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BACKGROUND: Patients with PR intervals >240ms have atrio-ventricular (AV) dyssynchrony, which can increase risk of atrial fibrillation and all-cause mortality. When requiring pacing, long AV delays (AVDs) have been programmed to avoid ventricular dyssychrony. His bundle pacing (HBP) may provide improved AV synchrony in patients with prolonged PR. METHODS: 10 patients with sinus node dysfunction and prolonged PR who received HBP were studied. Real-time echocardiographic was performed with 3 pacemaker modes (RV septal, non-selective HBP, and selective HBP) using the following pacemaker settings: control (no ventricular pacing), pacing with AVD of 180ms, 150ms, 120ms, 100ms, and 70ms. Echocardiographic Doppler measurements: EA/RR, >40% = AV synchrony; E/e’

Introduction The VICTORY AF Study was designed to evaluate the risk of the procedure and/or device-related strokes in patients with PersAF on warfarin undergoing ablation with a phased radiofrequency (RF) system. Methods The VICTORY AF trial was a prospective, multicenter, single-arm, investigational study. PersAF patients on vitamin K antagonism without major structural heart disease or history of stroke/transient ischemic attack undergoing phased RF ablation for atrial fibrillation (AF) were included. The primary outcome was the incidence of the procedure and/or device-related stroke within 30 days of the ablation by a board-certified neurologist's assessment. The secondary outcomes were an acute procedural success, 6 months effectiveness (defined as the reduction in AF/atrial flutter episodes lasting ≥10 minutes by 48-hour Holter 6 months postablation) and the number of patients with pulmonary vein (PV) stenosis. Results A total of 129 (108 PersAF, 21 long-standing PersAF) patients were treated (mean age: 60.6 ± 7.7; 79.8% male, 54.3% CHA2Ds2-VASc score ≥ 2). Two nondisabling strokes were reported (1.6%); one before discharge and the second diagnosed at the 30-day visit. Due to slow enrollment, the study was terminated before reaching the 95% one-sided upper confidence boundary for stroke incidence. Acute procedural success was 93.8%, and at 6 months, 72.8% of patients demonstrated ≥90% reduction in AF burden, 78.9% were off all antiarrhythmic drugs. There were no patients with PV stenosis of greater than 70%. Conclusions VICTORY AF demonstrated a 1.6% incidence of stroke in PersAF undergoing ablation with a phased RF system which did not meet statistical confidence due to poor enrollment. The secondary outcomes suggest comparable efficacy to phased RF in the tailored treatment of permanent AF trial. Rigorous clinical evaluation of the stroke risk of new AF ablation technologies as well as restriction to Vitamin K antagonist anticoagulation appears to be unachievable goals in a clinical multicenter IDE trial of AF ablation in the current era.

Objectives STOP AF PAS (Sustained Treatment of Paroxysmal Atrial Fibrillation Post-Approval Study) is the first prospective, multicenter, 3-year study in North America to assess long-term safety and effectiveness of the cryoballoon for treatment of patients with drug-refractory symptomatic pAF. Background The STOP AF PAS was required by the U.S. Food and Drug Administration at the time of approval of the first-generation cryoballoon for the treatment of paroxysmal atrial fibrillation (pAF). The second-generation cryoballoon (CB2) was commercially released shortly after this trial was initiated. Methods The study was nonrandomized. Enrollment was completed with 344 eligible patients undergoing pulmonary vein isolation (PVI) using the CB2. Procedure-related safety and freedom from AF and symptomatic atrial flutter/atrial tachycardia through 3 years were determined. Documented atrial arrhythmias ≥30 s were considered treatment failures. Results Acute PVI was achieved in 99.3% (1,341 of 1,350) of veins. Mean follow-up was 34 ± 7 months. The rate of major complications was 5.8%, including a 3.2% rate of phrenic nerve injury, which resolved in all but 1 patient by 36 months. At 36 months, 11.7% of patients were prescribed antiarrhythmic agents, inclusive of “pill-in-the-pocket” administration. Freedom from AF was 81.6% at 12 months, 73.8% at 24 months, and 68.1% at 36 months. Freedom from AF and symptomatic atrial flutter/atrial tachycardia was 79.0% at 12 months, 70.8% at 24 months, and 64.1% at 36 months. Freedom from a repeat ablation procedure was 80.9% at 36 months. Conclusions PVI using the CB2 was an effective treatment for patients with pAF, with freedom from all atrial arrhythmias of 64% at 36 months. (Sustained Treatment of Paroxysmal Atrial Fibrillation Post-Approval Study [STOP AF PAS]; NCT01456949)

