Abstract Background Low QRS amplitude (QRSa), QRS fractionation (QRSf) and longer QRS duration (QRSd) are markers of myocardial fibrosis and inflammation in non-ischemic cardiomyopathy (NICM). Objective To determine if reduction of inflammation with treatment of cardiac sarcoidosis (CS) may reverse these 12 lead ECG parameter changes. Methods 21 patients (pts) with CS and VT ablation with a positive baseline positron emission tomographic (PET 1) scan were studied. All pts received prednisone ≥40 mg for 4 to 8 weeks followed by a taper and maintenance with methotrexate ± low-dose prednisone, <10 mg/day, until clinically stable and resolution of inflammation on PET 2 one year after initial. In addition, pts with low LV ejection fraction (13/21) received guideline directed medical therapy for heart failure. Pts at 1yr with positive PET2 (9) were compared to those with negative PET2 (12). Baseline and 1yr 12-lead ECGs were analyzed for QRSd, ≥2QRSf contiguous leads and QRSa in the limb leads. Results Pts in PET2(+) vs PET2(−) groups has similar gender (men 89% vs 100%, p=0.42), age (57±8 vs 56±10 years, p=0.8) and LV ejection fraction (41±11 vs 46±11, p=0.31). Baseline 12-lead ECGs showed similar QRSd, ≥2QRSf contiguous leads and QRSa for PET2(+) vs PET2(−); P all >0.15 (Table 1). At 1 yr there was a lower prevalence of ≥2QRSf contiguous leads and strong trend for shorter QRS duration and larger QRSa in lead DI if PET2(−) vs PET2(+). 4 pts demonstrated loss of QRSf 2 contiguous leads and/or increase in QRSa in DI by at least 0.15 mV from baseline if PET2(−) and none if PET2(+). Conclusions In pts with CS and VT, reversal of inflammation may result in a greater QRSa and reduction in QRSf. An increase in QRSa in lead 1 by >0.15mV and/or loss of QRSf identifies a clear positive response to treatment and negative PET at 1 year. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Richard T and Angela Clark Innovation Fund in Cardiovascular Medicine, the Mark S Marchlinski EP Research and Education Fund and the Winkelman Family Fund in Cardiovascular Innovation. Table 1

Abstract Background Patients with idiopathic outflow tract ventricular arrhythmias (OTVAs) and structurally normal heart by ECG and echocardiogram often undergo cardiac magnetic resonance (CMR) study to evaluate for presence of concealed myocardial abnormalities with late gadolinium enhancement (LGE). However, the clinical impact of incidental LGE finding in the left ventricle (LV) in patients with idiopathic OT-VAs is unclear. Accordingly, the aim of the present study was to investigate the prevalence, characteristics and prognostic significance of isolated LV LGE in a large population of patients with OTVA undergoing CMR. Methods A total of 364 consecutive patients (43±16 years, 53% male) with OTVA and negative routine diagnostic work-up were included. All patients underwent a CMR study with LGE imaging for detection of scar/replacement fibrosis. Presence of LGE was correlated with long term major adverse cardiovascular events including sudden cardiac death (SCD), resuscitated cardiac arrest and nonfatal documented sustained ventricular tachycardia. Results Isolated LGE in the LV was identified in 15 patients (4%), typically involving the inferolateral wall (11 cases, 73%) and having a median extension of 3 (2–5)% of the LV mass. All cases showed a midmyocardial/subepicardial distribution consistent with a possible prior myocarditis. Patients with incidental finding of LV-LGE were older (55±13 years vs. 42±16 years; p<0.01) and were more frequently males (80% vs. 51%; p=0.03). After a median follow-up of 69 (47–98) months, none of the patients in the LV-LGE group and 1 patient (0.3%) in the non-LGE group (p=1.0) experienced the composite end-point which consisted in an episode of sustained VT with hypotension and dizziness. The patient subsequently underwent effective radiofrequency ablation of the VT from the right ventricular outflow tract. Conclusion In this large CMR study, isolated LV scar was found in 4% of patients with idiopathic OT-VAs, was small in size with distribution consistent with prior myocarditis. The LGE abnormality did not portend a negative prognosis. Funding Acknowledgement Type of funding source: None

January 22, 2019 551 This study used a Survival Tree analysis method to identify specific risk groups for mortality and ventricular tachycardia recurrence using risk factors at the time of ventricular tachycardia ablation. Left ventricular ejection fraction, electrical storm, and previous ablation were the most informative variables. The classification system provides estimates of ventricular tachycardia recurrence and mortality that can be used to help counsel patients and to plan for care after the procedure.

