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Fingolimod, a sphingosine-1-phosphate receptor (S1PR) modulator, was the first oral disease-modifying therapy approved for relapsing forms of multiple sclerosis; it reduces autoreactive lymphocytes' egress from lymphoid tissues by down-regulating S1PRs. Sphingosine-1-phosphate signaling is implicated in a range of physiologic functions, and S1PRs are expressed differentially in various tissues, including the cardiovascular system. Modulation of S1PRs on cardiac cells provides an explanation for the transient effects of fingolimod on heart rate and atrioventricular conduction at initiation of fingolimod therapy, and for the mild but more persistent effects on blood pressure observed in some patients on long-term treatment. This review describes the nontherapeutic actions of fingolimod in the context of sphingosine-1-phosphate signaling in the cardiovascular system, as well as providing a summary of the associated clinical implications useful to physicians considering initiation of fingolimod therapy in patients. A transient reduction in heart rate (mean decrease of 8 beats per minute) and, less commonly, a temporary delay in atrioventricular conduction observed in some patients when initiating fingolimod therapy are both due to activation of S1PR subtype 1 on cardiac myocytes. These effects are a reflection of fingolimod first acting as a full S1PR agonist and thereafter functioning as an S1PR antagonist after down-regulation of S1PR subtype 1 at the cell surface. For most individuals, first-dose effects of fingolimod are asymptomatic, but all patients need to be monitored for at least 6 hours after the first dose, in accordance with the label recommendations.

Patients with heart failure frequently exhibit intraventricular conduction delays, which contribute to asynchronous contraction patterns and impaired hemodynamic performance. Cardiac resynchronization therapy (CRT) with biventricular (BV) and left ventricular (LV) pacing has been shown to improve both hemodynamic and clinical performance. This study investigated the effects of CRT on LV Doppler indices in these patients.Thirty-two patients with advanced heart failure (New York Heart Association classor =III, QRS120 milliseconds, PR interval150 milliseconds) were studied 4 weeks after implantation of a CRT system. Doppler echocardiography was conducted in 3 separate CRT modes, right ventricular, LV, and BV stimulation at 3 different atrioventricular delays. CRT resulted in significant improvement of Doppler parameters such as filling time (FT, 313 +/- 111 milliseconds at baseline --363 +/- 154 milliseconds [BV], P.05), aortic velocity time integral (AO(VTI) 23.2 +/- 7.4 cm at baseline --26.8 +/- 8.8 cm [LV], P.05), and the myocardial performance index (MPI, 1.21 +/- 0.51 at baseline --0.85 +/- 0.34 [BV], P.05). The most improvement was observed with LV and BV stimulation at short and intermediate atrioventricular delays (80-120 milliseconds), independent of ischemic or idiopathic origin.CRT improves hemodynamic performance in patients with heart failure with intraventricular conduction delays. Doppler echocardiography allows noninvasive evaluation of acute CRT effects in patients with heart failure. In particular, FT, AO(VTI), and MPI are useful parameters for noninvasive follow-up and optimization of pacing parameters.

Background Radiofrequency ablation of the atrioventricular junction is a well-established procedure for the management of atrial fibrillation refractory to medical therapy. However, there are few data available on the prevalence and characteristics of the escape rhythms that are present after the procedure. Methods The Ablate and Pace Trial was a prospective, multicenter registry of atrioventricular junction ablation and pacing in atrial fibrillation. Ablation of the atrioventricular junction was accomplished with radiofrequency energy with standard techniques. Before discharge from the hospital, patients underwent a systematic analysis of the rate and morphologic features of the escape rhythm, if any, that was present when the pacing rate was gradually decreased. Results There were 156 patients from 16 centers who underwent attempted radiofrequency ablation of the atrioventricular junction. The procedure was successful in 155 (99%) of 156 patients. An escape rhythm was present in 104 patients (67%) after radiofrequency ablation. The escape rate ranged from 11 to 65 beats/min (mean 39 ± 10 beats/min). Only 49 patients (31%) had an escape rate ≥40 beats/min. Of the 104 patients with an escape rhythm, 53 patients (51%) had a QRS that was unchanged from baseline. There was no correlation between the number of radiofrequency applications and the presence of an escape rhythm. Conclusion The majority of patients who undergo radiofrequency catheter ablation of the atrioventricular junction are pacemaker dependent after the procedure, as defined by lack of an escape rhythm or the presence of an escape rhythm that is

The purpose of this study was to determine the incidence and origin of T-wave changes after ablation of an accessory atrioventricular connection (AC), which could either be a sign of damage to the coronary circulation or a result of persistent abnormal repolarization secondary to previously abnormal ventricular activation ("cardiac memory").Ninety of 107 consecutive patients (33 women and 57 men, mean age 36 +/- 5 years) undergoing successful catheter ablation of an AC were studied. Patients with bundle branch block or more than 1 AC were excluded. Sixty-four patients had manifest preexcitation (group 1) and 26 had a concealed AC (group 2). Immediately after loss of preexcitation, 38 (59%) patients with a manifest AC showed T-wave abnormalities. In contrast, none of the patients with a concealed AC had T-wave abnormalities after ablation (P.05). The T-wave changes (1) did not correlate with the number or duration of energy applications or with markers of tissue injury; (2) correlated with the location of the AC and the degree of preexcitation, respectively; and (3) completely resolved over a period of weeks to months. None of the patients had recurrence of preexcitation or tachycardia during a mean follow-up of 16 +/- 7 months.T-wave changes after ablation are most likely caused by "cardiac memory" and are not a sign of myocardial or coronary injury.

Background Patients with recurrent forms of atrial fibrillation may receive dual-chamber pacemakers after atrioventricular junction ablation for refractory symptoms. These patients are at risk for chronic atrial fibrillation, which would negate the benefits of dual-chamber pacing. The purpose of this study was to examine the survival of dual-chamber pacing modes in patients undergoing ablate and pace therapy. Methods and Results One hundred fifty-six patients underwent ablate and pace therapy for medically refractory chronic (70 patients) or recurrent (86 patients) atrial fibrillation. Seventy-eight percent of patients had structural heart disease. The mean age was 66 ± 11 years, with an average ejection fraction of 48% ± 18%. The choice of pacing mode and programming were at the discretion of the investigators. At implantation, 91 patients (58%) were programmed to VVI mode, 47 (30%) were programmed to DDD mode, and 18 (12%) were programmed to DDI mode. After 1 year of follow-up, 10 DDD patients were reprogrammed to VVI mode (7 patients) or DDI mode (3 patients), most frequently for chronic atrial fibrillation (7 patients). Two patients with DDI mode were reprogrammed to VVI and DDD modes (1 patient each). Survival of the DDD mode was 76% at 1 year by Kaplan-Meier analysis. Reprogramming from DDD mode was not associated with patient age, left ventricular ejection fraction, discontinuation of antiarrhythmic drugs, or the duration of atrial fibrillation symptoms before ablation. Conclusions Seventy-six percent of patients with recurrent atrial fibrillation who are initially programmed to DDD mode remain in DDD mode 1 year after ablation and pacing therapy. The modest rate of progression to chronic atrial fibrillation supports the use of dual-chamber pacing in this setting. (Am Heart J 1999;137:682-5.)

