Area Of Earliest Activation Research Articles

Effect of reference electrode on intracardiac electrograms: Close indifferent electrode vs Wilson central terminal

BackgroundUnipolar electrograms (uni-EGMs) are an essential part of intracardiac mapping. Although Wilson central terminal (WCT) is conventionally used as a reference for signals, avoidance of contamination by far-field and nonphysiologic signals is challenging. ObjectiveThe aim of the study was to explore the impact of an intracardiac indifferent reference electrode close to the recording electrodes, in lieu of WCT, on electrograms. MethodsSinus node activation was mapped in patients undergoing catheter ablation by a multielectrode array with a close indifferent electrode (CIE) embedded in the distal end of the catheter shaft. An equal number of points was sequentially acquired at each site with use of CIE as a reference first and subsequently with WCT. Uni-EGMs, bipolar EGMs, and the earliest activation area (defined as the area activated in the first 10 ms of the beat) were compared between CIE- and WCT-based activation maps. ResultsSeventeen patients (61 ± 18 years; 76% male) were studied. Uni-EGM voltages acquired with CIE were significantly larger than (n = 11) or comparable to (n = 4) those acquired with WCT. When points from the entire cohort were analyzed altogether, unipolar voltages and their maximum negative dV/dT and bipolar voltages recorded with CIE were significantly larger than those recorded with WCT (2.36 [1.42–3.79] mV vs 1.96 [1.25–3.03] mV, P < .0001; 0.40 [0.18–0.77] mV/s vs 0.35 [0.15–0.71] mV/s, P < .0001; and 1.46 [0.66–2.81] mV vs 1.33 [0.54–2.64] mV, P < .0001, respectively). The earliest activation area was significantly smaller in CIE-based activation maps than in WCT-based ones (0.3 [0.7–1.4] cm2 vs 0.6 [1.0–1.8] cm2, P = .01). ConclusionCIE-based maps were associated with an approximately 20% increase in unipolar voltage and may highlight the origin of a focal activation more clearly than WCT-based ones.

Characteristics and outcomes of catheter ablation of ventricular arrhythmias originating from the left ventricular summit

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Catheter ablation (CA) of the left ventricular summit (LVS) arrhythmias is a challenging procedure due to the inherent complexity anatomy of that region. Different anatomical approaches are usually performed for mapping this area including deep intramural location. The objective of this study is to investigate the procedural outcomes of ablation of LVS arrhythmias. Methods Retrospective analysis of 32 consecutive patients (mean age 58±12 years old) who underwent CA of LVS arrhythmia in a single center. Baseline characteristics, procedural parameters and clinical outcomes were analyzed. Results All LVS arrhythmias had inferior and vertical axis (positive inferior leads with negative aVR and aVL leads). LBBB pattern was found in 25/32 (78%) and RBBB pattern in 7/32 (22%). 14/32 (44%) patients presented a "w" morphology in DI lead. 18/32 (56%) cases showed abrupt V3 transition. 13/32 (41%) patients had a previous failed ablation. Direct mapping of the intramural septum, through the septal perforator veins, was performed using a wire or a multipolar 2Fr catheter in 19 patients (59%). The earliest activation area was recorded in LCC-RCC in 13 patients (41%) followed by a septal perforator vein in 9 patients (28%). Most patients required multisite sequential ablation for achieving success (20 patients, 62%). Acute arrhythmia suppression was achieved in 22 patients (69%) and only 1 patient presented a complication (pericardial tamponade). Late success was noted in 3 patients (9%). During a median follow up of 9,79±8,6 months, 23 patients (72%) maintained a sustained acute success (80% reduction of PVC burden at least) None of the 9 patients without sustained acute success needed to repeat ablation. Conclusions Ablation of LVS arrhythmias is a challenging procedure with frequent previous ablation attempts. The earliest activation area is commonly found between LCC-RCC junction and in the intramural septum. Multisite non-conventional anatomical mapping and ablation steps are required to obtain a sustained success.

The incidence and location of epicardial connections in the era of contact force guided ablation for pulmonary vein isolation.

