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Background Electrophysiology study (EPS) is an important part of the diagnosis and workup for supraventricular tachycardia (SVT). Provocative medications are used to induce arrhythmias, when they are not inducible at baseline. The most common medication is the β1-specific agonist, isoproterenol, but recent price increases have resulted in a shift toward the nonspecific agonist, epinephrine. Objective We hypothesize that isoproterenol is a better induction agent for SVT during EPS than epinephrine. Methods We created a retrospective cohort of 131 patients, who underwent EPS and required medication infusion with either isoproterenol or epinephrine for SVT induction. The primary outcome was arrhythmia induction. Results Successful induction was achieved in 71% of isoproterenol cases and 53% of epinephrine cases (P = 0.020). Isoproterenol was significantly better than epinephrine for SVT induction during EPS (odds ratio [OR], 2.35; 95% confidence interval [CI], 1.14-4.85; P = 0.021). There was no difference in baseline variables or complications between the two groups. Other variables associated with successful arrhythmia induction included a longer procedure duration and atrioventricular nodal re-entry tachycardia as the clinical arrhythmia. In a multivariable model, isoproterenol remained significantly associated with successful induction (OR, 2.57; 95% CI, 1.002-6.59; P = 0.05). Conclusions Isoproterenol was significantly better than epinephrine for SVT arrhythmia induction. However, epinephrine was safe and successfully induced arrhythmias in the majority of patients who received it. Furthermore, when atropine was added in epinephrine-refractory cases, in a post hoc analysis there was no difference in arrhythmia induction between medications. Cost savings could thus be significant without compromising safety.

A 25-year-old man with severe nonischemic dilated cardiomyopathy underwent subcutaneous implantable cardioverter defibrillator (S-ICD) implant and subsequently underwent HeartWare ventricular assist device (HVAD) placement. Postoperative interrogation revealed both primary and secondary S-ICD vectors inappropriately regarded sinus rhythm as "noise," and the alternate vector significantly undersensed sinus rhythm. The S-ICD was reinterrogated using high-resolution capture to visually confirm EMI with a dominant frequency in both the primary and secondary vectors of 46.67 Hz that fell within the S-ICD operational range of 9-60 Hz. The 46.67 Hz frequency correlated with the HVAD operational speed of 2,800 RPM. The HVAD pump speed was increased from 2,800 to 3,000 RPM, resulting in a dominant frequency of 50 Hz. The notch filter is nonprogrammable in S-ICDs. However, the built-in filter is 50 Hz for countries in European time zones as opposed to 60 Hz in US time zones due to differences in the anticipated noise from electrical sources within each continent. Thus, the S-ICD time zone was reprogrammed from EST to GMT, which reduced the notch filter from 60 to 50 Hz, resulting in S-ICD successfully eliminating EMI when the patient was in a supine position. The EMI interference was still intermittently present in the upright patient position. This case demonstrates the utility of high-resolution electrogram capture to identify the source and frequency of EMI in S-ICD and offers a potential avenue to troubleshoot dominant frequency oversensing by changing the device time zone.

A 55-year-old woman presented with severe dyspnea during acceleration-dependent left bundle branch block (LBBB). Metoprolol initially ameliorated symptoms by preventing the heart rate at which LBBB occurred. Over time LBBB presented at slower heart rates and the patient developed recurrent dyspnea during an activity that correlated with the development of LBBB on event monitors and exercise stress testing. A biventricular pacemaker was implanted, and the patient's symptoms remain resolved after a follow-up of over 4 years. More research is needed to define the use of cardiac resynchronization therapy in patients with normal heart function.