Impedance monitoring has been proposed as a method to assess the adequacy of tissue heating during catheter ablation procedures. The purpose of this study was to evaluate the relation among initial impedance, fall in impedance, and electrode temperature during catheter ablation procedures.Data from 248 applications of radiofrequency energy in 45 consecutive patients (26 with accessory pathways and 19 with atrioventricular nodal reentrant tachycardia) referred for catheter ablation were analyzed. The initial impedance was higher during ablation of accessory pathways than during atrioventricular nodal reentrant tachycardia (116+/-66 versus 106+/-80 omega, P.001). In both groups, a significant correlation was observed between the initial impedance and temperature (R = 0.98, P.001). After accounting for differences between patients and ablation targets, an even closer correlation was observed (accessory pathways: R = 0.95, P.0001; atrioventricular nodal reentrant tachycardia: R = 0.94, P.0001).These data suggest that monitoring of the initial impedance and the fall in impedance during ablation procedures may provide clinically valuable information to assess the efficacy of tissue heating and lesion formation.

Although radiofrequency catheter ablation of the atrioventricular (AV) node is an established treatment for atrial fibrillation (AF) with uncontrolled ventricular response, factors that predict clinical outcome in patients with associated congestive heart failure (CHF) are unknown.AV node ablation and permanent pacemaker implantation was performed in 44 consecutive patients (mean age 71+/-10 years) with CHF and AF associated with uncontrolled ventricular response. Immediately before ablation, mean left ventricular ejection fraction (EF) measured by 2-dimensional echocardiogram was 34.6%+/-9.8%, mean exercise tolerance time was 2.6+/-1.8 minutes, and mean quality of life score was 62.3+/-19.7. Complete AV block was achieved in all 44 patients but was complicated by death in 1 patient from cardiogenic shock soon after ablation. By 1 month after ablation, EF increased to 43.8%+/-13.7% (P.01), exercise tolerance time was 4.0+/-2.5 minutes (P.01), and mean quality of life score decreased to 35.6+/-18.1 (P.01). Improved cardiac performance (increase in EFor = 9% over baseline EF) was detected in 20 (45%) of the patients. During a mean follow-up of 17+/-9 months, 5 patients died suddenly of presumed ventricular tachyarrhythmia and 4 others died of progressive CHF. Multivariate Cox survival analysis identified baseline EFor = 30%, presence of significant mitral regurgitation (2+) before ablation, and failure to exhibit improved cardiac performance by 1 month after ablation as the only independent predictors of death.Baseline variables and failure of EF to improve soon after AV node ablation identifies patients with CHF and AF who have a high mortality rate. Adjunctive therapy to reduce sudden death and progressive heart failure should be evaluated in this subgroup.

Background Persistent inappropriate sinus tachycardia may evolve as a complication after radiofrequency (RF) fast pathway ablation of atrioventricular nodal reentrant tachycardia (AVNRT). Parasympathetic denervation may serve as one of the possible mechanisms. We performed a study to show the prevalence of this phenomenon in RF ablation of the slow pathway. Methods and Results Thirty-three patients (25 women, 8 men) aged 53 ± 16 years were investigated. A median of 3 pulses was used to selectively modify or ablate the slow pathway and render AVNRT noninducible. Heart rate (HR) and different indexes in the time and frequency domain of heart rate variability were evaluated in serial 24-hour Holter recordings. Data were obtained 1 day, 1 month, and 3 months after the procedure and compared with preablation values. Despite a trend of increasing HR and decreasing heart rate variability within the first month after RF ablation, no significant changes were detected. Conclusions RF ablation of the slow pathway in AVNRT does not change parameters of HR and heart rate variability significantly by means of serial 24-hour Holter recordings. (Am Heart J 1998;136:259-63.)

To determine whether precise left-sided accessory pathway localization is possible from the coronary sinus, electrocardiogram (ECG) characteristics from the coronary sinus pair demonstrating earliest activation via the accessory pathway were compared to simultaneous mitral annular ablation catheter ECGs at successful ablation sites in 48 patients. To define the coronary sinus-mitral annular relation, the coronary sinus to mitral annulus distance (D) was measured at sequential distances from the coronary sinus os in 10 cadaver hearts. Mitral annular ECGs demonstrated earliest activation via the accessory pathway more frequently than the earliest coronary sinus pair (p0.001), more frequent continuous electrical activity (p0.001), and more frequent accessory pathway potentials (p0.01). D was10 mm at 20, 40, and 60 mm, respectively, from the coronary sinus os. Coronary sinus ECGs do not precisely localize left-sided accessory pathways, which may be due in part to an average anatomic separation of more than 10 mm between the coronary sinus and accessory pathways bridging the mitral annulus.

This prospective study was conducted to determine the percentage of patients with long-term pacemaker dependency after successful radiofrequency ablation of the atrioventricular junction. Abrupt inhibition of the pacemaker was performed 13.5 ± 8.1 months after ablation in 59 patients. A ≥5-second asystole was considered to indicate pacemaker dependency. Pacemaker dependency was present in 18 patients. Absence of escape rhythm immediately after ablation was strongly associated with a higher incidence of long-term pacemaker dependency. The following variables were not associated with pacemaker dependency: age, presence of cardiac disease, presence of preablation bundle branch block, number of radiofrequency applications, a bilateral approach for ablation, and continuation of antiarrhythmic therapy after ablation. We concluded that (1) long-term pacemaker dependency is present in 30.5% of the patients after successful atrioventricular junction radiofrequency ablation and (2) absence of escape rhythm immediately after ablation predicts long-term pacemaker dependency. (Am Heart J 1997;133:580-4.)

