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AIMS: Recently, it has been shown that atrial fibrillation may be caused by spontaneously discharging foci located predominantly in the pulmonary veins. However, the effect of atrial overdrive pacing on these pulmonary vein foci has not been studied. METHODS AND RESULTS: In 58 patients with drug refractory paroxysmal or persistent atrial fibrillation we performed radiofrequency catheter ablation of arrhythmogenic triggers inside the pulmonary veins and/or an ostial pulmonary vein isolation with conventional mapping and ablation technology. Continuous bigeminal pattern of discharge from one or more arrhythmogenic pulmonary veins was recorded in 14 patients. Atrial overdrive pacing resulted in suppression of pulmonary vein 'focus' activity in all patients. The longest mean atrial pacing cycle length resulting in overdrive suppression was 587+/-114 ms. Independent of pacing rate and duration, bigeminal pulmonary vein focus activity reemerged 2.5+/-3.7s after cessation of pacing. Overdrive suppression of the pulmonary vein focus was incomplete in 9 pacing attempts, and resulted in induction of atrial fibrillation from the same vein in 3 of 31 pacing manoeuvres. At 2 years follow-up 79% of these patients were free of atrial fibrillation, 55% without antiarrhythmic drugs, 24% on previously ineffective antiarrhythmic drug therapy. CONCLUSION: Stable pulmonary vein 'focus' activity in patients with atrial fibrillation can be suppressed by atrial overdrive pacing. However, 'proarrhythmic' effects of atrial overdrive pacing, such as induction of atrial fibrillation, were also seen.

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INTRODUCTION: This study was designed to analyze dynamic changes in autonomic tone preceding the onset of sustained atrial arrhythmias in patients with focal atrial fibrillation (AF) to determine why patients with frequent discharge from the arrhythmogenic foci develop sustained AF. METHODS AND RESULTS: Holter tapes from 13 patients (10 men and 3 women; mean age 53 +/- 5 years) with paroxysmal "lone" AF (mean 18 +/- 13 episodes per week) and a proven focal origin (pulmonary veins in all cases) were analyzed. A total of 38 episodes of sustained (>30 min) were recorded and submitted to frequency-domain heart rate variability analysis. Six periods were studied using repeated measures analysis of variance: the 24-hour period, the hour preceding AF, and the 20 minutes before AF divided into four 5-minute periods. A significant increase in high-frequency (HF, HF-NU) components was observed during the 20 minutes preceding AF (P = 0.003 and 0.002, respectively), together with a progressive decrease in normalized low-frequency (LF-NU) components (P = 0.035). An increase in LF/HF ratio followed by a linear decrease starting 15 minutes before sustained AF also was observed, indicating fluctuations in autonomic tone, with a primary increase in adrenergic drive followed by a marked modulation toward vagal predominance immediately before AF onset. CONCLUSION: In patients with focal ectopy originating from the pulmonary veins, sustained episodes of atrial arrhythmias are mainly dependent on variations of autonomic tone, with a significant shift toward vagal predominance before AF onset.

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BACKGROUND AND OBJECTIVE: As has recently been discovered, paroxysmal atrial fibrillation (PAF) can be induced by focal extrasystoles or tachycardia. This raises the question of whether this form of atrial fibrillation can be cured by high-frequency catheter ablation of the focal trigger. PATIENTS AND METHODS: Seven men and eleven women (mean age 45.6 +/- 11 years) with severe symptoms and treatment-resistant PAF underwent electrophysiological tests with the aim of high-frequency catheter ablation, if long-term ECG monitoring had demonstrated frequent atrial extrasystoles or tachycardia as pointer to a focal origin. Ablation was performed at the point of earliest excitation after the origin of the ectopic focus had been localized. The end-point was reached if the atrial ectopic rhythm had ceased for more than 60 min. RESULTS: In 18 of the 20 patients an ectopic focus was found and successfully ablated (1 in the superior vena cava, 3 in the right atrium and 16 in a pulmonary vein). Atrial ectopic beats recurred within 24 hours of ablation in 6 of the 14 patients with a pulmonary vein focus: a second focus was found in two, re-emergence of the original focus in two, no re-investigation in another two. 13 of the 18 patients have had no further symptoms after a mean follow-up of 11 months without anti-arrhythmia treatment. CONCLUSION: The results indicate that focally induced paroxysmal atrial fibrillation can be cured by locally applied high-frequency ablation.