Introduction Focal impulse and rotor modulation (FIRM)-guided ablation has had mixed results of published success, and most studies have had a follow-up for a year or less. We aimed to study a consecutive group of patients followed for at least 1.5 years, subgrouped into those with an initial FIRM ablation and those with a previous, failed ablation who now received a FIRM guided one, to evaluate for success in each group and factors that might affect success. Methods Of 181 patients, 167 were available for analysis. Group 1 (n = 122) had a first or primary ablation (paroxysmal atrial fibrillation [PAF] 51; persistent atrial fibrillation [PeAF] 71) and group 2 (n = 45) had a redo ablation (PAF 18; PeAF 27). All patients were done under general anesthesia. FIRM mapping was done in the right atrium first and then the left, and only rotors consistently seen on multiple epochs were ablated, using 15 to 30 W. Rotor ablation was discontinued when remapping showed elimination of rotational activity at the site. Wide area catheter ablation was done for pulmonary vein isolation (PVI). Routine follow-up was at 3, 6, and 12 months of the first year, with a Holter monitor at 6 months, and then every 6 months thereafter. Event recorders were given to patients with potential arrhythmic symptoms. Results Mean follow-up was 16 months. Nearly 40% of patients had obstructive sleep apnea; mean body mass index was 32; and average left atrial size was 39.7 mm and 46.2 mm for PAF and PeAF patients, respectively. Freedom from atrial arrhythmia recurrence was: in group 1 patients, 82.4% for PAF and 67.6% for PeAF patients; in group 2 patients, 83.3% for PAF, but only 40.7% for PeAF patients. Comparing outcomes for the first 10 patients studied to the next 20 or more done by three operators showed no difference, suggesting no learning curve affecting the ablation results. Furthermore, the univariate analysis did not show any demographic factor to have an independent significance for ablation success or failure. Spontaneous termination during rotor ablation occurred in 76.8% of PAF and 27.6% of PeAF patients but did not affect the long-term outcomes for maintenance of sinus rhythm. Conclusions FIRM-guided atrial ablation plus PVI in our patient population resulted in good success from a recurrence of atrial arrhythmias in patients undergoing an initial ablation procedure. For those with persistent AF undergoing a second procedure now using FIRM guidance plus PVI, the results are lower. Further research is needed to define better the appropriate population for FIRM-guided ablation and the degree of ablation needed for success in these patients.

A 15-year-old girl with a history of paroxysmal supraventricular tachycardia underwent an electrophysiology study (EPS) for diagnosis and ablation. Her baseline electrocardiogram and echocardiogram were normal. At EPS, she had dual atrioventricular nodal (AVN) conduction, but isoproterenol was needed to initiate the slow-fast form of AVN reentry. Before ablation without any isoproterenol, she began to have a spontaneous block in the fast pathway with continuous conduction over the slow pathway. After ablation of the slow pathway, all complexes conducted over the fast pathway during a 25-year follow-up. Possible electrotonic interaction between the slow and fast pathways is proposed as the mechanism for this phenomenon.

