focal ablation or the creation of linear lines) and drug therapy that may reverse a remodelle. atrium.

Notes: Implantable Atrial Defibrillator. Introduction: The purpose of our study was to evaluate the effect of repeated cardioversion with an implantable atrial defibrillator on the clinical outcome of patients with atrial fibrillation. Methods and Results: The effects of the implantable atrial defibrillator on the total duration of atrial fibrillation, number of atrial fibrillation recurrences, and left atrial size were evaluated prospectively in 16 patients with atrial fibrillation (13 men and 3 women; mean age 58 ± 11 years). Seven patients bad no cardiovascular disease, 5 patients had hypertension. 3 patients had coronary heart disease, and 1 patient bad congenital heart disease. Eight patients had paroxysmal atrial fibrillation for a mean duration of 80 ± 61 months, and eight patients had persistent atrial fibrillation for a mean duration of 68 ± 119 months. Except for one patient who received digoxin throughout the study, alt patients received the same Class I or III antiarrhythmic agent throughout the study. The implantable atrial defibrillator successfully converted 50 (93%) of 54 spontaneous episodes of atrial fibrillation in 12 patients. During the initial 3 months of clinical follow-up, the atrial defibrillator documented 261 ± 270 hours of atrial fibrillation compared with 126 ± 172 hours (P = 0.01) during the subsequent 3 months. The left atrial size decreased from 4.4 ± 0.7 cm at the time of atrial defibrillator implantation to 4.1 ± 0.6 cm (P = 0.02) 6 months later. The number of atrial fibrillation recurrences did not change. These findings were observed in the absence of changes in drug therapy. No complications were observed. Conclusion: Restoration and maintenance of sinus rhythm in patients with atrial fibrillation by repeated cardioversion with an implantable atrial defibrillator was associated with a reduction in the total arrhythmia duration and a reduction in left atrial size. These results suggest that maintenance of sinus rhythm with the atrial defibrillator may reverse the remodeling process associated with atrial fibrillation.

Notes: Pulmonary Vein Arrhythmias. Introduction: Recent studies demonstrated that atrial arrhythmias may be generated within pulmonary veins. The purpose of this study was to compare the endocardial activation times at effective and ineffective ablation sites during radiofrequency catheter ablation of arrhythmias initiated or generated within pulmonary veins. Methods and Results: Twenty-one of 28 patients without structural heart disease underwent successful ablation of 23 arrhythmogenic foci within a pulmonary vein. Electrograms were recorded at 75 pulmonary venous sites and categorized into three groups: 23 successful ablation sites; 28 unsuccessful target sites within an arrhythmogenic pulmonary vein; and 24 sites within nonarrhythmogenic pulmonary veins. The endocardial activation time of premature depolarizations arising at successful target sites was significantly earlier than at other sites. During premature depolarizations, an endocardial activation time of -75 msec or earlier had a sensitivity of 83% and a specificity of 79% for identification of a successful ablation site. Endocardial activation times earlier than -100 msec were recorded only at successful ablation sites, and endocardial activation times later than -30 msec were recorded only at sites within nonarrhythmogenic pulmonary veins. The presence of a split potential during sinus rhythm or premature depolarizations was not a specific indicator of a successful ablation site. Conclusion: The endocardial activation times of premature depolarizations that arise within pulmonary veins and initiate atrial tachycardia/fibrillation are useful in identifying successful ablation sites.

Notes: Heterogeneous Changes in Atrial Electrophysiologic Properties. Introduction: The regional changes in atrial elettrophysiologic properties related to atrial fibrillation (AF) in patients with paroxysmal AF (PAF) and chronic AF (CAF) remain unclear. The purpose of this study was to investigate the regional changes in atrial electrophysiology in patients with AF. Methods and Results: We evaluated the atrial electrophysiology at different sites (high right atrium, low right atrium [LRAJ, and distal coronary sinus [DCS]) in 11 patients with CAF, 8 patients with PAF, and 10 controls. Patients with CAF had significantly prolonged interatrial conduction and corrected sinus node recovery time, and shortened atrial effective refractory period (ERP) with loss of rate-related adaptation in the DCS, hut had paradoxic prolongation of atrial ERP in the LRA, as compared with patients with PAF and the controls. As a result, the spatial distribution of atrial ERP that was observed in the controls and in patients with PAF was reversed in patients with CAF, without an increase in the dispersion of atrial refractoriness. Patients with PAF showed intermediate changes in atrial conduction times and atrial refractoriness as compared with patients with CAF and controls. Conclusion: There was a regional heterogeneity on the changes of atrial electrophysiology in different parts of the atrium, and the “normal” spatial distribution of atrial refractoriness was reversed in patients with CAF. The electrophysiologic changes observed in patients with PAF appear to behave as if in transition from the control state to CAF, suggesting progressive changes in atrial electropbysiologic properties.

