Endocardial Mapping Research Articles

Relationship of bipolar and unipolar electrogram voltage to scar transmurality and composition derived by magnetic resonance imaging in patients with nonischemic cardiomyopathy undergoing VT ablation

Bipolar voltage mapping has a role in defining endocardial-based scar in postinfarct patients undergoing ventricular tachycardia catheter ablation. The utility of bipolar and unipolar voltages in characterizing scar has not been evaluated in patients with nonischemic cardiomyopathy. To relate left ventricular (LV) endocardial bipolar and unipolar voltages in these patients to scar transmurality (endocardial vs nonendocardial) and composition (homogeneous core vs heterogeneous gray). Ten consecutive cardiomyopathy patients undergoing endocardial LV tachycardia ablation were included (age 48 ± 14 years; left ventricular ejection fraction 43% ± 15%). Preablation late gadolinium-enhanced magnetic resonance imaging was used to quantify core and gray scar by using signal-intensity thresholding. Electroanatomic LV endocardial mapping provided bipolar and unipolar voltages. Electroanatomic maps and late gadolinium-enhanced magnetic resonance imaging were rigidly registered in order to relate voltage to scar (registration error 3.6 ± 2.9 mm). Bipolar voltage was lower in endocardial core than in no scar (P <.001). Unipolar voltage was lower in endocardial core and nonendocardial core than in no scar (P <.001). Endocardial and nonendocardial gray scar had an effect similar to that of core in reducing bipolar and unipolar voltages (P <.001). The mass of healthy myocardium and endocardial core scar independently predicted bipolar and unipolar voltages using general estimating equation modeling. With receiver operating characteristic curve analysis, bipolar voltage >1.9 mV and unipolar voltage <6.7 mV had a high negative predictive value (91%) for detecting nonendocardial scar from either endocardial scar or no scar. In patients with nonischemic cardiomyopathy, LV endocardial bipolar voltage is dependent on endocardial core and gray scar, while the unipolar voltage is influenced by core and gray scar across the LV wall as defined by late gadolinium-enhanced magnetic resonance imaging.

P‐Wave Morphology: Underlying Mechanisms and Clinical Implications

Increasing awareness of atrial fibrillation (AF) and its impact on public health revives interest in identification of noninvasive markers of predisposition to AF and ECG-based risk stratification. P-wave duration is generally accepted as the most reliable noninvasive marker of atrial conduction, and its prolongation has been associated with history of AF. However, patients with paroxysmal AF without structural heart disease may not have any impressive P-wave prolongation, thus suggesting that global conduction slowing is not an obligatory requirement for development of AF. P-wave morphology is therefore drawing increasing attention as it reflects the three-dimensional course of atrial depolarization propagation and detects local conduction disturbances. The factors that determine P-wave appearance include (1) the origin of the sinus rhythm that defines right atrial depolarization vector, (2) localization of left atrial breakthrough that defines left atrial depolarization vector, and (3) the shape and size of atrial chambers. However, it is often difficult to distinguish whether P-wave abnormalities are caused by atrial enlargement or interatrial conduction delay. Recent advances in endocardial mapping technologies have linked certain P-wave morphologies with interatrial conduction patterns and the function of major interatrial conduction routes. The value of P-wave morphology extends beyond cardiac arrhythmias associated with atrial conduction delay and can be used for prediction of clinical outcome of a wide range of cardiovascular disorders, including ischemic heart disease and congestive heart failure.

Geoffrey O. Hartzler, MD

On Saturday, March 10, 2012, cardiology sadly lost one of its brightest stars. Geoffrey O. Hartzler died suddenly at his home at the Lake of the Ozarks; he was 65 years old. Geoff was a very special individual, intellectually brilliant, intense, energetic, and controversial. He was born in 1946 in Goshen, IN, the second of 3 brothers, the youngest of whom died tragically of a berry aneurysm as a teenager. His father was a Mennonite minister who in a later career was instrumental in establishing the first outpatient community mental health center in the United States. His mother contracted polio when Geoff was 4 years old and survived in an iron lung. She remained the focus of the family's energy for nearly 4 decades. Pictured from left to right, Dr Andreas Gruentzig (AG), Dr Geoffrey O. Hartzler (GOH), and Dr Barry D. Rutherford (BDR) at Saint Luke's Mid America Heart Institute catheterization laboratory in 1984. He entered medical school at Indiana University. While a freshman, he worked 10-hour shifts watching a telemetry monitor and responding to cardiac arrests. At that time, he developed a keen interest in acute care medicine. He won an essay contest sponsored by the Mayo Clinic and spent a 3-month summer externship at Mayo. During that externship, he met and worked with another student clerk, David R. Holmes, Jr. Both went on to complete internal medicine and cardiology training at the Mayo Clinic and became Mayo faculty members in 1977. I (B.D.R.) first encountered Geoff Hartzler in the early 1970s when he was a cardiology fellow at the Mayo Clinic. At that time, I was a young consultant working in the Coronary Care Unit at St. Mary's Hospital. We were floating polyethylene catheters at the bedside to the pulmonary artery in patients with acute myocardial infarction. …