Venice Chart International Consensus Document on Ventricular Tachycardia/Ventricular Fibrillation Ablation ANDREA NATALE, M.D.,∗ ANTONIO RAVIELE, M.D.,† AMIN AL-AHMAD, M.D.,‡ OTTAVIO ALFIERI, M.D.,¶ ETIENNE ALIOT, M.D.,∗∗ JESUS ALMENDRAL, M.D.,†† GUNTER BREITHARDT, M.D.,‡‡ JOSEP BRUGADA, M.D.,¶¶ HUGH CALKINS, M.D.,∗∗∗ DAVID CALLANS, M.D.,††† RICCARDO CAPPATO, M.D.,‡‡‡ JOHN A. CAMM, M.D.,¶¶¶ PAOLO DELLA BELLA, M.D.,∗∗∗∗ GERARD M. GUIRAUDON, M.D.,†††† MICHEL HAISSAGUERRE, M.D.,‡‡‡‡ GERHARD HINDRICKS, M.D.,¶¶¶¶ SIEW YEN HO, M.D.,∗∗∗∗∗ KARL H. KUCK, M.D.,††††† FRANCIS MARCHLINSKI, M.D.,‡‡‡‡‡ DOUGLAS L. PACKER, M.D.,¶¶¶¶¶ ERIC N. PRYSTOWSKY, M.D.,∗∗∗∗∗∗ VIVEK Y. REDDY, M.D.,†††††† JEREMY N. RUSKIN, M.D.,‡‡‡‡‡‡ MAURICIO SCANAVACCA, M.D.,¶¶¶¶¶¶ KALYANAM SHIVKUMAR, M.D.,∗∗∗∗∗∗∗ KYOKO SOEJIMA, M.D.,††††††† WILLIAM J. STEVENSON, M.D.,‡‡‡‡‡‡‡ SAKIS THEMISTOCLAKIS, M.D.,¶¶¶¶¶¶¶ ATUL VERMA, M.D.,∗∗∗∗∗∗∗∗ and DAVID WILBER, M.D.,†††††††† for the Venice Chart members From the ∗Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, Austin, TX, USA; †Cardiovascular Department, Ospedale dell’Angelo, Mestre-Venice, Italy; ‡Cardiac Arrhythmia Service, Stanford University Medical School, Stanford, USA; ¶Department of Cardiac Surgery, Ospedale San Raffaele, Milan, Italy; ∗∗Department of Cardio-Vascular Diseases, CHU de Nancy, Hopital de Brabois, Vandoeuvre-les-Nancy, France; ††Division of Cardiology, Hospital General Gregorio Maranon, Madrid, Spain; ‡‡Department of Cardiology and Angiology, University Hospital of Munster, Munster, Germany; ¶¶Thorax Institute-Cardiology, Hospital Clinic, University of Barcelona, Barcelona, Spain; ∗∗∗Department of Cardiology, The Johns Hopkins Hospital, Baltimore, MD, USA; †††Department of Medicine, Section of Cardiovascular Disease, Hospital of the University of Pennsylvania, Philadelphia, PA, USA; ‡‡‡Department of Electrophysiology, Policlinico San Donato, San Donato Milanese, Italy; ¶¶¶Cardiac and Vascular Sciences, St. George’s Hospital Medical School, London, UK; ∗∗∗∗Cardiology Division, Centro Cardiologico Monzino, Milan, Italy; ††††Cardiac Surgery, University of Western Ontario, London, Canada; ‡‡‡‡Hopital Cardiologique du Haut Leveque, Bordeaux, France; ¶¶¶¶Heart Center, Department of Cardiology, University of Leipzig, Leipzig, Germany; ∗∗∗∗∗Cardiac Morphology Unit, Royal Brompton Hospital, London and Imperial College, London, UK; †††††Department of Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany; ‡‡‡‡‡Department of Medicine, Section of Cardiovascular Disease, University of Pennsylvania, Philadelphia, PA, USA; ¶¶¶¶¶Cardiac Translational and Electrophysiology Laboratory, Saint Mary’s Hospital Complex, Mayo Clinic Foundation, Rochester, NY, USA; ∗∗∗∗∗∗The Care Group, Indianapolis, IN, USA; ††††††Cardiac Arrhythmia Service, Miller School of Medicine, University of Miami, Miami, USA; ‡‡‡‡‡‡Arrhythmia Service, Massachusetts General Hospital, Boston, MA, USA; ¶¶¶¶¶¶Heart Institute, University of San Paulo Medical School, San Paulo, Brazil; ∗∗∗∗∗∗∗Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; †††††††Cardiovascular Division, University of Miami Hospital, Miami USA; ‡‡‡‡‡‡‡Cardiovascular Division, Brigham and Women’s Hospital, Boston, MA, USA; ¶¶¶¶¶¶¶Cardiovascular Department, Ospedale dell’Angelo, Mestre-Venice, Italy; ∗∗∗∗∗∗∗∗Cardiology, Southlake Regional Health Center, Toronto, Canada; and ††††††††Department of Cardiology, Loyola University Medical Center, Chicago, IL, USA

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Introduction: Device recalls create problems for patients and physicians, for the risks associated with replacement may be greater than the device failure rate. In 2005, Medtronic, Guidant, and St. Jude had implantable cardioverter defibrillator (ICD) recalls on several of their devices. There were no national standards to guide physicians on the management of such patients. We report the reasons for and outcomes of ICD and pacemaker generator changes from our practice resulting from these advisories. Methods and Results: After an advisory was issued, the patients with an affected device were contacted, evaluated in the office by one of the electrophysiologists in our group, and a management plan was determined. Two hundred and twenty-two of 1,039 (Medtronic 273, Guidant 766) (21.4%) patients with advisory devices underwent device replacement. Nine minor complications occurred: hematoma managed conservatively (n = 6); local discomfort (n = 1); and incisional infections treated successfully with oral antibiotics (n = 2). Major complications occurred in nine patients (4.1%). Four atrial leads were damaged, two of which were repaired, one during the same procedure and the other at a later date. One patient required a reoperation to tighten a loose ventricular lead set screw. Hematoma requiring evacuation occurred in one patient, and pocket revision was necessary in two patients secondary to severe discomfort due to the positioning of the device in the pocket. One patient had a cerebrovascular accident preoperatively. There were no perioperative deaths or infections requiring system removal. Conclusion: Even with experienced operators complications can occur when replacing generators for a device recall. Careful risk assessment for each individual patient should be performed and efforts made to minimize generator changes.