The effects of epicardial connections (ECs) involving pulmonary veins (PVs) in atrial fibrillation (AF) ablation have been revealed recently. However, no systematic approaches to identify and ablate the ECs were established. Patients with AF undergoing radiofrequency (RF) catheter ablation were retrospectively analyzed. ECs were identified when (1) PV isolation (PVI) cannot be achieved after first-pass isolation; (2) PVI was still absent although the conduction gap was detected and ablated; (3) the earliest activation area (EAA) was revealed located within the PV antrum distant from the initial ablation line using high-density mapping (HDM) technique; (4) focal ablation at the EAA was effective to achieve PVI. Relevant pacing maneuvers were performed to elucidate ECs' bidirectional conduction. Overall, 36 ECs were identified and ablated in 35/597 (5.86%) patients. Among the 35 patients with ECs, at least one PV insertion of ECs was located at the carina region. The most common pattern was a single breakthrough in 31 (88.6%) patients, followed by multiple breakthroughs in 3 and wide breakthroughs in 1. The median distance from EAA to the initial ablation line was 10.0 mm. The average number of RF energy delivery was 1.75 ± 1.00, and single RF delivery was adequate in 16/36 (44.4%) patients. Continuous potentials were present at the EAA in 9/34 (26.5%) patients. ECs were confirmed and ablated successfully in 5.86% (35/597) AF patients using HDM. PV insertions of ECs were mainly located at the carina region. Continuous potentials might assist in the prediction of ECs.

Ultra-high resolution mapping and ablation of accessory pathway conduction.

Detailed mapping studies of accessory pathway (AP) conduction have not been previously performed using ultra-high resolution mapping systems. We sought to evaluate the clinical utility of ultra-high resolution mapping systems and the novel "Lumipoint" algorithm in AP ablation. This study included 17 patients who underwent AP mapping using minielectrode basket catheters and Rhythmia systems. Ablation was performed with 4-mm irrigated-tip catheters. Antegrade and retrograde AP conduction was observed in 6 and 16 patients. Atrial activation map was obtained during orthodromic tachycardia and ventricular pacing in 13 (76.5%) and 14 (82.3%) patients, and the earliest activation area was identical. Ventricular activation maps were created during atrial pacing in 3 patients. All maps showed focal activation patterns on global activation histograms, and the valley on the histogram highlighted the earliest activation area. "Complex activation" features further highlighted limited areas with continuous electrical activity during the time period in the majority. APs were located at the mitral and tricuspid annuli in 15 and 2 patients, and all were successfully eliminated with 3.4 ± 0.6s applications. No patients had recurrences during a median follow-up of 15 [10.5-22.5] months. At successful ablation sites, the local atrial and ventricular electrogram amplitudes and ratio tended to be greater, and fusion or continuous electrical activity between the atrial and ventricular components was more frequently observed on the minielectrode than ablation catheter (17/17 vs. 12/17, p = 0.005). Ultra-high resolution activation mapping and a novel algorithm facilitated the AP localization. The local electrogram characteristics differed between the minielectrode and ablation catheters.

Inverse Solution Mapping of Epicardial Potentials

Background— Catheter ablation of ventricular tachycardia (VT) is still one of the most challenging procedures in cardiac electrophysiology, limited, in part, by unmappable arrhythmias that are nonsustained or poorly tolerated. Calculation of the inverse solution from body surface potential mapping (sometimes known as ECG imaging) has shown tremendous promise and can rapidly map these arrhythmias, but we lack quantitative assessment of its accuracy in humans. We compared inverse solution mapping with computed tomography–registered electroanatomic epicardial contact catheter mapping to study the resolution of this technique, the influence of myocardial scar, and the ability to map VT. Methods and Results— For 4 patients undergoing epicardial catheter mapping and ablation of VT, 120-lead body surface potential mappings were obtained during implantable defibrillator pacing, catheter pacing from 79 epicardial sites, and induced VT. Inverse epicardial electrograms computed using individualized torso/epicardial surface geometries extracted from computed tomography images were compared with registered electroanatomic contact maps. The distance between estimated and actual epicardial pacing sites was 13±9 mm over normal myocardium with no stimulus-QRS delay but increased significantly over scar ( P =0.013) or was close to scar ( P =0.014). Contact maps during right ventricular pacing correlated closely to inverse solution isochrones. Maps of inverse epicardial potentials during 6 different induced VTs indicated areas of earliest activation, which correlated closely with clinically identified VT exit sites for 2 epicardial VTs. Conclusions— Inverse solution maps can identify sites of epicardial pacing with good accuracy, which diminishes over myocardial scar or over slowly conducting tissue. This approach can also identify epicardial VT exit sites and ventricular activation sequences.