Simultaneous coronary angiography during titration of radiofrequency energy for ablation of left ventricular summit tachycardia in the ‘inaccessible area’

A 45-year-old patient with an implantable cardioverter defibrillator and a decreased left ventricular (LV) ejection fraction (40%) due to non-ischaemic cardiomyopathy was referred for ablation of recurrent LV outflow tract tachycardia. Endocardial and coronary venous mapping revealed earliest electrical activation within the distal great cardiac vein (GCV). Endocardial LV ablation was unsuccessful and …

Acute Hemodynamic Effect of Left Ventricular Endocardial Pacing in Cardiac Resynchronization Therapy

Background— During cardiac resynchronization therapy (CRT) device implantation, the pacing lead is usually positioned in the coronary sinus (CS) to stimulate the left ventricular (LV) epicardium. Transvenous LV endocardial pacing via transseptal puncture has been proposed as an alternative method. In the present study, we evaluated the acute hemodynamic effects of CRT through LV endocardial pacing in heart failure patients by analyzing LV pressure–volume relationships. Methods and Results— LV pressure and volume data were determined via conductance catheter during CRT device implantation in 10 patients. In addition to the standard epicardial CS pacing, the following endocardial LV sites were systematically assessed: the site transmural to the CS lead, the LV apex, the septal midwall, the basal lateral free wall, and the midlateral free wall. Four atrioventricular delays were tested. There was a significant improvement of systolic function with CRT in all LV pacing configurations, whereas no differences in systolic or diastolic function were detected between LV epicardial and endocardial transmural sites. The optimal pacing site varied among patients but was rarely related to relatively longer activation delays, as assessed by analyzing endocardial electric activation maps. Nonetheless, positioning the pacing lead at the optimal endocardial LV site in each patient significantly improved LV performance in comparison with conventional CS site stimulation (stroke volume, 83 [79–112] mL versus 73 [62–89] mL; P =0.034). Conclusions— Pacing at the optimal individual LV endocardial site yields enhanced LV performance in comparison with conventional CS site stimulation. Endocardial LV pacing might constitute an alternative approach to CRT, when CS pacing is not viable.

Low Rate of Atrial Fibrillation Recurrence Verified by Implantable Loop Recorder Monitoring Following a Convergent Epicardial and Endocardial Ablation of Atrial Fibrillation

Evaluate long-term outcomes in patients undergoing the Convergent procedure (CP) for the treatment of atrial fibrillation (AF). The CP provides a multidisciplinary approach, combining endoscopic creation of epicardial linear lesions followed by endocardial mapping and ablation and targets persistent and longstanding persistent AF patients who are at increased risk of heart failure, stroke, and mortality. Outcomes from a prospective nonrandomized study were recorded for consecutive patients by interrogation of implanted Reveal monitors. Rhythm status and AF burden were quantified 6-24 months postprocedure, and compared relative to AF type, gender, age, body mass index, left atrial size, left ventricular ejection fraction, and congestive heart failure, hypertension, age >75 years, age between 65 and 74 years, stroke/TIA/TE, vascular disease (previous MI, peripheral arterial disease or aortic plaque), diabetes mellitus, female (CHA(2) DS(2) VASc). A total of 50 patients were enrolled with 94% having persistent or longstanding persistent AF. There were 2 atrioesophageal fistulas reported. In one patient, the fistula resulted in death at 33 days postprocedure; in the second, the fistula was surgically repaired but patient died 8 months postprocedure from a CVI. After CP, 95% of patients were in sinus rhythm at 6-month follow-up; 88% at 12 months; and 87% at 24 months. The median AF burden recorded with Reveal XT monitors was 0.0%, 0.1%, and 0.1% at 6, 12, and 24 months with 81%, 81%, and 87% of patients reporting a burden less than 3%, respectively. Using 24 × 7 continuous loop recording, the CP demonstrated success in treating persistent and longstanding persistent AF patients. Endocardial mapping and catheter ablation with diagnostic confirmation of procedural success complemented the endoscopic creation of epicardial linear lesions in restoring sinus rhythm.