The purpose of this study was to compare the atrial-His intervals generated during programmed atrial stimulation in patients with and without dual atrioventricular nodal physiology and with and without inducible atrioventricular nodal reentrant tachycardia. Programmed atrial stimulation at a basic-drive cycle length of 500 to 600 msec was performed in 180 patients. The minimum atrial-His interval was defined as the atrial-His interval of the basic-drive beats. The maximum atrial-His interval was defined as the longest A2H2 interval. The criterion for dual atrioventricular nodal physiology was an increment of 50 msec in the A2H2 interval in association with a 10 msec decrement in the A1A2 interval. The minimum atrial-His interval was significantly shorter (106 +/- 34 msec vs 116 +/- 29 msec; p0.05) and the maximum atrial-His interval significantly longer (304 +/- 101 msec vs 222 +/- 56 msec; p0.001) in the 87 patients who had atrioventricular nodal reentry than in the 93 patients who did not. Among the 87 patients who had atrioventricular nodal reentry, the maximum atrial-His interval was significantly longer in 53 patients who had dual atrioventricular nodal physiology than in 34 patients who did not (340 +/- 105 msec vs 249 +/- 62 msec; p0.001). Among the 66 patients who had dual atrioventricular nodal physiology, the maximum atrial-His interval was significantly longer in 53 patients who had atrioventricular nodal reentry than in 13 patients who did not (340 +/- 105 msec vs 268 +/- 61 msec; p0.01). The insensitivity of the conventional dual atrioventricular nodal physiology criterion for the detection of dual atrioventricular nodal pathways is in part attributable to a lesser degree of slowing of conduction in the slow pathway relative to the fast pathway in some patients who have atrioventricular nodal reentry. The inability to demonstrate atrioventricular nodal reentry despite the presence of dual atrioventricular nodal physiology in some persons may be attributable in part to an inadequate degree of conduction delay in the slow pathway.

Adenosine, verapamil, propranolol, and procainamide are widely used antiarrhythmic drugs. The interactions among them are still not known in human beings. Adenosine-induced negative dromotropic effects were assessed by rapid bolus injection of adenosine during constant high right atrial pacing in each patient. The initial dose of adenosine was 0.5 mg and was followed by a stepwise increment of 0.5 mg until atrioventricular (AV) nodal block occurred. The negative dromotropic actions of adenosine were examined in the control state and in the following three protocols in three groups of patients: (1) In 12 patients (group 1), intravenous verapamil, 0.15 mg/kg, was given; (2) In 12 patients (group 2), intravenous propranolol, 0.1 mg/kg, was given; and (3) in 10 patients (group 3), intravenous procainamide, 15 mg/kg, was given. The dose-response curves of adenosine on AV nodal conduction were almost identical in the control state and after verapamil, propranolol, or procainamide injection. However, verapamil, in contrast to propranolol, significantly reduced the dose of adenosine required to produce AV nodal block, from 4.4 +/- 0.7 mg to 2.7 +/- 0.3 mg (p0.01). Of note, procainamide exerted no significant effects on adenosine-induced negative dromotropism on AV nodal conduction or AV nodal block. In conclusion, the negative dromotropic effects of adenosine are preserved and independent even in the presence of verapamil, propranolol, or procainamide. Both verapamil and propranolol can exhibit additive effects with adenosine in prolonging AV nodal conduction time; however, only verapamil can reduce the dose of adenosine required to produce AV nodal block. This finding indicates that the dose of adenosine may be reduced for patients who have already been treated with verapamil.

This study evaluated the effects of flosequinan on ventricular rate in patients with congestive heart failure and atrial fibrillation to determine whether this agent has a facilitatory effect on atrioventricular conduction and whether such an effect may be deleterious. Flosequinan is known to have a dose-dependent positive chronotropic effect on the sinus node, but its effect on atrioventricular conduction has not been evaluated. An excessive increase in ventricular rate during the treatment of heart failure could raise a safety concern and counterbalance beneficial responses. Data were analyzed from 338 patients participating in three similarly designed placebo-controlled exercise trials with flosequinan who also underwent ambulatory electrocardiographic monitoring. The effects of two doses of flosequinan on supine, standing, ambulatory, and exercise heart rates and on exercise capacity in patients in sinus rhythm and atrial fibrillation were compared. Flosequinan increased heart rate in a dose-dependent manner, in patients both with sinus rhythm and atrial fibrillation. A 100 mg once daily dose produced significant increases, in both rhythms, ranging from 6 to 11 beats/min, in supine and standing heart rate, ambulatory heart rate, and exercise heart rate. With a dose of 75 mg twice daily, heart rates under these conditions increased by >20 beats/min in flosequinan-treated patients in atrial fibrillation, a change significantly greater than that observed with placebo or flosequinan, 100 mg once daily and also more than in patients in sinus rhythm treated with the same dose. These results indicate that flosequinan facilitates atrioventricular nodal conduction, increasing the ventricular response in atrial fibrillation, especially at higher dosages. This finding could result from a direct drug action, such as phosphodiesterase inhibition, or reflex sympathetic activation. This response is of sufficient magnitude potentially to impair left ventricular function and interfere with clinical benefit. The effect of heart-failure drugs on ventricular responses in atrial fibrillation should be examined to provide insight into potential mechanisms of both action and safety in this common patient group.

In an effort to reduce energy requirements for atrial defibrillation to a level low enough to perform painless electrical cardioversion with an implantable atrial defibrillator, we tested the hypothesis that drug therapy with the class III agent d-sotalol, when used concurrently with a low-energy shock, reduces atrial defibrillation threshold. In a nonthoracotomy canine model of atrial fibrillation, intracardiac shocks were delivered between the distal coronary sinus and the mid-right atrium. Based on a step-up energy delivery protocol the atrial defibrillation threshold was defined as the least amount of energy that resulted in a >10% and

A study during the era of surgical ablation suggested that atrioventricular (AV) nodal conduction is faster in patients with accessory pathways than in controls. In the present study, AV nodal characteristics were studied in 30 patients who underwent radiofrequency ablation of an accessory pathway and compared to 23 control patients. Sinus cycle length, AH and HV intervals, AV block cycle length, ventriculoatrial (VA) block cycle length, AV nodal effective refractory period, and VA effective refractory periods were measured in control and postablation accessory pathway patients before and after autonomic blockade with 0.04 mg/kg of atropine and 0.2 mg/kg of propranolol. The mean sinus cycle length in the control and accessory pathway groups did not differ significantly at baseline (798 +/- 211 and 766 +/- 156 msec, respectively) or after autonomic blockade (654 +/- 98 and 649 +/- 108 msec, respectively). The mean AH interval in the accessory pathway group (77 +/- 15 msec) was significantly shorter than in the control group (91 +/- 22 msec; p0.05) at baseline; however, there was no difference after autonomic blockade. No other significant differences were observed between the accessory pathway and control groups. These results demonstrate that AV nodal properties of patients with accessory pathways are not significantly different from controls and suggest that previously reported differences may have been due to selection bias.

10. George BS, Voorhees III WD, Roubin GS, Fearnot NE, Pinkerton CA, Raizner AE, King SB, Holmes DR, Topol EJ, Kereiakes DJ, Hartzler GO. Multicenter investigation of coronary stenting to treat acute or threatened closure after percutaneous transluminal coronary angioplasty: clinical and angiographic outcomes. J Am Coll Cardiol 1993; 22:135-43. 11. Rozenman Y, Lotan C, Mosseri M, Gotsman MS. Relation ofthrombotic occlusion of coronary stents to the indication for stenting, stent size, and anticoagulation. Am J Cardiol 1995;75:84-5.