Ventricular arrhythmias (VAs) commonly originate from the ventricular outflow tracts (OT) in the absence of structural heart disease. All patients undergoing successful idiopathic OT VAs ablation from septal region with structurally normal hearts between 2006 and 2010 were studied. Real-time 3-D electroanatomical map (EAM) of septal summit was constructed using intracardiac echocardiogram and CartoSound (Figure B). Activation and pacemapping were performed. VA arising from septal summit was defined by ICE, EAM and fluoroscopy. Variability in precordial transition and 12-lead ECG morphologies were observed. Characteristic 12-lead ECG features of VAs successfully ablated from the RCC were highlighted by LBBB, positive R wave in Lead I; taller R wave in Lead II than Lead III and S wave in aVR greater than aVL (A). Septal summit RFA was guided by ICE (C). Systematic pacemapping using the patient as their own control efficiently localised the earliest site of origin for successful RFA (D). Conclusions: Ventricular arrhythmias from the posterior septal summit(1)can be safely and successfully ablated by utilising the characteristics from 12-lead ECG, imaging with ICE, simultaneous EAM and fluoroscopy;(2)are characterised by +'ve R wave Lead I; R wave Lead II>III and S wave aVR>aVL;(3)variability in BBB morphology and precordial transition are due to normal anatomic variation and one can use patient as own control with pacemapping to confirm RCC origin.

The prerequisites for the development of uniform ventricular tachycardia (VT) late after myocardial infarction (MI) have been fairly well understood for many years. Compared with survivors of cardiac arrest or patients evaluated for nonsustained VT, patients with uniform VT have more extensive infarction, more profound left ventricular dysfunction, and more abnormal endocardial activation during sinus rhythm.1,2 The slow conduction required for formation of VT circuits is caused by tissue disruption secondary to myocyte death and secondary fibrosis, as well as electric remodeling (eg, altered connexin expression) of the surviving cells.3,4 Although infarct-related damage may be transmural, the importance of the endocardial substrate for the formation of VT circuits has been established by histological-electrophysiological correlation3,5,6 and by the effects of catheter and surgical ablation. Given the importance of the topic, it is puzzling that there have been few data collected on the influence of modern cardiovascular care on the development of VT. There is a general sense that current pharmacological therapy and appropriate revascularization have reduced the incidence of VT after MI, but it is not clear how these therapies might affect the underlying pathophysiology.Article see p 1887 In this light, the study by Wijnmaalen and coworkers in this issue of Circulation offers considerable promise.7 In this study, 36 consecutive patients with VT late after MI (mean 13±9 years) were carefully evaluated to compare the influence of acute reperfusion of the infarct-related artery on the characteristics of the spontaneous/induced VT and the underlying VT substrate. There were 14 patients in the reperfused group and 22 who were not reperfused. The baseline characteristics of the 2 groups were similar, although the reperfused group presented with VT earlier after MI and were slightly younger. The majority …

It is critical to begin any discussion on ablation of unstable ventricular tachycardia with background information supporting the importance of the effort. First, stable, mappable ventricular tachycardias represent the tip of the arrhythmia iceberg. In order for any arrhythmia to be mappable it must be reliably inducible and hemodynamically tolerable. The ventricular tachycardia must also be stable in response to the catheter manipulation and pacing required to identify the appropriate site for ablative therapy during activation and entrainment mapping [1–4]. In a consecutive series of “ideal” patients presenting with hemodynamically tolerated ventricular tachycardia and referred for catheter ablation, 30% had only unmappable VT at the time of electrophysiological evaluation [5]. Secondly, ICD event monitoring after device implantation has documented rapid unmappable VT in most patients regardless of the clinical indication for initial device therapy [6–8]. Finally, in looking to the future, a strategy for prevention of sudden cardiac death that uses ablative therapy must target the substrate for unmappable ventricular tachycardia [9].