Atrial fibrillation cannot always be converted to sinus rhythm by transthoracic electrical cardioversion. We examined the effect of ibutilide, a class III antiarrhythmic agent, on the energy requirement for atrial defibrillation and assessed the value of this agent in facilitating cardioversion in patients with atrial fibrillation that is resistant to conventional transthoracic cardioversion.One hundred patients who had had atrial fibrillation for a mean (+/-SD) of 117+/-201 days were randomly assigned to undergo transthoracic cardioversion with or without pretreatment with 1 mg of ibutilide. We designed a step-up protocol in which shocks at 50, 100, 200, 300, and 360 J were used for transthoracic cardioversion. If transthoracic cardioversion was unsuccessful in a patient who had not received ibutilide pretreatment, ibutilide was administered and transthoracic cardioversion attempted again.Conversion to sinus rhythm occurred in 36 of 50 patients who had not received ibutilide (72 percent) and in all 50 patients who had received ibutilide (100 percent, P0.001). In all 14 patients in whom transthoracic cardioversion alone failed, sinus rhythm was restored when cardioversion was attempted again after the administration of ibutilide. Pretreatment with ibutilide was associated with a reduction in the mean energy required for defibrillation (166+/-80 J, as compared with 228+/-93 J without pretreatment; P0.001). Sustained polymorphic ventricular tachycardia occurred in 2 of the 64 patients who received ibutilide (3 percent), both of whom had an ejection fraction of 0.20 or less. The rates of freedom from atrial fibrillation after six months of follow-up were similar in the two randomized groups.The efficacy of transthoracic cardioversion for converting atrial fibrillation to sinus rhythm was enhanced by pretreatment with ibutilide. However, use of this drug should be avoided in patients with very low ejection fractions.

OBJECTIVE The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was categorized as “atrial-ventricular” (A-V) or “atrial-atrial-ventricular” (A-A-V). RESULTS The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.

With use of transesophageal echocardiography, the short-term effects of transthoracic electrical cardioversion of atrial flutter (AFI) on atrial mechanical function and spontaneous echo contrast were determined. Thirty patients who had AFI for a mean of 6.4 +/- 12.2 months underwent transthoracic cardioversion. A transesophageal echocardiogram was recorded immediately before cardioversion, and left atrial appendage emptying velocity and spontaneous contrast were assessed serially at 1, 3, and 5 minutes after cardioversion in 28 patients, and also at 8, 10, and 15 minutes after cardioversion in a subgroup of 13 patients. Cardioversion was deferred in 2 patients (7%) because a thrombus was found in the left atrial appendage. Before cardioversion, spontaneous contrast was present in the left atrium in 7 of 28 patients (25%) who underwent cardioversion. The mean left atrial appendage emptying velocity of 54 +/- 22 cm/s before cardioversion fell by 26% to 40 +/- 25 cm/s at 1 minute after restoration of sinus rhythm (p

Purpose: Adenosine is a useful agent for the diagnosis and termination of tachycardias. The purpose of this study was to identify the rhythms for which adenosine is prescribed in hospitalized adults and to identify the reasons for its misuse. Patients and Methods: Data were collected from the medical records of 100 patients who received intravenous adenosine while hospitalized at a university medical center. The characteristics of the patients, rhythms treated with adenosine, and dosages of adenosine were analyzed. In addition, internal medicine house officers were administered a questionnaire referring to an electrocardiogram of atrial fibrillation with a rapid ventricular response. Results: The arrhythmias for which adenosine was administered consisted of regular, narrow-QRS complex tachycardias in 33% of patients; atrial fibrillation in 32% of patients; regular, wide-QRS complex tachycardias in 23% of patients; atrial flutter in 10% of patients, and multifocal atrial tachycardia in 2% of patients. The mean (± SD) number of doses of adenosine given to each patient was 1.6 ± 0.8, and the mean dose of adenosine was 7.8 ± 2.8 mg. Internal medicine house officers prescribed 70% of the doses of adenosine and were as likely to use it for patients with atrial fibrillation as were surgical house officers. There was a 2% incidence of proarrhythmia, including asystole and polymorphic ventricular tachycardia. Thirty-one percent of the 100 house officers in our survey misdiagnosed a 12-lead electrocardiogram of rapid atrial fibrillation as paroxysmal supraventricular tachycardia, suggesting that adenosine may have been misused for atrial fibrillation because of errors in rhythm diagnosis. Only 5% of those who correctly diagnosed atrial fibrillation also answered that adenosine would be likely to terminate the arrhythmia, suggesting that a misunderstanding that adenosine terminates atrial fibrillation is not a common reason for its misuse. Conclusions: Approximately 40% of hospitalized adults who are treated with adenosine receive the medication unnecessarily for atrial fibrillation or atrial flutter, and this misuse results in unnecessary expenses and risks of adverse effects. The primary reason that adenosine is misused for atrial fibrillation is the inability to recognize that rhythm on an electrocardiogram. House officers need additional education on the electrocardiographic recognition of atrial fibrillation.