Application of L1-Norm Regularization to Epicardial Potential Solution of the Inverse Electrocardiography Problem

The electrocardiographic inverse problem of computing epicardial potentials from multi-electrode body-surface ECG measurements, is an ill-posed problem. Tikhonov regularization is commonly employed, which imposes penalty on the L2-norm of the potentials (zero-order) or their derivatives. Previous work has indicated superior results using L2-norm of the normal derivative of the solution (a first order regularization). However, L2-norm penalty function can cause considerable smoothing of the solution. Here, we use the L1-norm of the normal derivative of the potential as a penalty function. L1-norm solutions were compared to zero-order and first-order L2-norm Tikhonov solutions and to measured 'gold standards' in previous experiments with isolated canine hearts. Solutions with L1-norm penalty function (average relative error [RE] = 0.36) were more accurate than L2-norm (average RE = 0.62). In addition, the L1-norm method localized epicardial pacing sites with better accuracy (3.8 +/- 1.5 mm) compared to L2-norm (9.2 +/- 2.6 mm) during pacing in five pediatric patients with congenital heart disease. In a pediatric patient with Wolff-Parkinson-White syndrome, the L1-norm method also detected and localized two distinct areas of early activation around the mitral valve annulus, indicating the presence of two left-sided pathways which were not distinguished using L2 regularization.

Use of electroanatomic mapping in the assessment of atrial tachycardia aetiology

The present case report is of a 36-year-old man who had been symptomatic for frequent palpitations for 4 years after a prolonged febrile episode. The electrocardiogram on admission revealed an iterative supraventricular tachycardia at rate of 110 bpm, with ventriculoatrial interval of 180 ms and superior P-wave axis. Electroanatomic mapping showed substantially normal values in the right atrium other than an area along the posteroseptal region of the tricuspid annulus, with a low-voltage region that correlated with the area of earliest activation.

Reentrant and nonreentrant focal left atrial tachycardias occur after pulmonary vein isolation

Both focal and macroreentrant atrial tachycardia (ATs) can occur after pulmonary vein (PV) isolation for treatment of atrial fibrillation (AF). We report the response to pacing and pharmacologic maneuvers performed in patients with stable focal ATs after segmental PV isolation. The purpose of this study was to determine the mechanism of focal ATs occurring after PV isolation. Patients with persistent left AT after cessation of antiarrhythmic drug therapy presented for mapping and ablation. Electroanatomic mapping during AT was performed. Entrainment was performed from multiple right and left atrial sites. Single-beat resetting was performed. Adenosine was infused intravenously to determine the effect on the tachycardia. Five patients (3 men and 2 women; age 65 +/- 10 years) had focal left AT that persisted in response to pacing maneuvers. Four patients had ATs (cycle length 265 +/- 18 ms) that demonstrated focal areas of early activation at the septal aspect of the right lower (3 patients) or right upper (1 patient) PV ostium. Resetting demonstrated a flat-plus increasing curve in two patients. Adenosine was infused with transient AV block and no change to the tachycardia cycle length in three patients. Tachycardias were entrained from multiple left atrial sites. Recordings from the ablation catheter at the critical isthmus typically demonstrated mid-diastolic or long fractionated potentials. One tachycardia with a longer and more variable cycle length (480-598 ms) did not demonstrate fusion during pacing from distant sites. Persistent focal left ATs may occur after segmental PV isolation. Many of these tachycardias are caused by a focal reentrant circuit located at the PV ostium; however, focal nonreentrant rhythms also may occur.