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INTRODUCTION: We assessed the mode of reinitiation of atrial fibrillation (AF) after cardioversion and the efficacy of ablating these foci of reinitiation in patients with chronic AF. METHODS AND RESULTS: Fifteen patients, 7 with structural heart disease, underwent mapping and catheter ablation of drug-resistant AF documented to be persistent for 5 +/- 4 months. In all patients, cardioversion was followed by documentation of P on T atrial ectopy and early recurrence, which allowed mapping of the reinitiating trigger or the source of ectopy. Radiofrequency (RF) ablation was performed at pulmonary vein (PV) ostia using a target temperature of 50 degrees C and a power limit of 30 to 40 W, with the endpoint being interruption of all local muscle conduction. A total of 32 arrhythmogenic PVs and 2 atrial foci (left septum and left appendage) were identified: 1, 2, and 3 or 4 PVs in 5, 3, and 6 patients. RF applications at the ostial perimeter resulted in progressively increasing delay, followed by abolition of PV potentials in 8, but potentials persisted in 6. A single ablation session was performed in 7 patients and 8 underwent two or three sessions because of recurrence of AF; ablation was directed at the same source due to recovery of local PV potential or at a different PV. No PV stenosis was noted either acutely or at repeated follow-up angiograms. Nine patients (60%) were in stable sinus rhythm without antiarrhythmic drugs at follow-up of 11 +/- 8 months. Anticoagulants were interrupted in 7 patients. CONCLUSION: PVs are the dominant triggers reinitiating chronic AF in this patient population. Elimination of PV potentials by ostial RF applications results in stable sinus rhythm in 60%. A larger group and longer follow-up are needed to investigate further the role of trigger ablation in curative therapy for chronic AF.

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Atrial fibrillation is the most common sustained arrhythmia causing substantial morbidity and probably increasing the risk of death. Most commonly, it is divided into a paroxysmal form, when--by definition--episodes end spontaneously, or a persistent one that lasts and requires a medical or electrical intervention for its termination. It might be called permanent, when no further attempts seem to be indicated for its elimination. Until recently, therapeutic strategies aimed at preventing cardiac embolism and at restoring and maintaining sinus rhythm by antiarrhythmic drugs. Long-term efficacy of the latter approach is poor, since less than 50% of patients can be maintained in stable sinus rhythm when periods of more than 1 year are considered. Can atrial fibrillation be cured? More than ten years ago Cox and coworkers demonstrated that the surgical compartimentation of both atria (MAZE procedure) is able to abolish atrial fibrillation in up to 90% of patients with chronic paroxysmal and also persistent atrial fibrillation. However, all studies trying to imitate the MAZE procedure by electrophysiological catheter-based techniques applying radiofrequency energy to produce transmural linear lesions were either not successful or showed a non-acceptable complication rate, especially a high rate of cerebrovascular accidents. The rationale behind the principle of compartimentation of the atria is the reduction of the critical atrial muscle mass necessary to facilitate fibrillation of the atria. A different approach aiming especially at the problem of paroxysmal atial fibrillation is based on the observation that there might be a "focal trigger" responsible for the initiation of the atrial tachyarrhythmia and that by eliminating this focal trigger atrial fibrillation can be avoided. This hypothesis was first verified in patients by Haïssaguerre et al., in fact experimental creation of "focal atrial fibrillation" was presented by Moe and Abildskov more than 30 years ago. During the last 3 years the concept of curing paroxysmal atrial fibrillation by applying focal radiofrequency lesions was supported by the results of several groups in more than 200 patients: 60 to 85% of patients can be cured, but in almost half of the cases more than one procedure is necessary. Most interestingly--and this is a finding of all investigators--more than 90% of the triggering ectopic foci are located in the pulmonary veins or in the pulmonary vein/left atrial junction. This concept is also supported by surgical experience from performing pulmonary vein isolations during open heart surgery. Most recently, the concept of eliminating the trigger was extended and applied to patients with established persistent atrial fibrillation. Until now, it has not been well established how many patients with paroxysmal atrial fibrillation are "good candidates" for a focal RF ablation procedure, nor is the risk of the procedure well defined. Besides the necessity of performing a transseptal catheterization there is the risk of cardiac embolism and pulmonary vein stenosis. The endpoint of the procedure is also not well defined: instead of trying to eliminate the "trigger" located in a pulmonary vein, it might be safer to isolate the "arrhythmogenic vein". This however, is a difficult task with current catheter technologies. It can be expected that new catheter designs for mapping and ablation and--maybe--the use of alternative energy sources--e.g., ultrasound, microwave--will make the procedure easier and applicable to more patients with drug refractory atrial fibrillation.