Canine left ventricle electromechanical behavior under different pacing modes

Cardiac resynchronization therapy may improve survival and quality of life in patients suffering from heart failure with left ventricular (LV) contraction dyssynchrony. While several studies have investigated electrical or mechanical determinants of synchronous contraction, few have focused on activation contraction coupling at a macroscopic level. The objective of the study was to characterize LV electromechanical behavior and response to pacing in a heart failure model. We analyzed data from 3D electroanatomic non-contact mapping and blood pool SPECT for 12 dogs with right ventricular (RV) tachycardia pacing-induced dilated cardiomyopathy. Surfaces generated by the two modalities were registered. Electrical signals were analyzed, and endocardial wall displacement curves were portrayed. Rapid pacing decreased the mean LV ejection fraction (LVEF) to 20.9 % and prolonged the QRS duration to 79 ± 10 ms (normal range: 40-50 ms). QRS duration remained unchanged with biventricular pacing (88.5 ms), while single site pacing further prolonged the QRS duration (113.3 ms for RV pacing and 111.6 ms for LV pacing). No trend was observed in LV systolic function. Activation duration time was significantly increased with all pacing modes compared to baseline. Finally, electromechanical delay, as defined by the delay between electrical activation and mechanical response, was increased by single site pacing (172.9 ms for RV pacing and 174.6 ms for LV pacing) but not by biventricular pacing (162.4 ms). Combined temporal and spatial coregistration electroanatomic maps and baseline gated blood pool SPECT imaging allowed us to quantify activation duration time, electromechanical delay, and LVEF for different pacing modes. Even if pacing modes did not significantly modify LVEF or activation duration, they produced alterations in electromechanical delay, with biventricular pacing significantly decreasing the electromechanical delay as measured by surface tracings and endocardial non-contact mapping.

050 Automated analysis of atrial delayed enhancement cardiac MRI correlates with voltage, AF recurrence post-ablation, and high stroke risk

IntroductionVisualisation of atrial scar using delayed-enhanced MRI (DE-MRI) may reveal causes for atrial fibrillation recurrence following ablation. To develop an objective method for delineating ablation-scar we compared DE-MRI before and...

Isolated epicardial ultrarapid activity

fi A 28-year-old man with arrhythmogenic right ventricular cardiomyopathy/dysplasia was admitted to our center for appropriate shocks to treat polymorphic ventricular tachycardia (VT) that recurred despite therapy with amiodarone, sotalol, and the combination of both drugs. He had undergone endocardial catheter ablation of VT 10 years ago. The recording from the interrogation of the implantable cardioverter-defibrillator demonstrated the irregular cycle length of VT when the shock was delivered. He underwent a second catheter ablation procedure for the recurrent VT. Endocardial mapping using the ablation catheter (Thermocool, Biosense Webster, Diamond Bar, CA) failed to reveal delayed electrograms. Epicardial mapping revealed that the low bipolar voltage area ( 1.0 mV for epicardium and 1.5 mV for endocardium) was more extensive on the epicardium (Figure 1A) and was uniformly marked by multicomponent and late electrograms. Furthermore, maping of the epicardial surface showed on a discrete area of he right ventricle (Figure 1A, white arrow) an ultrarapid ctivity with an irregular cycle length of 80–160 ms and a ean signal amplitude of 0.13 mV, which was dissociated rom ventricular activity (Figure 1B). This rapid activity as reproducibly recorded intermittently over an area of pproximately 2 cm despite catheter movement ensuring ontact. Epicardial delayed electrograms and rapid activity ere eliminated by radiofrequency application. The patient has been free from any VTs since 3 months after the procedure. A previous report showed a detailed characterization of he electroanatomic substrate of the right ventricular endoardial and epicardial surfaces in patients with arrhythmoenic right ventricular cardiomyopathy/dysplasia presenting ith recurrent ventricular arrhythmias despite endocardial blation. Patients with arrhythmogenic right ventricular cariomyopathy/dysplasia and VT after endocardial ablation ave a more extensive epicardial area of electrogram abnoralities and frequently have basal right ventricular wall hickening. Although the exact mechanism of this focal