Atrial Fibrillation (AF) is often initiated by pulmonary vein (PV) depolarizations. However, sustained PV firing (PVF) is infrequently observed in this population and has not been characterized. In 15 patients undergoing AF ablation we report the response of sustained PVF to pacing and pharmacological maneuvers. Sustained PVF was defined as discrete, repetitive, electrical activity during sinus rhythm that did not correspond with other electrical events (P, QRS, T wave), persisting ≥5 minutes and recorded at/or distal to PV ostium prior to ablation. During sustained PVF, pacing was performed from coronary sinus and/or posterior right atrium at different cycle lengths (900 to 400 ms; duration: 30 to 60 s) following which, if PVF persisted, in random order, isoproterenol and adenosine were administered and carotid sinus massage (CSM) was performed. PVF response was classified as: suppressed (complete quiescence), augmented (increase in frequency of PVF/AF initiation) and “no effect.” Sustained PVF was observed in 16 veins. In 13 (81%) patients, PVF was suppressed during overdrive pacing with early recurrence (≤5 s) postpacing regardless of pacing cycle length in 11 (85%) patients. PVF was augmented by isoproterenol in the majority of patients (88%) and showed mixed response to adenosine (augmented 40%, suppressed 20%, and no effect 40%). CSM appeared to have no effect on PVF in the majority of patients (86%). Sustained PVF is seen infrequently in patients undergoing AF ablation. Its response to pacing maneuvers argues against sustained reentry and supports triggered activity and/or abnormal automaticity as the mechanisms underlying the phenomenon.

We have shown that pacemapping from each of the pulmonary veins reveals unique surface ECG characteristics. However, application of these criteria to spontaneous atrial premature complexes is often difficult because of obscuration by the prior T wave. We hypothesized that the pulmonary vein of origin of spontaneous atrial premature complexes can be determined by measuring characteristics of the P wave whether or not the P wave was superimposed on the prior T wave. We analyzed 58 spontaneous atrial premature complexes of known pulmonary vein origin in 30 patients referred for atrial fibrillation ablation. The origin of all the atrial premature complexes was documented by detailed, intracardiac multipolar catheter mapping. Based on previous work, the criteria for distinguishing right‐sided from left‐sided pulmonary vein origin of atrial premature complex includes: (1) P wave duration < 120 ms; (2) P wave amplitude in lead I > 0.05 mV; and (3) P wave amplitude in leads II/III > 1.25. The criteria to separate superior from inferior pulmonary veins included the sum of the P wave amplitude in all the inferior leads greater than 0.3 mV. The combination of the P wave duration < 120 ms and the ratio of the P wave amplitude in leads II/III > 1.25, distinguished right‐sided from left‐sided pulmonary vein origin of spontaneous atrial premature complexes with a sensitivity of 82% and specificity of 100%. The sum of the P wave amplitude in leads II, III, and aVF > 0.3mV distinguished superior from inferior pulmonary vein of origin with a sensitivity of 39% and specificity of 73%. The pulmonary vein origin of spontaneous atrial premature complexes can often be localized using careful quantitative analysis of the surface ECG despite superimposition of the P wave upon the T wave. Separation of right‐sided from left‐sided pulmonary vein origin of spontaneous atrial premature complexes can be determined with good specificity and sensitivity, while the ability to distinguish inferior from superior pulmonary vein origin is limited. (PACE 2004; 27:182–188)