Atrioventricular (AV) node reentrant tachycardia is now routinely cured by selective radiofrequency ablation of slow AV node pathway conduction. However, debate remains concerning the optimum method for localizing the site at which radiofrequency energy should be delivered to eliminate slow-pathway conduction. Some investigators have proposed simple anatomy-guided ablations posteriorly near the ostium of the coronary sinus, whereas others suggest an electrophysiology-guided ablation using either recorded “slow potentials” or mapping of the retrograde atrial exit site of slow AV node pathway conduction when possible. To examine these issues, we systematically studied slow potentials recorded in the AV junction of patients undergoing radiofrequency catheter ablation for medically refractory AV node reentrant tachycardia. In 67 patients with the slow-fast form of AV node reentrant tachycardia, we performed detailed atrial mapping along the tricuspid annulus within the triangle of Koch. Two types of slow potentials were identified. Low-amplitude, low-frequency potentials, found in 48% of patients, were localized to the mid to posterior portions of the triangle of Koch, whereas high-amplitude, high-frequency potentials, observed in 22% of patients, were located only posteriorly near the ostium of the coronary sinus. In response to a bolus infusion of adenosine or incremental atrial pacing-induced AV node Wenckebach periodicity, the low-amplitude, low-frequency potentials showed an increased duration and further reduction in amplitude and frequency and often totally disappeared. In contrast, in spite of these maneuvers, the high-amplitude and high-frequency potentials remained unchanged. Of the 25 (37%) of 67 patients in whom the earliest retrograde atrial activation during ventriculoatrial slow AV nodal pathway conduction could be recorded, no patient exhibited low-amplitude, low-frequency potentials, and only 7 (28%) of 25 of these patients showed high-amplitude, high-frequency potentials. High-amplitude, high-frequency potentials persisted after successful radiofrequency ablation of slow pathway conduction. Fewer applications of radiofrequency energy were required for successful elimination of slow pathway conduction in patients in whom the retrograde atrial exit site of slow-pathway conduction could be localized, compared with those patients who only exhibited retrograde fast AV nodal pathway conduction. We conclude that high-amplitude, high-frequency potentials are part of atrial activity, whereas the origin of low-amplitude, low-frequency potentials is unclear and may represent either true intranodal biophysical electrical activity or merely artifact or far-field potentials. Regardless, the recording of high-amplitude or low-amplitude potentials is not required for successful ablation of slow-pathway conduction, although the ability to localize the retrograde atrial exit of slow-pathway conduction may assist in the ablation procedure.

Pacing the right ventricle in the apex profoundly modifies the sequence of activation and thus the sequence of contraction and relaxation of the left ventricle. To evaluate the relative importance of preserving normal ventricular activation sequence and optimal atrioventricular (AV) synchrony in permanent pacing, we compared the effects of three pacing modes: AAI, preserving both normal AV synchrony and normal activation sequence; DDD, with complete ventricular capture that preserves only AV synchrony; and VVI, disrupting both, at rest and during exercise. Hemodynamic and radionuclide studies were performed in 11 patients who had normal intrinsic conduction and who were implanted on a long-term basis with a DDDR pacemaker for isolated sinus node dysfunction. AAI versus DDD and VVI significantly increased cardiac output at rest (6.6 +/- 1.3 L/min vs 6 +/- 0.9 L/min vs 5 +/- 1 L/min; p0.01) and during exercise (13.5 +/- 2 L/min vs 12.1 +/- 2.2 L/min vs 14.4 +/- 2.1 L/min; p0.01). Pulmonary capillary wedge pressure was lowest with AAI (15.4 +/- 4.5 mm Hg), with an average reduction of 17% compared with DDD (19.6 +/- 5 mm Hg; p0.01) and of 30% compared with VVI (25.8 +/- 7 mm Hg; p0.01) during exercise. Identical benefits were observed for all other hemodynamic parameters: right atrial pressure, pulmonary artery pressure, left ventricular (LV) stroke work index, and systemic vascular resistances. LV ejection fraction was significantly higher in AAI than in DDD at rest (61% vs 58%, respectively; p0.05) and during exercise (65% vs 60%, respectively; p0.05). This improvement in LV systolic function resulted principally from the increase in septal ejection fraction. LV filling also was improved in AAI as demonstrated by a significant increase in peak filling rate at rest and during exercise. These data show the importance of preserving, whenever possible, not only normal AV synchrony but also normal ventricular activation sequence in permanent cardiac pacing.

Fourteen men with intermittent ventricular bigeminy were selected for this study because coupling intervals of the extrasystoles were considerably long and usually fixed, and bradycardia-dependent (10 cases) and/or tachycardia-dependent (12 cases) termination of bigeminy occurred. In all cases, when the heart rate ranged between two certain values, ventricular bigeminy with fixed-coupled extrasystoles was sustained. In all cases showing bradycardia-dependent termination, bigeminy was suddenly terminated with no changes in coupling of the preceding extrasystoles when the heart rate was decreased below a certain lower value. In all cases showing tachycardia-dependent termination except one, when the heart rate increased beyond a certain higher value, coupling intervals gradually lengthened until bigeminy was terminated. These findings strongly suggest the possibility that, in a considerably large number of clinical cases, ventricular extrasystoles with fixed coupling are caused by longitudinal dissociation of conduction in the reentrant pathway of extrasytoles.

The safety and efficacy of radiofrequency catheter modification of the atrioventricular node for atrioventricular nodal reentrant tachycardia in the pediatric population is described. Twenty-one patients with a mean age of 14.9 ± 3.6 years underwent slow-pathway atrioventricular nodal modification with a stepwise anatomic approach. The average cumulative fluoroscopy exposure time (22 procedures in 21 patients) inclusive of the electrophysiologic study was 36.1 ± 22 minutes. Noninducibility of tachycardia was achieved in all patients with one procedural complication (hemothorax). During a mean follow-up of 15 ± 9.06 months, tachycardia recurred in one patient. Patient and family acceptance and satisfaction with the procedure was high. Because of the curative potential of radiofrequency catheter modification with low associated short- and long-term risks, it may be considered as a primary treatment option in pediatric patients with symptomatic atrioventricular nodal reentrant tachycardia.