Notes: Slow Pathway Ablation. Introduction: The relationship between temperature at the electrode-tissue interface and the loss of AV and ventriculoatrial (VA) conduction is not established, and the optimal target temperature for the slow pathway approach to radiofrequency ablation of AV nodal reentrant tachycardia (AVNRT) is unknown. Therefore, the purpose of this study was to compare target temperatures of 48°C and 60°C during the slow pathway approach to ablation of AVNRT. Methods and Results: The study included 138 patients undergoing ablation for AVNRT. Patients undergoing slow pathway ablation using closed-loop temperature monitoring were randomly assigned to a target temperature of either 48°C or 60°C. The primary success rates were 76% in the patients assigned to 48°C and 100% in the patients assigned to 60°C (P 〈 0.01). The ablation procedure duration (33 ± 31 min vs 26 ± 28 min; P = 0.2), fluoroscopic time (25 ± 15 min vs 24 ± 16 min; P = 0.5), and mean number of applications (9.3 ± 6.5 vs 7.8 ± 8.1; P = 0.3) were similar in patients assigned to 48° and 60°C, respectively. The mean temperature (46.1°± 24.8°C vs 48.7°± 3.2°C; P 〈 0.01), the temperature associated with junctional ectopy (48.1°± 2.0°C vs 53.5°± 3.5°C, P 〈 0.0001), and the frequency of VA block during junctional ectopy (24.6% vs 37.2%; P 〈 0.0001) were less in the patients assigned to 48°C compared to 60°C. The frequency of transient or permanent AV block was similar in each group (2.8% vs 3.6%; P = 0.2). In the 60°C group, only 12% of applications achieved an electrode temperature of 60°C. During follow-up of 9.9 ± 4.2 months, there was one recurrence of AVNRT in the 48°C group and none in the 60°C group. Conclusions: Compared to 48°C, a target temperature of 60°C during radiofrequency slow pathway ablation is associated with a higher primary success rate and a higher incidence of VA block during junctional ectopy induced by the radiofrequency energy. AV block is not more common with the higher target temperature, but only if VA conduction is aggressively monitored during applications of radiofrequency energy.

Notes: The dose-response relationship for successful defibrillation has been determined in man for the ventricle but not for the atrium. The purpose of this study was to determine the dose-response relationship for internal atrial defibrillation in humans. Seventy-seven consecutive patients underwent internal atrial defibrillation for acute (n = 14) or chronic AF (n = 63). Shocks were delivered in 40-V increments between electrodes positioned in the coronary sinus and the right atrium until successful conversion or a maximum of 400 V was reached. The shock strength versus success of shock data were subjected to a Kaplan-Meier survival analysis combined with a nonparametric probability analysis to arrive at the dose-response relationship. Using this relationship, comparisons were made between acute and chronic AF and clinical relevant conversion percentages (20, 50, 80 and 95%) were estimated and were compared with the conventional mean threshold. There were significant dose-response relationships in both patients groups (P 〈 0.05). The Kaplan-Meier analysis comparing patients with chronic and acute AF showed significant differences in their dose-response relationships (P 〈 0.001). The estimated shock intensity for 95% conversion in patients with acute and chronic AF was 279 V (2.9 J) and 433 V (6.6 J), respectively (P 〈 0.001). The conventional mean defibrillation threshold in patients with acute (192 ± 15 V. 1.4 ± 0.2 J) and chronic AF (343 ± 8 V, 4.4 ± 0.2 J) predicted the 60% and 45% chance of successful conversion, respectively. In conclusion, this study demonstrates that single shock conversion data can be used to determine a dose-response relationship, which can be used to estimate the shock intensity required for specific successful atrial defibrillation efficacy and to compare different clinical factors that affect defibrillation efficacy. (PACE 2003; 26:1249–1253)

Notes: Automatic mode switching (AMS) is a useful means to avoid rapid ventricular response during atrial fibrillation (AF), but AMS cannot occur if the detected atrial rate during AF is below the mode switching criteria. This may be the result of antiarrhythmic medications, or when the atrial events fall within the atrial blanking period, or if the atrial amplitudes during AF are too small to be sensed. We hypothesize that the addition of an automatic rate switching (ARS) algorithm may complement AMS response during AF with different detected atrial rates. We studied the Marathon DDDR pacemaker (Model 294–09, Intermedics Inc.) with the AMS and ARS algorithms that are independently programmable but can also operate in combination. AF sensed above the AMS rate (160 beats/mm) will lead to VDIR pacing, whereas AF below AMS rate will be tracked at an interim rate as dictate by the ARS, at a ventricular response that is 20 beats/min above the sensor indicated rate. Atrial tachyarrhythmias were simulated by chest wall stimulation (CWS). CWS was applied to 33 patients (16 men, 17 women, mean age 69 ± 11 years) with a Marathon DDDR pacemaker using an external pacer to simulate AF occurring at two rate levels: above the AMS rate (programmed at 160 beats/min) at 180 beats/min and below the AMS rate at 120 beats/min. The maximum, minimum, and mean ventricular rates during CWS in DDDR mode with AMS alone, ARS alone, and their combination were compared. During CWS at 120 beats/min, the AMS plus ARS setting showed a mean ventricular rate of 79 ± 3 beats/min and 124 ± 14 beats/mm in the AMS setting alone (P 〈 0.01). With CWS at 180 beats/min, the mean ventricular rate in the AMS plus ARS setting compared to the AMS setting alone was not significantly different. However, the variation in ventricular pacing rate was 7 ± 14 beats/min in the AMS plus ARS setting and 40 ± 42 beats/min in the AMS setting (P 〈 0.05). In conclusion, AMS is effective for simulated atrial tachyarrhythmias sensed above the AMS rate. Combined AMS with ARS is useful to handle simulated atrial tachyarrhythmia at a slower rate and to avoid rate fluctuation during AMS. There is also a possibility that this can be applied to the naturally occurring atrial tachyarrhythmias.