Unipolar Electrogram. introduction: The purpose (if this study was to determine the accuruey of the unipolar electrogram tor identifying the earliest site of ventricular activation. The earliest site of ventricular activation may he identified with the unipolar electrogram hy the absence of an R wave. However, the accuracy of this technique is unknown. Methods and Results: A sJn^^Ie ventricular premature complex was induced mechanically at the tip of an electrode catheter to simulate a ventricular premature depolarization site of origin. Unipolar electrograms were recorded from the right ventricular septum at the tip electrode and at 2, 5, 8, and 11 nmi from the electrode tip in 20 patients. No R waves were detected at the ventricular premature depolarization site of origin. R waves were detected in 4 of 20 patients (20%) at 2 mm from the tip electrode and 7 of 20 patients (35%) at 5. 8. and 11 mm from the tip electrode. An R wave was not ohserved at distances < 11 mm from the site of tachycardia origin in 13 of 20 patients (65%), Conclusions: While an R wave in the unipolar electrogram can he seen as close as 2 mm fnmi the site of impulse origin, the ahsence of an R wave as an indicator of the site of impulse origin in the right ventricle is highly inaccurate. Therefore, the ahsence of an R wave in the unipolar electrogram is unlikely to he an adequate guide for identiHcation of an effective target site for ahlation of right ventricular tachycardia. (./ Cardiovusc Electrophysiol. Vol. H. pp. 974-979, Scptemlwr

Postdefibrillation Ventricular Arrhythmias. Background: The relationship between postdefibrillation ventricular arrhythmias and shock strength is poorly understood in patients with implantable defibrillators. The purpose of this study was to characterize the relationship between postdefibrillation ventricular arrhythmias and shock strength. Methods and Results: Forty-three patients with an implanted defibrillator underwent six separate inductions of ventricular fibrillation (VF) after a step-down defibrillation energy requirement (7.3 ± 4.6 J) was determined. For each of the first three inductions of VF, the first two shocks were low energy and equal to approximately 75 % of the defibrillation energy requirement (5.4 ± 3.3 J), or to the defibrillation energy requirement plus 10 J (17.5 ± 4.3 J). After the first two shocks, subsequent shocks were programmed to the maximum available energy (29.0 ± 2.5 J). The alternate technique was used for the subsequent three inductions of VF. Post defibrillation ventricular arrhythmias were noted. Post defibrillation ventricular arrhythmias with a cycle length ≤ 300 msec were more frequent after a low-energy shock (19%), than after a high-energy shock (1.5 %; P = 0.005). Postdefibrillation ventricular arrhythmias with a cycle length > 300 msec were more frequent after a high-energy shock (32%), than after a low-energy shock (7.1%; P = 0.002). A relationship between the cycle length of the post defibrillation ventricular arrhythmias and the absolute defibrillation energy was observed (P 300 msec were uncommon after shocks ≤ 10 J (P = 0.001). The characteristics of ventricular arrhythmias after maximum-energy shocks were similar to those that occurred after high-energy shocks. Conclusions: Post defibrillation ventricular arrhythmias with a cycle length ≤ 300 msec are more common after shocks of strength associated with a low probability of successful defibrillation. Postdefibrillation ventricular arrhythmias with a cycle length of > 300 msec are more common after high- and maximum-energy shocks, and are directly related to the absolute defibrillation energy.