Electrophysiologic study and radiofrequency ablation therapy were performed in 23 patients with atypical (8 patients) or multiple (15) atrioventricular node reentry tachycardias. Dual pathways with anterograde fast and slow pathway conductions were demonstrated in 16 patients. Studies on retrograde conduction revealed the presence of three different pathways, including fast (15 patients), intermediate (17), and slow (16). The radiofrequency current was applied to the inferior aspect, one-third anterior two-thirds posterior between the His bundle and the ostium of the coronary sinus, of Koch's triangle along the tricuspid annulus in all patients. Application of the current resulted in selective ablation or modification of both retrograde intermediate and slow pathway conductions in 20 patients. In two patients retrograde fast pathway conduction was also modified. Complete atrioventricular block occurred in the remaining patient. Sixteen patients had no induction of tachycardia or echo, 4 had induction of a single echo, and 2 had induction of the slow-fast form tachycardia; one of those 2 patients underwent a second trial and was successful. A median application of 2 was delivered at a power of 25 +/- 5 W and a duration of 18 +/- 4 sec. The total fluoroscopic time was 25 +/- 21 minutes. The anterograde fast pathway conduction was unaffected; the shortest atrial paced cycle length that sustained 1:1 fast pathway conduction was 329 +/- 65 msec and 330 +/- 68 msec before and after ablation, respectively. A follow-up electrophysiologic study was performed in 16 patients 60 +/- 15 days after ablation. Eleven had no induction of tachycardia or echo, and five had induction of < 3 echoes. This study demonstrated that radiofrequency ablation with the inferior approach is effective and safe in atypical or multiple atrioventricular node reentry tachycardias. It resulted in ablation of the slow pathway and retrograde intermediate pathway conduction with preserved atrioventricular conduction.

A late electrophysiologic study was conducted in 182 of 289 patients with slow-fast atrioventricular node reentry tachycardia 81 +/- 36 days after radiofrequency ablation therapy by the inferior approach. Of these 182 patients, electrophysiologic study immediately after ablation revealed a selective modification of the slow pathway in 159, a modification of both the slow and fast pathways in 15, a modification of the fast pathway alone in 3, and failure of ablation in 5. One hundred two patients had no induction of echoes; 75 had induction of fewer than four echoes; and 5 had induction of sustained tachycardia with or without isoproterenol infusion. The late electrophysiologic study in these 182 patients revealed a persistent effect without changes in conduction properties in 161 (88%) patients. A change in conduction properties was noted in 21 patients, including 5 with resumption of slow- or fast-pathway conduction with induction of sustained tachycardia, 8 with improved fast- or slow-pathway conduction, and 8 with an additional depression of fast- or slow-pathway conduction. Of the 102 patients with no induction of echoes and the 75 patients with induction of fewer than four echoes during the immediate postablation electrophysiologic study, 5 (3 and 2, respectively) patients had induction of tachycardia. Of the 5 patients with induction of sustained tachycardia in the immediate postablation electrophysiologic study, 3 continued to have induction of sustained tachycardia; 1 had induction of echoes only; and 1 had no induction of echoes.(ABSTRACT TRUNCATED AT 250 WORDS)

Local electrograms from 47 consecutive patients who underwent successful radiofrequency catheter ablation of 49 accessory atrioventricular (AV) connections were analyzed. One hundred twenty-two local electrograms were recorded at 27 successful and 95 unsuccessful sites immediately before radiofrequency catheter ablation of 27 manifest accessory AV connections during preexcited sinus rhythm or atrial pacing. Continuous electric activity was found in 96% of successful sites versus 71% of unsuccessful sites (p < 0.01). Possible accessory pathway (AP) potentials were present only in 15% of successful and 2% of unsuccessful sites, respectively (p < 0.05). All measured time intervals were significantly shorter for successful sites as compared to unsuccessful sites of ablation of manifest accessory AV connections. Unipolar electrograms from the tip of the ablation catheter of each successful and unsuccessful ablation site were available for the last 16 patients with manifest accessory AV connections. A PQS pattern of the unipolar electrogram was associated with a higher success rate, whereas a PrS pattern never resulted in successful ablation of an accessory AV connection. Multivariate logistic regression analysis of the local electrogram characteristics of rapidly conducting, concealed accessory AV connections revealed the interval between the onset of the local ventricular and atrial electrogram (VoAo interval) as the only independent variable associated with successful sites for radiofrequency catheter ablation. The only study patient with a slowly conducting, concealed accessory AV connection underwent successful ablation with the first lesion of radiofrequency energy at the site with the shortest VoAo interval. We conclude that (1) the shortest local AV intervals and local ventricular electrograms preceding the earliest onset of the delta wave in any surface lead are predictive of successful ablation of manifest accessory AV connections; (2) the shortest local VA intervals during orthodromic AV reentry tachycardia or right ventricular pacing are predictive of successful ablation of concealed accessory AV connections; and (3) unipolar recordings from the tip of the ablation catheter should be recorded routinely during mapping of manifest accessory AV connections to identify appropriate target sites for radiofrequency energy applications.

The acute anatomic and valvular consequences of radiofrequency catheter ablation of accessory pathways were evaluated in 62 patients by means of serial echocardiographic examinations. Semiquantitative assessment of valvular incompetence and classification into one of four grades according to the width and the extension of the jet from the valvular orifice were carried out. Segmental wall motion abnormalities were evaluated semiquantitatively with four grades of severity (normal, hypokinesia, akinesia, or dyskinesia). New echocardiographic abnormalities were observed in five patients. One thrombus on the ventricular aspect of the mitral valve, three hemodynamically insignificant pericardial effusions, and one increase in severity of tricuspid incompetence were found 1 day after radiofrequency catheter ablation. We conclude that echocardiographic changes after radiofrequency ablation of accessory pathways are rare and of minor significance. These findings confirm the safety of the procedure.

A total of 408 patients received radiofrequency catheter ablation for paroxysmal supraventricular tachycardia, and 326 patients underwent serial follow-up electrophysiologic studies (early and late) after initially successful radiofrequency catheter ablation of accessory pathways (group 1, 186 patients with Wolff-Parkinson-White syndrome) and slow atrioventricular (AV) nodal pathways (group 2, 140 patients with AV nodal reentrant tachycardia). Among the patients in group 1, early (4 +/- 1 days) and late (129 +/- 14 days) studies found recurrent conduction through the accessory pathways in 12 and 16 patients, respectively. During a follow-up period of 21 +/- 7 months, recurrence of accessory pathway-mediated tachyarrhythmias was noted in six patients. Of these six patients, all had tachycardia inducible in the late study but not in the early study. Among the patients in group 2, four had recurrence of AV nodal reentrant tachycardia during a follow-up of 16 +/- 6 months. Of the four patients, one had tachycardia inducible in the early (4 +/- 1 days) study and three in the late (130 +/- 12 days) study. The results demonstrated that the early study was not as sensitive as the late follow-up electrophysiologic study in predicting late outcome of radiofrequency ablation, but both the early and late studies had a high total predictive accuracy (90%) in groups 1 and 2. Furthermore, only 4 of the 326 patients had initial evidence of recurrent tachycardia activated by programmed electrical stimuli during follow-up studies, suggesting that follow-up electrophysiologic studies in asymptomatic patients are not warranted.