INTRODUCTION Continuous mobile cardiac outpatient telemetry (MCOT) may have several advantages over traditional ambulatory monitoring systems in the diagnostic evaluation of symptoms such as palpitations, dizziness, and syncope. However, only limited published data are available showing its advantages. METHODS AND RESULTS We reviewed the records of 122 consecutive patients evaluated using MCOT for palpitations, presyncope/syncope, or to monitor the efficacy of a specific antiarrhythmic therapy. Ten of 17 patients (59%) studied for presyncope/syncope had a diagnosis made with MCOT. Eight of these 17 patients had a previous negative evaluation for presyncope/syncope and five had an event correlated with the heart rhythm during the monitoring period. Nineteen patients monitored for palpitations or presyncope/syncope were asymptomatic during monitoring but had a prespecified arrhythmia detected. When MCOT was used as the first ambulatory monitoring system to evaluate palpitations (n = 18), 73% of patients correlated their symptoms with the underlying cardiac rhythm. Seven of 21 patients monitored for medication titration had dosage adjustments during outpatient monitoring. CONCLUSIONS MCOT can detect asymptomatic clinically significant arrhythmias, and was especially useful to identify the cause of presyncope/syncope, even in patients with a previous negative workup. This outpatient monitoring system allows patients to undergo daily medication dose titration in the outpatient setting, thus avoiding hospitalization.

New Antiarrhythmic Agents for Prevention and Treatment of AF. Rhythm control could become the preferred treatment strategy for atrial fibrillation (AF) if the available antiarrhythmic agents were more effective and safe. A subanalysis of the AFFIRM trial data suggested that rhythm control, if achieved without the adverse effects related to antiarrhythmic medications, may offer a significant survival advantage over rate control. This article reviews the new investigational pharmacologic and dietary agents being considered for the prevention and treatment of AF. Dronederone is a benzofurane similar to amiodarone, but without the iodine component, and is devoid of many of the amiodarone systemic toxicities. Azimilide is a delayed rectifier potassium channel blocker with use-dependent effects. Agents that target the ultra rapid component of the delayed rectifier potassium current (I Kur ) have atrial myocyte specific properties and may be devoid of QT prolongation and torsade de pointes in clinical usage. Newer agents being studied also include fish oil, gap junction modulators, 5HT4 receptor antagonists, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and HMG CoA reductase inhibitors. There is considerable hope that at least some of these agents will ultimately be available for more effective and safe clinical treatment and prevention of AF.

Rhythm and Rate Control in Patients with AF. A recent series of randomized prospective clinical trials that compared rate control with rhythm control in patients with atrial fibrillation (AF) found no significant difference in primary outcome between the two strategies. However, these trials lacked clear criteria for defining “successful” rate or rhythm control. Various measures have been used to gauge the success of antiarrhythmic drug therapy, including time to first recurrence of AF, any AF recurrence, AF burden, and a reduction in symptoms. Determining the success of antiarrhythmic therapy can be relatively straightforward by using how patients feel during therapy as a key endpoint. Most patients are satisfied with a major reduction in symptomatic AF episodes and can live comfortably with occasional episodes of AF. For those who are bothered by even infrequent, brief AF episodes, a treatment regimen that eliminates nearly all AF recurrences is required, although often hard to achieve. Catheter ablation may be necessary to achieve a successful outcome in these patients. Suppression of AF in a patient at high risk of stroke does not, however, remove the need for concomitant warfarin therapy. The endpoints of ventricular rate control are not clear, and the recently published rhythm versus rate control trials lacked standard criteria for judging acceptable rate control. One relatively simple method is to try and achieve a 24-hour heart rate that mimics expected normal sinus rhythm. It is important to achieve good rate control to minimize symptoms and the risk of tachycardia-mediated cardiomyopathy. (J Cardiovasc Electrophysiol, Vol. 17

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.