Defibriiiation Energy Requirements. Introduction: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months alter implantation. However, the stability of the defibrillation energy requirement beyond I year has not heen reported. The purpose of this study was to characterize the defihrillation energy requirement during 2 years of clinical follow-up. Methods and Results: Thirty-one consecutive patients with u biphasic nonthoracotomy defihrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12. 10, 8, 6, 5, 4, 3, 2, and I J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defihrillation energy requirement during these evaluations was 10.9 ± 5.5 J, 12.3 ± 7.3 J, 11.7 ± 5.6 J, 10.2 ± 4.0 ,|, and 11.7 ± 7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased hy 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defihrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defihrillation system. There were no identifiahle clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defihrillation energy requirement. Conclusion: The mean defibrillation energy requirement does not change significantly after 2 years of hiphasic nonthoracotomy detihrillator system implantation. However, approximately 15% of patients develop a 1((-J or greater elevation in the defihrillation energy requirement, and 3% may require a defihrillation system revision. Therefore, a yearly evaluation of the defibrillation euergy requirement may he appropriate. (J Cardiovasc Electrophysiol, Vol. 9, pp. 916-920. Septemtwr 1998)

The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics.The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 +/- 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 +/- 0.45 L/min per m2 immediately afterwards (P = 0.001). This effect persisted for4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P = 0.003) and 10-J shocks (P = 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P = 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P0.0001). This effect persisted for4 minutes. A 1-J shock during the baseline rhythm did not effect the cardiac index.Defibrillator shocks9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for this effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. Methods and Results: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 ± 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA hlock cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV hlock cycle length (374 ± 78 vs 333 ± 74 msec, P < 0.01), a shorter VA hlock cycle length (383 ± 121 vs 307 ± 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 ± 23 vs 41 ± 17 msec, P < 0.01). Conclusion: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked hy adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway. (J Cardiovasc Electrophysiol, Voi 9. pp. 820-824, August 1998)

Background: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. Methods: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 ± 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of β-blockade while in continuous NE infusion. Results: The baseline NE plasma concentration of 298 ± 153 pg/ml increased to 708 ± 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. Conclusion: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by β-adrenergic stimulation. (Am Heart J 1998;135:945-51.)

Cardiac Memory. Introduction: “Cardiac memory” (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. Methods and Results: Thirty-one patients (ages 43 ± 14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9 ± 1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1,5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. Conclusion: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Background Because it is not clear which technique is less expensive, the purpose of this study was to compare the cost of radiofrequency modification and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrillation and an uncontrolled ventricular rate. Methods and Results The initial nominal charges for a successful procedure were compared in 10 patients with chronic atrial fibrillation who underwent modification of the AV node ($13 109±2002) and 14 similar patients who underwent ablation and pacemaker implantation ($28 302±2023, P P Conclusions The initial charges generated by AV node modification are significantly lower than for AV node ablation in patients with chronic atrial fibrillation. Even when adjusted for higher failure and recurrence rates, the modification procedure retains a major cost advantage over ablation during long-term follow-up.

Atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia may have different ages of tachycardia onset. Symptom onset data were obtained in 519 patients (atrioventricular nodal reentrant tachycardia, 231, accessory pathway-mediated tachycardia, 288). The mean age of the patients at the time of evaluation was 47 +/- 17 years (atrioventricular nodal reentrant tachycardia) and 37 +/- 15 years (accessory pathway-mediated tachycardia). The mean age of symptom onset was 32 +/- 18 years for atrioventricular nodal reentrant tachycardia and 23 +/- 14 years for accessory pathway-mediated tachycardia. A significantly greater proportion of patients with atrioventricular nodal reentrant tachycardia had the initial onset of symptoms after the age of 20 years (atrioventricular nodal reentrant tachycardia, 67% vs accessory pathway-mediated tachycardia, 41%, p < 0.001). In summary, there is a different mean age of symptom onset for patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia.

Four of 12 patients (33%) with paroxysmal supraventricular tachycardia (PSVT) and tachycardia-induced atrial fibrillation (AF) had recurrences of paroxysmal AF after successful catheter ablation of the PSVT. This study demonstrates that AF often remains a problem after radiofrequency catheter ablation of PSVT in patients with tachycardia-induced AF, and it may not be possible to predict in which patients this will be the case.

In a retrospective analysis of patients referred for atrioventricular node radiofrequency ablation, male gender and a history of hypertension were found to be predictors of crossover to a left ventricular approach for success. This subgroup of patients may benefit from early crossover if initial attempts at right-sided ablation fail.