By means of a new quantitative index for concealed conduction, we evaluated the effects of diltiazem on atrioventricular (AV) node concealment and correlated this index with the variability of the ventricular response during atrial fibrillation in 16 anesthetized mongrel dogs. After determination of the atrial effective refractory period (ERP), AV nodal ERP (AVNERP), concealment zone, and concealment index (AVNERP of blocked atrial extrasystole/AVNERP of conducted atrial extrasystole), the R-R intervals during atrial fibrillation induced by electrical stimulation were measured. Both low (0.1 mg/kg) and medium (0.2 to 0.4 mg/kg) doses of diltiazem prolonged the AVNERP and increased the mean R-R interval during atrial fibrillation. Only medium doses of diltiazem increased the degree of concealed conduction in the AV node and accentuated the variability of R-R intervals. There was a good positive correlation between the variability of the ventricular response during atrial fibrillation and the concealment index. In conclusion, medium doses of diltiazem are more effective in reducing heart rate during atrial fibrillation than a low dose. However, medium doses also increase the degree of concealed conduction in the AV node and enhance the irregularity of the ventricular response during atrial fibrillation. Measurement of the concealment index is useful for quantitating the degree of concealed conduction in the AV node, which is actually an important determinant of the ventricular response during atrial fibrillation.

Atrial fibrillation in the Wolff-Parkinson-White syndrome may be related to microreentry in the accessory pathway. If such is the case, catheter ablation of the accessory pathway should eliminate atrial fibrillation. Among 95 patients undergoing catheter ablation, 20 had atrial fibrillation during standard electrophysiologic study (atrial vulnerability) before ablation. There were 16 women and four men with a mean age of 32 years. Before ablation six patients required electrical cardioversion. Thirty minutes after ablation, 11 continued to have inducible atrial fibrillation. Atrial fibrillation terminated spontaneously in every patient after ablation. A control group of 20 patients with accessory pathway ablation had no inducible atrial fibrillation before or after ablation. Catheter ablation had no effect on atrial properties including functional refractory period (227 +/- 37 vs 215 +/- 29 msec before versus after ablation, mean +/- SD) or wavelength (7.4 +/- 3.2 vs 7.2 +/- 2.7 before versus after ablation). These data suggest that an intact accessory pathway is not necessary for initiation of atrial fibrillation in most patients with Wolff-Parkinson-White syndrome. A rapid ventricular response over the accessory pathway may facilitate the perpetuation of atrial fibrillation in persons prone to this arrhythmia.

To evaluate arrhythmogenicity in patients who receive a modified direct-current (DC) shock ablation (distal pair of electrodes connected in common as the cathode) or radiofrequency (RF) ablation of supraventricular tachycardia, a prospective study was performed with signal-averaged ECG, 24-hour Holter monitoring, electrophysiologic study (EPS) for ventricular tachycardia (VT), and treadmill exercise test. Sixty-nine consecutive patients with documented paroxysmal supraventricular tachycardia were included. Twenty-eight patients proved to have atrioventricular nodal reentrant tachycardia, and 41 patients had atrioventricular reciprocating tachycardia that involved accessory atrioventricular pathways. The first 34 patients received DC shock ablation and the other 35 patients received RF ablation. Signal-averaged ECG, Holter monitoring, and EPS for VT were performed before ablation, immediately after ablation, then 1 week, 2 weeks (Holter monitoring), 1 month (except EPS), and 3 months after ablation. Treadmill exercise testing was performed before ablation, and at 1 week and 3 months after ablation. The root mean square, low-amplitude signal and QRS duration of signal-averaged ECG disclosed no significant change after either DC or RF ablation up to 3 months. Late potential developed in only one patient in the DC shock group and it was considered to be innocuous because neither VT nor ventricular fibrillation was noted or induced. Increases in the number of ventricular premature contractions and in short-run VT were detected by Holter monitoring in the first week after either mode of ablation (p < 0.001 for the DC shock group; p < 0.05 for the RF group), which were greater (p < 0.05) and lasted longer in the DC shock group than in the RF group.(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the electrophysiologic properties of human atrial flutter and its response to various classes of antiarrhythmic drugs, 39 patients were identified as having inducible sustained atrial flutter with atrial extra-stimulation techniques. Measurement of intra-atrial, interatrial, atrioventricular node and His-Purkinje-conduction intervals, atrial refractory periods, and atrial flutter-cycle length were made before and after intravenous administration of verapamil, ouabain, or cedilanid, propranolol, and procainamide in these 39 patients, as well as in seven control patients. Verapamil significantly shortened flutter-cycle length but suppressed atrial-flutter induction in only one of seven patients. Two of nine patients who received propranolol proved resistant to flutter provocation; the seven patients who remained nonsuppressible exhibited greater prolongation of interatrial-conduction time. Ouabain and cedilanid suppressed flutter inducibility in four of seven patients, and flutter-cycle length increased in those patients remaining inducible. Procainamide suppressed flutter induction in nine of 11 patients. These results suggest that procainamide is the most effective agent of those agents tested in suppressing atrial flutter induced by atrial extra-stimulation. Verapamil and propranolol proved quite ineffective in suppressing inducible atrial flutter.

We continuously observed successive pairs of R-R intervals during atrial fibrillation and hypothesized that the shortest R-R interval for a given preceding R-R interval in a pair represents the functional refractory period of the atrioventricular node at that preceding interval. To test this hypothesis we simulated atrial fibrillation in 28 isolated cross-perfused canine hearts and obtained an R-R interval scatterplot by plotting the R-R intervals as a function of the immediately preceding R-R interval. This scatterplot enabled us to detect a series of the shortest R-R intervals for a wide range of preceding R-R intervals, and this allowed us to estimate the rate-dependent functional refractory period of the atrioventricular node in simulated atrial fibrillation. The estimated functional refractory periods correlated well with those measured by the conventional method (r = 0.93). We conclude that the proposed method makes it possible to estimate the rate-dependent functional refractory periods of the atrioventricular node in atrial fibrillation.