Mechanism of Induction of Atrioventricular Node Reentry. Introduction: AV node reentry (AVNRT) is typically induced with anterograde (Ant) block over the fast pathway (FP) and conduction over the slow pathway (SP), with subsequent retrograde (Ret) conduction over the FP. Rarely, a premature atrial complex (PAC) conducts simultaneously over the FP and SP to induce AVNRT (2 for 1). This study investigates the mechanism of 2 for 1 induction. Methods and Results: Of 192 consecutive patients (pts) undergoing posteroseptal radiofrequency ablation to treat AVNRT, 4 pts (2%) had 2 for 1 AVNRT induction. All needed isoproterenol for AVNRT initiation, and Ant conduction was over the SP during AVNRT. Controls (n = 15) were randomly selected from the remaining 188 pts and required isoproterenol to induce AVNRT with Ant block over the FP. For 2 for 1 versus control, respectively, there was no difference in mean age (55 vs. 46 yr), AVNRT cycle length (420 vs. 320 ms), or the Ant effective refractory period of the FP (320 vs. 344 ms). Of note, the PAC that induced AVNRT had a significantly longer AH interval over the SP in pts with 2 for 1 versus control (470 vs. 320 ms, P = 0.016), even though the A1A2 interval for induction was longer for 2 for 1 (315 vs. 260 ms, P = 0.003). Ret conduction over the SP was relatively poor in the 2 for 1 group as evidenced by 4/4 pts with induction of AVNRT during incremental ventricular pacing versus only 1/15 control pts (P < 0.001). Conclusion: The unique induction of AVNRT by a PAC with simultaneous conduction over the FP and SP is best explained by minimal to no retrograde invasion of the SP from the anterogradely conducted fast pathway impulse, and consistent with this observation is the initiation of slow/fast AVN reentry during incremental RV pacing.

Introduction: Dofetilide is the newest drug approved by the United States Food and Drug Administration for the treatment of patients with atrial fibrillation (AF). Few data on the efficacy and safety of dofetilide in a diverse group of patients are available. The aim of this study was to evaluate the results of dofetilide in a consecutive series of 69 patients with AF. Methods and Results: Sixty-nine patients with persistent (n = 53) or paroxysmal (n = 16) AF were administered dofetilide in-hospital. Prior to starting dofetilide, all patients had been adequately anticoagulated, and concomitant agents contraindicated in the presence of dofetilide were discontinued. Heart rhythms were monitored continuously by telemetry in all patients. The initial dose, which was determined using the Cockroft-Gault calculated creatinine clearance, was 500 μg bid, 250 μg bid, and 125 μg bid in 51, 13, and 5 patients, respectively. Reductions in subsequent dosage occurred in 12 patients, 4 for QT prolongation. Dofetilide was discontinued in-hospital in 7 patients, 2 for adverse arrhythmic events and 3 for unacceptable QT prolongation. Twenty-seven (63%) of 43 patients in AF converted spontaneously to sinus rhythm. Fifty-eight patients were discharged receiving dofetilide treatment and were followed as outpatients for 21 ± 7 months. One third of patients continued to take dofetilide at 1 year. One patient had a cardiac arrest 1 day after hospital discharge. Conclusion: Dofetilide is a well-tolerated antiarrhythmic drug with a high conversion rate of AF to sinus rhythm. One third of patients maintained sinus rhythm at 1 year. Proarrhythmia can occur and initiation of therapy must be performed in-hospital. (J Cardiovasc Electrophysiol, Vol. 14, pp. S287-S290, December 2003, Suppl.)

Arrhythmias and the Athlete.Introduction: This consensus statement summarizes the proceedings of The Expert Consensus Conference on Arrhythmias in the Athlete of the North American Society of Pacing and Electrophysiology (NASPE) on detecting, evaluating, and treating athletes with cardiovascular disorders that predispose to cardiac arrhythmias. Methods and Results: The participants in the open policy conference were selected by the codirectors (Drs. Estes and Olshansky) based on expertise and contributions to the literature. All participants provided a referenced summary of their presentation. The writing group used the information from all published scientific studies, clinical trials, registries, clinical experience, and expert opinion to make recommendations regarding screening, evaluation, management, eligibility for competition, and a range of other medical, social, and legal issues regarding the recreational and competitive athlete. The codirectors of the symposium synthesized the participants' reports for this and made revisions according to suggestions of all members of the writing committee. The manuscript was reviewed by four independent reviewers assigned by the NASPE Committee for the Development of Position Statements and NASPE Board of Trustees. Conclusion: Despite considerable advances in knowledge regarding the diagnosis, therapy, and mechanisms of arrhythmias in the athlete, much remains unknown. Continued basic, clinical, and epidemiologic research is needed. Current screening techniques to detect athletes lack sensitivity and specificity. Evaluation of standardized screening programs with tracking of long-term outcomes is needed. Officials from athletic, academic, medical, and legal institutions need to form strategic partnerships to develop policy related to assessment of risk and assumption of responsibility for athletic activities.