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Electrocardiograms of 37 consecutive patients with minimal preexcitation (i.e., PR >120 ms, QRS <120 ms) were compared before and after ablation with electrocardiograms of 37 age-matched patients with atrioventricular nodal reentrant tachycardia. The presence of a septal Q wave could be used to exclude minimal preexcitation with a high degree of reliability in both patients and controls before and after radiofrequency ablation.

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BACKGROUND: Modification of AV nodal conduction by means of radiofrequency catheter ablation has become the accepted mode of therapy for patients with symptomatic AV nodal re-entry tachycardias (AVN-RT). The published results demonstrate high success rates and a low incidence of severe complications. However, published series have primarily dealt with relatively young patient populations. Little is known about the efficacy and risks of radiofrequency catheter ablation of AVN-RT in the elderly. METHODS: We retrospectively analysed our data of 404 patients who underwent a catheter ablation therapy for AVN-RT between 1992 and June 1997. Nine patients were excluded from further analysis because of presence of more than one tachycardia mechanism. The ablation procedure was performed at the time of the diagnostic electrophysiologic study. RESULTS: The mean age of 395 patients undergoing catheter ablation for AVN-RT was 52.3 years (19-90 years); 85 patients were 65 years old or older. Compared with the younger subgroup, these elderly patients (mean age 70.4 years) more often had organic heart disease (coronary heart disease with or without myocardial infarction 19.3% versus 2.6%; P < 0.02), more often had syncopes or presyncopes with AVN-RT (43.2% versus 29.8%; P < 0.05), had more hospitalisations and emergency treatments because of their symptoms (56.8% versus 39.5%; P < 0.05) although the cycle length of the induced AVN-RT was significantly shorter in the younger patient group (325 ms versus 368 ms; P < 0.001). Slow pathway ablation was performed in 94% of the young and 82% of the elderly (P < 0.001). In 17.5% of the elderly patients versus 6.5% of the young (P < 0.05) the fast pathway approach was chosen as the first therapy or tried after an unsuccessful approach to the slow pathway. The overall success rate (96.8% in the young and 95.3% in the elderly) and the recurrence rate (5.8% in the elderly versus 4.9% in the young) were similar in both patient groups. There were no differences regarding the total procedure of fluoroscopy time, radiation exposure or the incidence of high-degree AV-block necessitating pacemaker implantation (2.3% in the elderly versus 1.6% in the young). CONCLUSIONS: In patients older than 65 years, AVN-RT may lead to severe, sometimes life-threatening symptoms, despite the fact that the tachycardia is not as fast as in younger patients. Radiofrequency catheter ablation can be performed effectively and safely and should be offered to these patients as first-choice therapy.

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INTRODUCTION: Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection. METHODS AND RESULTS: In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197% +/- 51% during drug-free tilting and 75% +/- 33% during repeated testing while on beta-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137% +/- 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156% +/- 104%; P = NS compared to baseline). CONCLUSION: In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, beta-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.

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Atrial fibrillation is one of the most common arrhythmias, leading at least in a subset of patients to severe symptoms (palpitations, weakness, syncope), and to hemodynamic impairment especially in the clinical setting of left ventricular dysfunction. Thus, in many cases restauration of sinus rhythm is indicated because of the negative effects of reduced cardiac output. Quinidine has been the first line drug for many years and has been proven to be highly effective especially when combined with Verapamil. But there is growing concern about using quinidine and other class I-anti-arrhythmic agents because of some hints in clinical trials for increased longterm mortality on these drugs. This study was undertaken to test the efficacy of Sotalol, a beta-blocker with additional strong class-III antiarrhythmic action, compared to a fixed combination of Quinidine and Verapamil for conversion of chronic atrial fibrillation and maintenance of sinus rhythm after medical or electrical cardioversion. To avoid early proarrhythmic effects, potassium values in the range of "high"-normal values (> 4.3 mval/L) were tried to be obtained. 82 patients were randomly assigned to receive either Sotalol or Quinidine/Verapamil. There was no difference between the groups as far as the underlying heart disease, duration of atrial fibrillation (mean 219 days) and other clinical features including echocardiographic parameters were concerned. The dose of the drug was weight-related individually adjusted, and the drug was continued thereafter. If sinus rhythm could not be established at that time, electric cardioversion was performed and the drug was continued in lower dosage thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