Atrioventricular (AV) nodal reentry requires intact retrograde ventriculoatrial (VA) conduction. The purpose of this study was to assess the contribution of various pacing and pharmacologic techniques to uncover VA conduction during apparent unidirectional VA block, and to evaluate the role of several biologic and electrophysiologic factors in concealment of retrograde conduction. Forty healthy dogs underwent catheter-electrophysiologic studies of AV and VA conduction. Group I (20 animals) had intact VA conduction. Group II (six animals) had VA dissociation with ventricular pacing initiated during sinus rhythm, but the presence of VA conduction was confirmed by isoproterenol infusion or by premature ventricular stimulation. In group III (14 animals), the above techniques failed to uncover VA conduction. Eight of 14 group III animals underwent thoracotomy and crushing or freezing of the sinoatrial (SA) node. Ventricular pacing initiated during sinus standstill was associated with 1:1 VA conduction in each experiment. VA conduction time and retrograde Wenckebach cycle length, both in the baseline state and during isoproterenol infusion, were significantly longer in the eight animals in group III than in those in group I. Age, gender, weight, breed, sinus cycle length, and anterograde AV conduction properties were not significantly different between groups I, II, and III. The data suggest that (1) in normal dogs, complete unidirectional VA block probably does not exist; (2) in the presence of anterograde input to the AV node, even sophisticated pacing and pharmacologic maneuvers may fail to uncover the presence of VA conduction; (3) although anterograde input is essential for concealment of VA conduction, the phenomenon is more closely associated with depressed retrograde than with anterograde AV nodal characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the relation between a new quantitative index of concealed atrioventricular nodal (AVN) conduction and the variability of ventricular response during atrial fibrillation in 12 patients without preexcitation. The second atrial extrastimulus (A3) was introduced following the first extrastimulus (A2), which was fixed at a coupling interval 20 to 40 msec longer than the AVN effective refractory period (ERP) during a basic atrial drive (A1) cycle length of 400 to 750 msec. The AVNERP of conducted A2 defined as the longest A2A3 interval at which A3 was not conducted to the His bundle was determined. This pacing sequence was repeated, whereas A2 was fixed at a coupling interval 20 to 40 msec shorter than the AVNERP, which means A2 was concealed within the AVN. Thus AVNERP of blocked A2, defined as the longest A2A3 interval at which A3 was not conducted to the His bundle, was measured. Concealment index (AVNERP of blocked A2/AVNERP of conducted A2) was developed to quantitate the magnitude of concealed penetration into the AVN by A2. During atrial fibrillation induced by premature or rapid atrial stimulation, the coefficient of variation (SD/mean) of R-R intervals and the maximum R-R/minimum R-R interval were significantly correlated with the concealment index (r = 0.838, p < 0.001; r = 0.678, p < 0.05). However, neither of these parameters was correlated with AVNERP. Both the minimum R-R and the mean R-R interval were related to the AVNERP (r = 0.946, r = 0.823, p < 0.001). The maximum R-R interval was not related to the AVNERP (r = 0.567, p = NS). We conclude that the concealment index may be a useful predictor of the magnitude of concealed AVN conduction, which may have an important role in determining irregularity of the ventricular response to atrial fibrillation.

Background Both “physiologic” (dual-chamber or atrial only) or ventricular-pacing-only permanent pacemakers provide chronotropic competence, with unknown health-related quality of life (QOL) differences between these options. The QOL studies within the Canadian Trial of Physiologic Pacing were performed to assess whether QOL differences exist in patients randomized to these 2 pacing modes. Methods Two QOL protocols were performed: 1) a substudy of 269 patients with detailed QOL measures (The Medical Outcomes Study, Short-Form [SF-36], the Pacemaker Syndrome Scale, an activity scale, and a pacemaker-specific scale) at baseline and 6 months after implantation; and 2) a parent study assessment of QOL in 1721 patients with a 12-item QOL instrument package (SF-6, “ladder of life,” and pacemaker syndrome scale) given 6 months after implantation only. Results In the substudy, pacing was associated with an average significant (P < .05) 0.36 SD unit improvement in QOL across all domains (SF-36: 38 ± 9 to 41 ± 11 for physical scores, 47 ± 11 to 52 ± 9 for mental health scores, both P < .001). Similar improvements were seen with the pacemaker-specific scales. There were no significant differences in the absolute or relative improvement in QOL between assigned pacing modes. The parent study similarly showed no differences in QOL between pacing modalities. Presyncope occurred in 31% of patients in the physiological pacing group, compared with 38% of the patients in the ventricular pacing group (P < .01). No other symptoms were different between the 2 groups. Pacemaker dependency, defined as an escape heart rate

Background The conduction system in right atrial isomerism may be complicated by the presence of paired sinus nodes and twin atrioventricular nodes. With a large cohort of infants and children with right atrial isomerism, we sought to investigate the nature of atrial rhythm, its prevalence, factors predisposing patients to symptomatic cardiac arrhythmia, and the relation of arrhythmia to long-term morbidity and mortality. Methods Standard 12-lead baseline electrocardiograms were performed in 110 infants and children with right atrial isomerism at a median age of 1 day, and their clinical records were reviewed. The type, timing, and precipitating factors of symptomatic cardiac arrhythmia that occurred in 15 patients, among a cohort of 85 patients who had or were awaiting surgical interventions, were noted. Results All patients except 1 had a sinus rhythm with intact atrioventricular conduction. Of these, 87% (95/109) had single P-wave morphology, whereas 13% (14/109) had multiple P-wave morphologies. For patients with a single P-wave morphology, the frontal P-wave axis was between 0 degrees and 90 degrees in 62% (59/95), 90 degrees and 180 degrees in 23% (22/95), and superior in 15% (14/95). There was no relation between either P-wave axis or morphology and cardiac anatomy. Symptomatic cardiac arrhythmia occurred in 15 of 85 patients (18%); 11 of the 15 patients had supraventricular tachycardia, and 1 patient each had atrial tachycardia, atrial flutter, ventricular tachycardia, and congenital complete heart block. The arrhythmias occurred before surgery in 4 patients, early after surgery in 5 patients, and late after surgery in 6 patients. Although 3 of the 7 patients who died suddenly had a history of symptomatic arrhythmia, arrhythmia was the documented cause of mortality in only 1 of the 32 fatalities (3.1%). Freedom from arrhythmia at 1, 5, 10, 15, and 20 years was 93% ± 3%, 86% ± 4%, 80% ± 6%, 73% ± 9%, and 48% ± 15% (mean ± SE), respectively. No risk factors for symptomatic arrhythmia were identified by means of logistic regression. Conclusions The atrial pacemaker varies in location within and between patients with right atrial isomerism. Although symptomatic cardiac arrhythmias are not uncommon, they do not seem to relate to the overall high mortality rate and occurrence of sudden death in this patient group. Nonetheless, detailed assessment and aggressive management of cardiac arrhythmias once they occur are warranted because of the precarious single ventricular hemodynamics. (Am Heart J 2002;144:159-64.)

are not known. A recent in vitro study7 showed that the marked prolongation of action potential duration in Purkinje fibers induced by erythromycin is not caused by activation of the “late sodium” current or by a-adrenoceptor stimulation. A potential blocking effect on the potassium currents involved in ventricular repolarization (inward rectifier, Ik; delayed rectifier, Ikl; transient outward, Ito) cannot be excluded as a possible mechanism. The association between spiramycin and QT interval prolongation must of course be confirmed prospectively in a larger population by recording the ECG before and during antibiotic therapy. However, extreme caution should be used in the choice of macrolide agents when antibiotic therapy is necessary in subjects with alterations of ventricular repolarization or in those with reduced cardiac electrical stability.