We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 +/- 6 shocks (mean +/- SD) per patient compared with the endocardial group, which received 181 total shocks and 6 +/- 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41%) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 +/- 9 J, lower than the endocardial mean energy of 20 +/- 9 J (P0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 +/- 6 defibrillator shocks15 J and 4 +/- 2 shocksor = 15 J, yet AF occurred in only 2.3% versus 9.6% (P0.05) of defibrillator shocks15 J andor = 15 J, respectively. Of note, AF was not induced with energy4 J or31 J.In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.

Venice Chart International Consensus Document on Atrial Fibrillation Ablation : 2011 Update

AF Treatment Strategies. Introduction: The Atrial Fibrillation (AF) Exchange Group, an international multidisciplinary group concerned with the management of AF, was convened to review recent advances in the field and the potential impact on treatment strategies. Methods: Issues discussed included epidemiology and the impact of the rising incidence of AF on health care systems, developments in pharmacological and surgical interventions in the management of arrhythmias and thromboprophylaxis, the potential to affect treatment strategies, and barriers to implementing them. Results: The incidence of AF and the associated burden on health care systems are increasing with aging populations, prevalence of comorbidities and more effective treatment of cardiovascular diseases. Advances in available medical treatments, in particular dronedarone and dabigatran, with other products in development, offer the possibility of changes in treatment paradigms and a greater emphasis on reducing hospitalizations and improvement in long-term outcomes instead of a symptom/safety-driven approach in which the priority is symptom suppression without provoking drug toxicity. Developments in catheter ablation techniques may mean that, in experienced centers, ablation may be offered as first-line treatment in selected patient populations. Barriers to optimal treatment include underdiagnosis, lack of recognition as a serious condition and as a risk factor for stroke, limited access to care, inadequate implementation of guidelines, and poor adherence to treatment. Conclusions: The focus of the management of AF may be changing as a consequence of new treatments based on the outcome improvements they offer. However, the benefits will not be fully realized if guidelines and guidance are not observed in routine clinical practice. (J Cardiovasc Electrophysiol, Vol. 21, pp. 946-958, August 2010)

LBBB and Heart Block. Background: Patients with left bundle branch block (LBBB) undergoing right heart catheterization can develop complete heart block (CHB) or right bundle branch block (RBBB) in response to right bundle branch (RBB) trauma. We hypothesized that LBBB patients with an initial r wave (≥1 mm) in lead V1 have intact left to right ventricular septal (VS) activation suggesting persistent conduction over the left bundle branch. Trauma to the RBB should result in RBBB pattern rather than CHB in such patients. Methods: Between January 2002 and February 2007, we prospectively evaluated 27 consecutive patients with LBBB developing either CHB or RBBB during right heart catheterization. The prevalence of an r wave ≥1 mm in lead V1 was determined using 118 serial LBBB electrocardiographs (ECGs) from our hospital database. Results: Catheter trauma to the RBB resulted in CHB in 18 patients and RBBB in 9 patients. All 6 patients with ≥1 mm r wave in V1 developed RBBB. Among these 6 patients q wave in lead I, V5, or V6 were present in 3. Four patients (3 in CHB group and 1 in RBBB group) developed spontaneous CHB during a median follow-up of 61 months. V1 q wave ≥1 mm was present in 28% of hospitalized complete LBBB patients. Conclusions: An initial r wave of ≥1 mm in lead V1 suggests intact left to right VS activation and identifies LBBB patients at low risk of CHB during right heart catheterization. These preliminary findings indicate that an initial r wave of ≥1 mm in lead V1, present in approximately 28% of ECGs with classically defined LBBB, may constitute a new exclusion criterion when defining complete LBBB. (J Cardiovasc Electrophysiol, Vol. pp. 781-785, July 2010)