RHO, R.W., et al.: Elevations in Ventricular Pacing Threshold with the Use of the Y Adaptor: Implications for Biventricular Pacing. Cardiac resynchronization therapy (CRT) is a new and promising therapeutic option for patients with severe heart failure and intraventricular conduction delay. Patients who are candidates for CRT and have a previously implanted device may utilize a “Y” IS 1 connector to accommodate the coronary sinus lead. This modification has the potential to alter biventricular pacing thresholds. During an 18 month period, successful biventricular pacemaker implantation was performed in 72 patients (age: 67 ± 11 years, left ventricular ejection fraction: 20.5 ± 5.6% ). All of these patients had severe symptomatic congestive heart failure (NYHA Class III and IV). In 20 patients a special “Y” adaptor that bifurcates the ventricular IS 1 bipolar output to two bipolar outputs or one unipolar and one bipolar output was utilized. During initial implantation, LV thresholds obtained in a unipolar configuration prior to connecting to the “Y” adaptor were significantly lower than thresholds obtained after connecting to the “Y” adaptor ( 1.7 ± 1.11 V at 0.5 ms pulse width versus 2.8 ± 1.5 V at 0.5 ms pulse width [P = 0.01] ). Two patients (10%) required left ventricular lead revisions due to unacceptably high left ventricular thresholds during device follow‐up. The difference in measured left ventricular thresholds between the two configurations is best explained by a resistive element that is added to the circuit when performing threshold measurement of the LV lead through the “Y” adaptor (combined tip to RV ring configuration) versus measurement of the LV lead in a unipolar configuration. This resistive element represents multiple factors including anode surface area, resistive polarization at the tissue‐electrode interface, and transmyocardial resistance. LV thresholds should be measured in an LV tip to RV ring configuration or ideally in a combined tip (LV and RV) to shared ring configuration in order to accurately assess LV thresholds. This observation has significant clinical implications as loss of capture may occur as a result of improper measurement of left ventricular thresholds at the time of implantation. (PACE 2003; 26:747–751)

Introduction: The etiology of atrial fibrillation (AF) recurrences after pulmonary vein (PV) isolation is not well described. The aim of this study was to examine the reason for recurrent AF in patients undergoing a repeat attempt at AF trigger ablation.

Atrial activation from a site in the low lateral right atrium will typically proceed in a superior direction. We present a case of a low lateral right atrial tachycardia with a surface electrocardiographic P wave morphology that appeared to have an inferiorly directed axis. The tachycardia occurred 2 years after successful atrial flutter ablation. The use of a multipolar basket catheter allowed confirmation of the focal origin of the tachycardia, permitted its rapid localization, facilitated catheter ablation, and provided clues to atrial activation that helped describe the appearance of the P wave.

Uniform success for ablation of focal athaJ tachycardias has been difficult to achieve using standard catheter mapping and ablation techniques. In addition, our understanding of the complex relationship between atrial anatomy, electrophysiology. and surface ECG P wave morphology remains primitive. The magnetic electroanatomical mapping and display system (CARTO) offers an on‐line display of electrical activation and/or signal amplitude related to the anatomical location of the recorded sites in the mapped chamber. A window of electrical interest is established based on signals timed from an electrical reference that usually represents a fixed electrogram recording from the coronary sinus or the atrial appendage. This window of electrical interest is established to include atrial activation prior to the onset of the P wave activity associated with the site of origin of a focal atrial tachycardia. Anatomical and electrical landmarks are defined with limited fluoroscopic imaging support and more detailed global chamber and more focal atrial mapping can be performed with minimal fluoroscopic guidance. A three‐dimensional color map representing atrial activation or voltage amplitude at the magnetically defined anatomical sites is displayed with on‐line data acquisition. This display can be manipulated to facilitate viewing from any angle. Altering the zoom control, triangle fill threshold, clipping plane, or color range can all enhance the display of a more focal area of interest. We documented the feasibility of using this single mapping catheter technique for localizing and ablating focal atrial tachycardias. In a consecutive series of 8 patients with 9 focal atrial tachycardias, the use of the single catheter CARTO mapping system was associated with ablation success in all but one patient who had a left atrial tachycardia localized to the medial aspect of the orifice of the left atrial appendage. Only low power energy deHvery was used in this patient because of the unavaHahiHty of temperature monitoring in the early version of the Navistar catheter, the location of the arrhythmia, and the history of arrhythmia control with flecainide. No attempt was made to Umit fluoroscopy time in our study population. Nevertheless, despite data acquisition from 120–320 anatomically distinct sites during global and more detaHed focal atrial mapping, total fluoroscopy exposure was typically < 30 minutes and was as little as 12 minutes. The detailed display capabilities of the CARTO system appear to offer the potential of enhancing our understanding of atrial anatomy, atrial activation, and their relationship to surface ECC P wave morphology during focal atrial tachycardias.