Accelerated junctional rhythm (AJR) has been considered as a sensitive but rather nonspecific marker of successful radiofrequency (RF) ablation of slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, AJR also occurs commonly during isoproterenol infusion. We therefore investigated the effect of isoproterenol on the significance of AJR while attempting slow pathway ablation.Forty patients with AVNRT underwent slow pathway ablation. Sixty-nine RF applications accompanied by AJR were observed and were separated into 2 groups: applications performed without (group I, n = 26) and with (group II, n = 43) isoproterenol infusion. The specificity of AJR for successful ablation for each group was calculated.The specificity of AJR in groups I and II was 73% (19/26) and 49% (21/43), respectively (P.05). There was no significant difference between the groups in the atrial electrogram width, atrial/ventricular electrogram amplitude ratio, the time from application onset to AJR emergence, or AJR cycle length. The catheter-tip temperature at AJR emergence was significantly lower (47 degrees C +/- 3 degrees C vs 52 degrees C +/- 3 degrees C, P.001) and the ratio of junctional beats to total heart beats during RF application was significantly greater (46% +/- 24% vs 33% +/- 18%, P.05) in group II compared with group I.Isoproterenol lowers the threshold of AJR emergence during RF application and thereby lowers the specificity of AJR for successful ablation. Complete washout of isoproterenol may therefore improve the specificity of AJR during RF ablation in patients with AVNRT.

6. Prichard CL, Mudd GJ, Barner HB. Coronary ostial stenosis. Circulation 1978;52:46-8. Thompson R. Isolated coronary ostial stenosis in women. J Am Co11 Cardiol 1986;7:997-1003. Rissanen V. Occurrence of coronary ostial stenosis in necropsy series of myocardial infarction, sudden death and violent death. Br Heart J 1975;37:182-91. Tillman CH, Mukerji V, Alpert AM, Sanfillipo JF. Isolated coronary ostial stenosis in men. AM HEART J 1988,115:1127-8. Mathias DN, Mooney FJ, Lange HW, et al. Frequency of success and complications of coronary angioplasty of stenosis at ostium of branch vessel. Am J Cardiol 1991:67:491-5. Top01 EJ, Ellis SG. Fishman J, Leimgraber P, et al. Multicenter study of percutaneous transluminal angioplasty for right coronary ostial stenosis. J Am Co11 Cardiol 1987;9:121418.

Radiofrequency ablation of the atrioventricular junction is a well-established procedure for the management of atrial fibrillation refractory to medical therapy. However, there are few data available on the prevalence and characteristics of the escape rhythms that are present after the procedure.The Ablate and Pace Trial was a prospective, multicenter registry of atrioventricular junction ablation and pacing in atrial fibrillation. Ablation of the atrioventricular junction was accomplished with radiofrequency energy with standard techniques. Before discharge from the hospital, patients underwent a systematic analysis of the rate and morphologic features of the escape rhythm, if any, that was present when the pacing rate was gradually decreased.There were 156 patients from 16 centers who underwent attempted radiofrequency ablation of the atrioventricular junction. The procedure was successful in 155 (99%) of 156 patients. An escape rhythm was present in 104 patients (67%) after radiofrequency ablation. The escape rate ranged from 11 to 65 beats/min (mean 39 +/- 10 beats/min). Only 49 patients (31%) had an escape rate/=40 beats/min. Of the 104 patients with an escape rhythm, 53 patients (51%) had a QRS that was unchanged from baseline. There was no correlation between the number of radiofrequency applications and the presence of an escape rhythm.The majority of patients who undergo radiofrequency catheter ablation of the atrioventricular junction are pacemaker dependent after the procedure, as defined by lack of an escape rhythm or the presence of an escape rhythm that is40 beats/min.

1. Haft JI, Habbab MA. Treatment of atria1 arrhythmias: effectiveness of verapamil when preceded by calcium infusion. Arch Intern Med 1986;146:1085-9. 2. Weiss AT, Lewis BS, Halon DA, et al. The use of calcium with verapamil in the management of supraventricular tachyarrhvthmias. Int J Cardiol 1983:4:275-80. 3. Stringer KA, Hicks P, Royal SR, et al. Verapamil preceded by calcium in supraventricular tachycardia. Drug Intel1 Clin Pharm 1988;22:575-6. 4. Salerno DM, Anderson B, Sharkey PJ, et al. Intravenous verapamil for treatment of multifocal atria1 tachycardia with and without calcium pretreatment. Ann Intern Med 1987;107: 623-8. 5. Guadagnino V, Greengart A, Hollander G, et al. Treatment of severe left ventricular dysfunction with calcium chloride in patients receiving verapamil. J Clin Pharmacol 1987;27:407-9. 6. Smallwood RA. Some effects of the intravenous administration of calcium in man. Aust Acad Med 1967;16:126-31. 7. Hariman RJ. Manniardi LM. McAllister RG, et al. Reversal of the cardiovasculare59:797-804. 8. Lang J, Chah QT, Charve P, et al. Role of calcium in the ratedependent depression of atrioventricular nodal conduction in the dog heart under vagal influence. Int J Cardiol 1987;15:6576.

Background Radiofrequency catheter ablation of the atrioventricular node and pacemaker insertion have been associated with occasional development of mitral regurgitation (MR). Ventricular pacing might result in MR if (1) left ventricular (LV) compliance is decreased and/or (2) mitral valve leaflet apposition is disturbed. We studied acute hemodynamic changes resulting from initiation of ventricular pacing in patients undergoing ablation. Methods and Results Thirteen patients (10 men and 3 women) with a mean age of 73.4 ± 8.6 years, with chronic atrial fibrillation and congestive heart failure, had permanent ventricular pacemaker insertion with lead placement at the right ventricular (RV) apex. The following hemodynamic recordings were obtained before ablation (during atrial fibrillation) and then immediately after ablation (during RV pacing): heart rate, mean arterial pressure, LV end-diastolic pressure (LVEDP), mean pulmonary capillary wedge pressure, V-wave amplitude, and cardiac index. Presence of MR was assessed by V-wave amplitude and the results of LV angiography. In patients who had MR, recordings were also obtained during temporary ventricular pacing from the RV outflow tract (RVOT). As a group there were no significant changes in any hemodynamic measurement. Before ablation, mild MR by LV angiogram was present in 5 patients, but none had large V-wave amplitude. After ablation, mild MR was present by LV angiogram in 6 patients, and in 3 of these patients large V-wave amplitude developed (mean amplitude 42.7 ± 2.2 mm Hg; assigned to group 1). This was associated with a rise in LVEDP in 1 patient (consistent with reduced LV compliance), but LVEDP was unchanged in the other 2 patients (suggesting abnormal mitral valve leaflet apposition). All patients in group 1 exhibited a fall in V-wave amplitude when the pacing site was moved to the RVOT. Conclusions Both reduced LV compliance and disturbed mitral valve leaflet apposition contribute to MR after ablation. MR is reduced by pacing from the RVOT. (Am Heart J 1999;138:1166-75.)