Background: A properly placed stimulus on the T-wave during ventricular repolarization can result in ventricular fibrillation (VF). Initiation of VF with pacing on T-wave is a rare event with a few reported cases in the literature. We present a unique case of induced VF attributed to a pacing stimulus on T-wave during ventricular pacing threshold testing of a permanent pacemaker. Case Report: A 64-year-old woman with persistent atrial fibrillation (AF) and a permanent pacemaker for tachycardia–bradycardia syndrome presented with symptomatic AF with rapid ventricular response. Acute rate control was achieved with intravenous diltiazem. During ventricular pacing threshold testing, noncapture occurred followed by a pacing spike on T-wave initiating VF. Cardiopulmonary resuscitation and defibrillation converted the rhythm to rate-controlled AF. An acute prolongation of the QT was noted and normalized within 12 hours. No antiarrhythmic medications were used. Postevent laboratory values were within normal limits. She was free of ischemia and an echocardiogram revealed normal left ventricular function. She recovered from the event and was discharged with rate-controlled AF. No further pacing-induced arrhythmias have occurred during follow-up pacemaker interrogation and 12-lead electrocardiograms continued to show normal QT intervals. Conclusion: Pacemaker-induced VF is an extraordinarily rare complication of cardiac pacing. Alterations in ventricular repolarization with rapid slowing of the heart rate demonstrated by acute prolongation of QT intervals may play a role. This report should alert physicians to the possibility of QT prolongation and an increased risk of ventricular arrhythmias following acute rate control of AF.

Introduction: Programmed stimulation is an important prognostic tool in the evaluation of patients with an ejection fraction ≤40% after myocardial infarction. Many believe that ventricular tachycardia (VT) requiring 3 ventricular extrastimuli (VES) for induction is less likely to occur spontaneously and has less predictive value. However, it is unknown whether the mode of VT induction is associated with long-term prognosis. Methods and Results: We analyzed a cohort of 371 patients enrolled in MUSTT who had inducible monomorphic VT and who were not treated with antiarrhythmic drugs or an implantable cardioverter defibrillator during the trial. Patients in whom sustained VT was induced with 1 or 2 VES or burst pacing (single VES n = 15, double VES n = 127, burst n = 7, total n = 149) were compared with those in whom VT was induced with 3 VES (n = 222). Compared with the others, patients requiring 3 VES were closer to their most recent myocardial infarction (17 vs 51 months, P = 0.035) and showed a trend toward a lower ejection fraction (26% vs 30%, P = 0.057). VT requiring 3 VES had a shorter cycle length (240 vs 260 ms, P < 0.001). Despite these findings, there was no difference in the incidence of arrhythmic death or cardiac arrest (HR 1.02; 95% CI 0.69-1.51) or all-cause mortality (HR 1.03; 95% CI 0.76-1.39) according to the mode of induction in adjusted analyses. Conclusions: The prognostic significance of VT induced by 3 VES is similar to that of VT induced by 1 or 2 VES, or burst pacing, in patients with coronary disease and abnormal LV function.

Venice Chart International Consensus Document on Atrial Fibrillation Ablation ANDREA NATALE, M.D.,∗ ANTONIO RAVIELE, M.D.,† THOMAS ARENTZ, M.D.,‡ HUGH CALKINS, M.D.,¶ SHIH-ANN CHEN, M.D.,∗∗ MICHEL HAISSAGUERRE, M.D.,†† GERHARD HINDRICKS, M.D.,‡‡ YEN HO, M.D.,¶¶ KARL HEINZ KUCK, M.D.,∗∗∗ FRANCIS MARCHLINSKI, M.D.,††† CARLO NAPOLITANO, M.D.,‡‡‡ DOUGLAS PACKER, M.D.,¶¶¶ CARLO PAPPONE, M.D.,∗∗∗∗ ERIC N. PRYSTOWSKY, M.D.,†††† RICHARD SCHILLING, M.D.,‡‡‡‡ DIPEN SHAH, M.D.,¶¶¶¶ SAKIS THEMISTOCLAKIS, M.D.,† and ATUL VERMA, M.D.,∗∗∗∗∗ for the Venice Chart members From the ∗Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, USA; †Department of Cardiology, Arrhythmologic Section, Umberto I Hospital, Venice-Mestre, Italy; ‡Arrhythmia Service, Herz-Zentrum, Bad Krozingen, Germany; ¶Department of Cardiology, The Johns Hopkins Hospital, Baltimore, USA; ∗∗Division of Cardiology, Department of Medicine, National Yang-Ming University School of Medicine and Taipei Veterans General Hospital, Taipei, Taiwan; ††Hospital du Haut Leveque, CHU Bordeaux, Bordeaux, France; ‡‡University Leipzig, Heart Center, Department of Cardiology, Leipzig, Germany; ¶¶National Heart and Lung Institute, Imperial College and Royal Brompton & Harefield Hospitals, London, UK; ∗∗∗Second Medical Department, St Georg General Hospital, Hamburg, Germany; †††Cardiovascular Division, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, USA; ‡‡‡Molecular Cardiology Laboratory, University of Pavia, Salvatore Maugeri Foundation, Pavia, Italy; ¶¶¶Department of Clinical Cardiac Electrophysiology and Internal Medicine, Mayo Clinic, Rochester, USA; ∗∗∗∗Department of Cardiology, Electrophysiology and Cardiac Pacing Unit, San Raffaele University Hospital, Milan, Italy; ††††St. Vincent Hospital and Health Care Center Program, Indianapolis, USA; ‡‡‡‡St. Bartholomew’s Hospital, London, UK; ¶¶¶¶Cardiology Cantonal Hospital of Geneva, Geneva, Switzerland; ∗∗∗∗∗University of Toronto, Toronto, Canada.