The main trunk of the left bundle branch is not part of the re-entry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

We report the case of a 19-year-old man with verapamil-sensitive idiopathic left ventricular tachycardia (ILVT), who had paroxysmal palpitations for 3 years. Programmed right atrial and ventricular stimulation easily induced ventricular tachycardia (VT) with QRS duration of 125ms, right bundle branch block pattern, and right inferior axis, which are characteristics of ILVT. Left ventricular endocardial mapping accidentally produced a complete left bundle branch block and provoked prolongation of the QRS duration of VT, which was 143ms. However, no changes occurred in the cycle length, inducibility, or maintenance of VT. The VT was eliminated successfully by catheter ablation at the pre-Purkinje potential (PP) recording site. These findings suggest that the main trunk of the left bundle branch is not a critical component of the re-entry circuit of ILVT.

Correlation between substrate location and ablation strategy in patients with ventricular tachycardia late after myocardial infarction

The requirement for epicardial radiofrequency ablation (RFA) is still undefined in ventricular tachycardia (VT) late after myocardial infarction (MI). The purpose of this study was to evaluate the correlation between the need for epicardial RFA and the clinical and electrophysiologic characteristics of VT late after MI. Endocardial mapping and RFA were performed for VT late after MI, followed by epicardial mapping and RFA if no endocardial substrate was present or endocardial RFA failed. Seventy patients with VT late after MI (30 anterior MI [A-MI] and 40 posteroinferior MI [PI-MI]) were included in the study. Forty-one VTs in patients with A-MI and 64 VTs in patients with PI-MI were targeted for RFA. Epicardial mapping and ablation were attempted in 6 patients and performed successfully in only 4 patients. All 6 (100%) patients requiring epicardial access had PI-MIs. Patients with epicardial RFA had endocardial low-voltage areas of smaller size compared to patients without epicardial RFA (21 ± 13 cm(2) vs 68 ± 40 cm(2); P <.01). During 25 ± 19 months of follow-up, recurrence after the initial procedure was noted in 12 of 30 patients (40%) with A-MI and in 18 of 40 patients (45%) with PI-MI. There was no significant difference between groups. In the majority of patients, clinical and slower VTs late after MI can be abolished using endocardial RFA. Rarely indicated, epicardial RFA is more commonly required in patients with small-sized PI-MI. During follow-up, VT recurrence after successful RFA is common.

Disparate Activation of the Coronary Sinus and Inferior Left Atrium During Atrial Tachycardia After Persistent Atrial Fibrillation Ablation: Prevalence, Pitfalls, and Impact on Mapping

Persistent atrial fibrillation (AF) ablation may lead to partial disconnection of the coronary sinus (CS). As a result, disparate activation sequences of the local CS versus contiguous left atrium (LA) may be observed during atrial tachycardia (AT). We aimed to evaluate the prevalence of this phenomenon and its impact on activation mapping. AT occurring after persistent AF ablation were investigated in 74 consecutive patients. Partial CS disconnection during AT was suspected when double potentials with disparate activation sequences were observed on the CS catheter. Endocardial mapping facing CS bipoles was performed to differentiate LA far-field from local CS potentials. A total of 149 ATs were observed. Disparate LA-CS activations were apparent in 20 ATs after magnifying the recording scale (13%). The most common pattern (90%) was distal to proximal endocardial LA activation against proximal to distal CS activation, the latter involving the whole CS or its distal part. Perimitral macroreentry was more common when disparate LA-CS activations were observed (67% vs 29%; P = 0.002). Partial CS disconnection also resulted in "pseudo" mitral isthmus (MI) block during LA appendage pacing in 20% of patients as local CS activation was proximal to distal despite distal to proximal activation of the contiguous LA. Careful analysis of CS recordings during AT following persistent AF ablation often reveals disparate patterns of activation. Recognizing when endocardial LA activation occurs in the opposite direction to the more obvious local CS signals is critical to avoid misleading interpretations during mapping of AT and evaluation of MI block.