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1 The steady-state plasma concentrations of metoprolol and propafenone were determined in patients being treated with one of these drugs alone and during combined treatment with both drugs. In addition, single dose studies with metoprolol, propafenone and the combination of both drugs were performed in healthy volunteers to determine the pharmacokinetics and the time course of beta-adrenoceptor blocking activity. 2 In four patients being treated with metoprolol first and subsequently with propafenone in addition steady-state levels of metoprolol increased two to five fold with simultaneous treatment with propafenone. 3 In four patients being treated with the drug combination first and thereafter with propafenone alone no changes in the steady-state levels of propafenone were observed between both treatment periods. 4 Adverse effects of the drug combination were observed in two patients (one patient experienced severe nightmares and the other left ventricular failure). 5 When single oral doses of metoprolol (50 mg) and propafenone (150 mg) and the combination of both were administered to healthy subjects, an approximately two-fold decrease of the oral clearance of metoprolol was seen when propafenone was given in addition. No conclusive changes in the pharmacokinetics of propafenone could be detected in the presence of metoprolol. 6 Duration of beta-adrenoceptor blocking activity of a single dose of metoprolol in healthy volunteers as measured by reduction of exercise-induced tachycardia increased when propafenone was given in addition. 7 The dose of metoprolol should be reduced when propafenone is given in addition.

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A 55-year old male patient, with dizzy spells during everyday activity and a complete right bundle branch block as the sole electrocardiographic abnormality, reproducibly demonstrated tachycardia-dependent Mobitz Type II- and 2:1 second degree atrioventricular block. An electrophysiologic study revealed a provocable block within the distal portion of the bundle of His without evidence of a split His potential. Because of the truly tachycardia-dependent AV-block, beta-blocker medication was initiated to prevent high sinus rates during everyday activity. This therapy abolished symptoms totally.

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The incidence and prognostic significance of intraventricular conduction disturbances following aortic valve replacement was studied in a retrospective analysis of the records of 210 patients who had undergone aortic valve replacement for calcified aortic valve disease (dominant stenosis) between 05/01/1978 and 09/30/1983. Preoperatively, left anterior hemiblock was a common finding (9.6%), whereas LBBB, RBBB, and RBBB + LAFB were only found in 1.9, 1.0, and 1.0%, respectively. Following aortic valve replacement, the incidence of new conduction disturbances was 22.1% (n = 46): 19 LBBB, 16 LAFB, 6 RBBB, 3 RBBB + LAFB, 2 complete AV-blocks. In about half of the cases of LBBB and LAFB the ECG normalized within one week postoperatively. Thus, the incidence of persisting conduction disturbances was only 14.4%. Four patients died early (early mortality rate 1.9%), and 11 patients died later postoperatively during a 38 month follow-up. The 4-year cardiac survival rate of patients with pre- and/or postoperative conduction disturbances was similar to the 4-year cardiac survival rate of those patients who had never shown this complication (93.2 +/- 4.1 vs. 94.7 +/- 2.1%).

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Electrophysiological studies with prenalterol in 19 patients (6 women, 13 men, 5 with sinus node disease, 4 with AV node disease, 7 with double node disease, 2 with conduction disturbance below His bundle, 1 normal) showed that sinus node function (heart rate, sinus node recovery time) is uniformly improved by this beta-stimulator. Also AV conduction is significantly and uniformly improved (shortening of AH interval and of the functional refractory period of AV conduction). There is no or little influence on intra-atrial conduction and on conduction below the His bundle. However, spontaneous depolarisation in His-Purkinje fibers--as tested in patients with complete AV block and ventricular demand pacemaker--is increased through beta-stimulation with prenalterol as reflected by shorter escape intervals and higher frequency escape rhythm. Prenalterol may be of clinical use in patients with cardiomyopathies who developed bradycardia under digitalisation or patients with severe bradyarrhythmia either with or without digitalis. It might also be useful in rare emergency situations, when complete pacemaker failure develops.

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Standstill and inexcitability (quiescence) of the high right atrium could be demonstrated in a patient with sinus node dysfunction and bradycardia--tachycardia syndrome. The onset of P wave in surface electrocardiogram did not represent the beginning of atrial excitation but followed 130 msec the high right atrial and 50 msec the low right atrial deflection, leading thereby to a short PR interval which gave misinformation on the atrioventricular conduction. A pacemaker implant with right ventricular stimulation freed the patient of his previous complaints. 4 wk after the implantation the demand unit was inhibited for 5 h by external stimulation. Continuous ECG monitoring, esophageal ECG recording and fluoroscopic study could not reveal any atrial activity. The conditions for atrial pacemaker implantation are discussed.

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Excitability, maximum velocity of depolarization (MVD), conduction velocity, discharge rate and the duration of transmembrane action potentials as a function of frequency of stimulation were studied in isolated cardiac tissues exposed to the optical isomers of verapamil and D 600.

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