Post-CABG Nonsustained VT.Introduction: Nonsustained ventricular tachycardia (NSVT) occurs frequently in the postoperative period (≤30 days) after coronary artery bypass graft (CABG) surgery, a setting where many factors may play a role in its genesis. The prognosis of NSVT in this setting in patients with left ventricular (LV) dysfunction is unknown. This study was designed to assess its significance. Methods and Results: We compared the outcome of untreated patients enrolled in the Multicenter Unsustained Tachycardia Trial with coronary artery disease (CAD), LV dysfunction, and NSVT identified postoperatively after CABG (n = 228; mean age 67 years, 84% males) versus nonpostoperative settings (n = 1,302; mean age 66 years, 85% males). Sustained monomorphic ventricular tachycardia was induced in 27% and 33% (P = 0.046) of patients with postoperative and nonpostoperative NSVT, respectively. The 2- and 5-year rates of arrhythmic events were 6% and 16%, respectively, in postoperative patients versus 15% and 29% in nonpostoperative patients (unadjusted P = 0.0020, adjusted P = 0.0082). The 2- and 5-year overall mortality rates were 15% and 36%, respectively, for postoperative patients versus 24% and 47% for nonpostoperative patients (unadjusted P = 0.0005, adjusted P = 0.027). Patients whose NSVT was identified early (

Late Occurrence of Heart Block.Introduction: There are few data regarding the occurrence of delayed heart block at least 24 hours after radiofrequency catheter ablation (RFCA) of AV nodal reentry or posteroseptal accessory pathways (APs). We investigated the late occurrence of heart block in this population, the clinical outcome, and whether findings at electrophysiologic study could have predicted its development. Methods and Results: Two of 418 patients with AV nodal reentry undergoing RFCA using a posterior approach and 1 of 54 patients with RFCA of a posteroseptal AP developed late heart block. Anterograde and retrograde AV nodal conduction before and after RFCA were normal. Patients received 12, 15, and 32 RFCA lesions, respectively, using a mean maximum power of 44 W. The RFCA sites were the posterior septum for posteroseptal AP and the posterior and mid-septum for patients with AV nodal reentry, with no His electrogram ever recorded at the ablation site. During RFCA, junctional tachycardia occurred with 1:1 VA conduction in the patient with a posteroseptal AP, but occasional intermittent single retrograde blocked complexes were present in both patients with AV nodal reentry. No rapid junctional tachycardia or > 1 consecutive retrograde blocked complex was ever observed during RFCA. Persistent high-degree AV block with junctional escape developed 2 days after RFCA in the posteroseptal AP patient. A permanent pacemaker was implanted, and normal conduction was noted 16 days after RFCA. Both patients with AV nodal reentry complained of fatigue, mainly on exertion, 3 to 4 days after RFCA, and ECG-documented exercise-induced variable AV block was obtained. Because heart block resolved in our initial patient, a prolonged monitoring period was allowed. Symptoms disappeared at 13 and 8 days, and a follow-up treadmill test showed normal PR interval and no heart block. No recurrence of heart block has been seen in any of these three patients. Conclusion: Late unexpected heart block after RFCA of AV nodal reentry and posteroseptal AP is rare, often resolves uneventfully in 1 to 2 weeks, and no specific electrophysiologic findings predicted its occurrence. Prolonged clinical observation is preferable to immediate pacemaker implantation in such patients.