Two-dimensional speckle-tracking echocardiography for atrioventricular accessory pathways persistent ventricular pre-excitation despite successful radiofrequency ablation

The present study was undertaken to investigate the concordance between longitudinal two-dimensional (2D)-speckle-tracking data and endocardial mapping for localizing atrioventricular accessory pathways (AP), and whether longitudinal 2D-speckle-tracking imaging accurately identifies the contractile abnormalities associated with AP and the effect of radiofrequency ablation. Echocardiograms were repeated twice in 40 patients with Wolff-Parkinson-White (WPW) syndrome (before and early after ablation) and in 40 healthy controls to obtain longitudinal 2D strain and strain rate data. The site of ablation was considered as the gold standard for the AP localization. While control patients had a homogeneous strain pattern, all but two patients with WPW had an abnormal deformation pattern with three peaks in one or two basal contiguous segments: an early peak concomitantly with the delta wave followed by a systolic and a post-sytolic one. The rapid increase in LV longitudinal deformation within the basal pre-excited zone resulted in a pre-systolic peak strain rate at the beginning of the delta wave by SR imaging that was not found in controls. The early basal contraction spread towards the mid-ventricle before merging with the normal activated segments in 15 patients (39%). Contractile abnormalities were no more than one adjacent segment different compared with the AP ablation site in all these 38 patients. Regional strain was impaired in the pre-excited areas especially in AP localized in the interventricular septum. The abnormal deformation pattern persisted in 16 (42%) patients despite successful radiofrequency ablation. However, the difference in the regional strain between WPW patients and controls did not remain after ablation. Longitudinal 2D-speckle-tracking data accurately match with endocardial mapping findings for localizing AP. Longitudinal 2D-speckle-tracking imaging accurately identifies AP-associated contractile abnormalities. Longitudinal 2D-speckle-tracking identifies persistence of local ventricular pre-excitation immediately after successful ablation.

Imaging Study of Ventricular Scar in Arrhythmogenic Right Ventricular Cardiomyopathy

Background— The hallmark lesion of arrhythmogenic right ventricular cardiomyopathy (ARVC) is fibrofatty scar replacement. We compared endocardial voltage mapping (EVM) and contrast-enhanced cardiac magnetic resonance (CE-CMR) for imaging scar lesions in ARVC patients. Methods and Results— We studied 23 consecutive ARVC patients (16 males; mean age, 38±12 years) who underwent RV EVM and CE-CMR and 37 control subjects. In 21 (91%) of 23 ARVC patients, RV EVM was abnormal, with a total of 45 electroanatomical scars (EAS): 17 (38%) in the inferobasal region, 12 (26.6%) in the anterolateral region, 8 (17.7%) in the RV outflow tract (RVOT), and 8 (17.7%) in the apex. RV delayed contrast enhancement (DCE) was found in 9 (39%) of 23 patients, with a total of 23 RV DCE scars: 4 (17.4%) in the inferobasal region, 9 (39.1%) in the anterolateral region, 4 (17.4%) in the RVOT, and 6 (26.1%) in the apex. There was a mismatch in 24 RV scars, with 22 EAS not confirmed by DCE and 2 DCE scars (both in the RVOT) undetected by EVM. In 9 (75%) of 12 patients with abnormal RV EVM/normal RV DCE, ≥1 DCEs were identified in the left ventricle (LV). Overall, ventricular DCE was detected in 78% of patients. No control subjects showed either EAS or DCE. Conclusions— EVM and CE-CMR allow identification of RV scar lesions in most ARVC patients. CE-CMR is less sensitive than EVM in identifying RV scar lesions. The high prevalence of LV DCE confirms the frequent biventricular involvement and indicates the diagnostic relevance of LV scar detection by CE-CMR.

Nature of Electrogram Fractionation During Atrial Fibrillation

The study by Jadidi et al1 described the locations of areas of continuously fractionated atrial electrograms during atrial fibrillation (AF) using high-resolution endocardial mapping in 9 patients with paroxysmal AF and 9 patients with persistent AF. This study then correlated these areas with the locations of fractionated atrial potentials during sinus rhythm and coronary sinus (CS) pacing in the same patients. Their premise was that fractionation resulted from conduction abnormalities (conduction slowing/block, pivot points, asynchronous activation, and wave collision).2,3 They postulated that areas exhibiting fractionation during all 3 rhythms (AF, sinus rhythm, and CS pacing) may differentiate fixed atrial/anatomic substrate (structural remodeling) from wave collision or functional slow conduction. They were hopeful that a better understanding of these patterns would help identify which of the areas of fractionation were optimal targets for ablation. Article see p 32 The study was carefully designed and executed, as expected from one of the premier AF laboratories in the world. Some of the findings were expected. The left atrial area was greater, the global left atrial bipolar voltage during AF was lower, and the area of continuously fractionated electrograms was greater (although not as a percentage of the overall area) in patients with persistent AF than in patients with paroxysmal AF. Perhaps most important were the findings that were not expected under the premise that fractionated electrograms were exclusively due to conduction abnormalities. First, the continuously fractionated areas during AF (CFE mean, <80 milliseconds) did not exhibit lower voltage than the surrounding areas during AF, nor did those sites exhibit low voltage (<1 mV) during sinus rhythm or CS pacing. The voltage during AF was actually higher in the fractionated areas than in the surrounding areas. There was a surprising inverse relationship between the mean bipolar voltage in AF and …

Isorhythmic Atrioventricular Dissociation in Labrador Retrievers

Isorhythmic atrioventricular dissociation (IAVD) is a rhythm disturbance in which atria and ventricles are driven by independent pacemakers at equal or nearly equal rates. To describe electrocardiographic and electrophysiologic features of IAVD in a group of 11 Labrador Retrievers and its possible correlation with focal junctional tachycardia (FJT). Between December 2004 and October 2010, medical records of 11 Labrador Retrievers with surface electrocardiographic findings compatible with IAVD were retrospectively analyzed. Twelve-lead surface electrocardiograms, thoracic radiographs, and echocardiographic findings of each dog and electrophysiologic mapping results of 3 dogs were retrospectively analyzed. In 10 of 11 dogs, the ECG pattern revealed the presence of IAVD with type I synchronization. In 5 of 10 dogs, IAVD with type I synchronization was interrupted by periods of junctional tachycardia with 1 : 1 ventriculo-atrial conduction. One of 11 dogs presented IAVD with type II synchronization. The ECG diagnosis of IAVD with type I and type II synchronization, and junctional rhythm with 1 : 1 ventriculo-atrial conduction was confirmed in 3 of 11 dogs with endocardial mapping in which the diagnosis of focal junctional tachycardia was made. IAVD with type I synchronization is more common than IAVD with type II synchronization in Labrador Retrievers, and a correlation between IAVD and FJT can be hypothesized.

Epicardial and endocardial mapping determine most successful site of ablation for ventricular tachyarrhythmias originating from left ventricular summit

A 34-year-old woman presented with idiopathic premature ventricular complex (PVC) and ventricular tachycardia (VT) originating from the area called the left ventricular summit. Radiofrequency (RF) application both through the coronary sinus and to the epicardial surface transiently suppressed the VT/PVC. Radiofrequency with sufficient energy was only applicable from the endocardial site, and the VT/PVC was successfully eliminated.

Abstract 9250: Endocardial Electrogram Characteristics Indicating an Epicardial Origin of Focal Ventricular Arrhythmias

Introduction: While most ventricular arrhythmias (VA) can be ablated successfully using an endocardial (ENDO) approach, epicardial (EPI) mapping and ablation is sometimes required. There may be clues on the surface electrocardiogram related to intrinsicoid deflection and QRS width; however, identification of an EPI origin of VA with certainty remains problematic, and there are no reported ENDO electrogram (EGM) characteristics that may direct ablation strategy. Methods: All patients referred for ablation of ventricular tachycardia or frequent ventricular ectopy from June 2006 through July 2010 were evaluated. Only patients with completed electroanatomical activation maps of a focal VA from ENDO and EPI were included. EGMs recorded by a bipolar mapping catheter in the area of earliest ENDO activation were analyzed and compared to the area of early EPI activation. Results: There were 17 patients with completed ENDO and EPI electroanatomical maps of a focal VA identified. We identified 3 characteristics from ENDO mapping that consistently indicated an EPI VA origin: 1) Diffusely early activation (&gt; 2cm2 region of sites with equally earliest activation within 10 msec; figure); 2) Sequence of a far-field EGM followed by a near-field EGM in the region of earliest ENDO activation; and 3) Inability to capture the far-field component of the earliest ENDO EGM (stimulus-QRS &lt; egm-QRS time) or reproduce the PVC or VT QRS complex morphology with pacing at the earliest ENDO activation site. Conclusions: The presence of a diffuse area of early activation and inability to capture a far-field electrogram from the endocardium indicates an epicardial origin of a focal ventricular arrhythmia.

Abstract 16917: Enodcardial Scar Size Predicts Adverse Outcomes Following Radiofrequency Catheter Ablation in Patients with Recurrent Ventricular Tachycardia

Introduction: Sustained Ventricular Tachycardia (VT) often occurs in the setting of structural heart disease and myocardial scar. Little is known about the prognostic value of endocardial scar or border zone after VT ablation. Methods 48 consecutive ICD patients with structural heart disease and documented VT underwent detailed endocardial voltage mapping (&gt; 200 LV points). Endocardial scar and border zone were defined as &lt; 0.5mV and 0.5-1.5 mV, respectively. Scar burden was defined as the ratio between endocardial scar and total left ventricular (LV) endocardial area, scar + border zone burden as the ratio between scar plus border area divided by LV area. Follow-up was included if ICD clinic notes or interrogations could be obtained at &lt; 6 month intervals. VT recurrence (VTR) was defined as any VT &gt;30s or causing appropriate ICD shocks. Mortality was determined using the Social Security Database. Results: All patients (46 male, age 62+12.18; 81% CAD; EF 26.39+12.47) underwent clinically indicated VT ablation with a mean follow-up of 31.5±8.7 months. A scar burden of &gt;10% was associated with a higher rate of first VT recurrence (VTR) with 1.9, 1.5,and 1.2 fold increases seen at 12, 24 and 36 moths, respectively. Similarly, a scar+border zone burden of &gt;25% resulted in 2.0, 1.6 and 1.2 fold increases of VTR at 12, 24 and 36 months, respectively. A scar burden of &gt;10%was also associated with a 4.0, 3.7 and 3.9 fold increase in mortality at 12, 24 and 36 months, respectively. Similarly, a scar+border zone burden of &gt;25% was associated with a 6.0, 3.8 and 3.8 fold increase in mortality at 12, 24 and 36 months, respectively. Conclusions: Large myocardial scar/border zone substrate correlates with earlier recurrence of VT and higher long-term mortality after VT ablation. This finding may allow for more refined risk stratification and guide an individualized pharmacologic/ablation-based approach to VT.

Abstract 9133: Abnormal Response of Superior Sinoatrial Node to Sympathetic Stimulation is a Characteristic Finding in Patients with Atrial Fibrillation and Symptomatic Bradycardia

Introduction: We hypothesize that unresponsiveness of superior sinoatrial node (SAN) to sympathetic stimulation is strongly associated with the development of symptomatic bradycardia in patients with atrial fibrillation (AF). Methods and Results: We performed 3-dimensional endocardial mapping in healthy control (Group 1, n=10) and in patients with AF without (Group 2, n=57) or with (Group 3, n=15) symptomatic bradycardia at baseline and during isoproterenol infusion. Sympatomatic bradycardia includes cardiac syncope, presyncope or dizziness associated with either sinus bradycardia (&lt;40 bpm; n=7) or prolonged sinus pauses (&gt;3.0 seconds; n=8) Corrected SAN recovery time (CSNRT) was abnormal (&gt; 550ms) in 0%, 11% and 36% of groups 1, 2 and 3, respectively (p=0.02). At baseline, 90%, 36% and 7% (p&lt;0.001) of the patients had multicentric SAN activation patterns. For groups 1, 2 and 3, respectively, the median distance from the superior vena cava-right atrial junction to the most cranial earliest activation site (EAS) was 5.0 (25-75 percentile range, 3.5-21.3) mm, 10.0 (4-20) mm and 17.5 (12-34) mm at baseline (p=0.01), and was 4.0 (0-5) mm, 5.0 (1-10) mm and 15.0 (5.4-33.3) mm during isoproterenol infusion (p=0.01), suggesting upward shift of EAS during isoproterenol infusion. However, while the EAS during isoproterenol infusion was at the upper 1/3 of crista terminalis in 100% of Group 1 and 78% of Group 2 patients, only 20% of the groups 3 patients moved EAS to that region (p &lt; 0.001). We analyzed the comparative efficacy of CSNRT and 3D mapping in differentiating Group 2 and Group 3 patients. The sensitivity and specificity of CSNRT test are 35% and 89%, respectively, and of the 3D mapping test are 78% and 78%, respectively. Conclusions: Superior SAN serves as the EAS during sympathetic stimulation in normal patients and in most patients with AF without symptomatic bradycardia. In contrast, unresponsiveness of superior SAN to sympathetic stimulation is a characteristic finding in patients with AF and symptomatic bradycardia.