Mechanism of focal atrial tachycardias occurring after pulmonary veins isolation

Introduction: A proarrhythmic consequence of pulmonary vein isolation (PVI) to treat atrial fibrillation can be a persistent left atrial tachycardia (LAT). We previously described that focal LATs can occur; however it is unclear whether the mechanism of these focal arrhythmias is reentry, triggered activity, or abnormal automaticity. We performed detailed pacing and pharmacologic maneuvers to determine the mechanism of focal LATs occurring after PVI. Methods: PVI was performed by segmental ostial ablation guided by a circular mapping catheter (Lasso). Patients whose recurrent arrhythmia was a LAT that persisted for more then 8 weeks returned for mapping and ablation. Results: Of 15 pts with persistent LAT, three (age 66 14, all male) had focal LAT (cycle length 268 21 ms) that remained stable in response to pacing. Electroanatomic maps demonstrated focal areas of early activation at the septal aspect of the right lower (2 pts) or right upper (1 pt) PV. Adenosine caused transient AV block but no change in tachycardia cycle length (TCL). Entrainment from multiple LA sites (N 23) outside the PVs demonstrated long post-pacing-intervals (PPI) (mean PPI-TCL 73 27 ms, range 46-127 ms). Entrainment from multiple poles around the Lasso catheter had a wide range of PPIs (PPI-TCL 22 18 ms, range -3 to 50 ms), suggesting both isthmus sites and sites outside the circuit. Septal Lasso sites and not lateral sites had PPI TCL. A single beat resetting curve in 2 pts demonstrated a mixed flat-increasing curve, consistent with reentry. In one pt, burst atrial pacing terminated and reinitiated the same tachycardia. Recordings at the critical isthmus demonstrated mid diastolic potentials or a long fractionated signal suggesting slow conduction. Ablation at the site of mid diastolic electrograms or best PPI (PPI-TCL 2 6 ms) resulted in LAT termination. Conclusions: Focal left atrial tachycardias may occur after segmental PVI, particularly at the septal aspect of the right pulmonary veins. Detailed entrainment mapping and resetting confirm that the mechanism of the stable tachycardias we studied is reentry. RF application at the critical isthmus results in tachycardia termination.

Voltage-sensitive dye mapping in Langendorff-perfused rat hearts.

An imaging system suitable for recordings from Langendorff-perfused rat hearts using the voltage-sensitive dye 4-[beta-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) has been developed. Conduction velocity was measured under hyper- and hypokalemic conditions, as well as at physiological and reduced temperature. Elevation of extracellular [K(+)] to 9 mM from 5.9 mM caused a slowing of conduction velocity from 0.66 +/- 0.08 to 0.43 +/- 0.07 mm/ms (35%), and reduction of the temperature to 32 degrees C from 37 degrees C caused a slowing from 0.64 +/- 0.07 to 0.46 +/- 0.05 mm/ms (28%). Ventricular activation patterns in sinus rhythm showed areas of early activation (breakthrough) in both the right and left ventricle, with breakthrough at a site near the apex of the right ventricle usually occurring first. The effects of mechanically immobilizing the preparation to reduce motion artifact were also characterized. Activation patterns in epicardially paced rhythm were insensitive to this procedure over the range of applied force tested. In sinus rhythm, however, a relatively large immobilizing force caused prolonged PQ intervals as well as altered ventricular activation patterns. The time-dependent effects of the dye on the rat heart were characterized and include 1) a transient vasodilation at the onset of dye perfusion and 2) a long-lasting prolongation of the PQ interval of the electrocardiogram, frequently resulting in brief episodes of atrioventricular block.

Transseptal activation during left atrial pacing in humans: electroanatomic mapping using a noncontact catheter and the intracardiac echocardiography.

A better understanding of transseptal activation may be important for the treatment of atrial fibrillation, but little is known about preferential routes of conduction from the left atrium (LA) to the right atrium (RA) in humans. Twelve patients were studied. A noncontact mapping system was used to map the RA during pacing from several sites of LA at different cycle lengths. The location of the Bachmann's bundle (BB), the fossa ovalis (FO) and the coronary sinus (CS) ostium were determined using intracardiac echocardiography. The BB was the earliest area of right atrial activation during pacing from the atrial appendage, roof and postero-superior wall in 94% of cases. The FO was the area of earliest activation during pacing from the septum and the right superior pulmonary veins (PV) in 95% of cases. The CS ostium (alone or associated with the FO) was the region of transseptal breakthrough in all patients during pacing from the right inferior PV, postero-inferior wall and distal CS. Various patterns of activation with 2 or 3 distinct areas of transseptal breakthrough were observed during pacing from the lateral wall and the left superior PV. The pacing cycle length did not influence the modality of transseptal activation. Different patterns of transseptal activation were found during pacing from LA. The preferential routes of conduction from the LA to the RA were related to the sites of stimulation and were not influenced by the pacing cycle length.

Global repolarization sequence of the ventricular endocardium: monophasic action potential mapping in swine and humans.

The aim of this study was to evaluate the global sequence of repolarization over the ventricular endocardium. Disturbances in myocardial repolarization are associated with the genesis of arrhythmias. However, little is known about the global sequence of repolarization. Monophasic action potentials (MAPs) were recordedfrom 61 +/- 18 LV and/or RV sites in ten healthy pigs and from 43 +/- 15 LV or RV sites in eight patients using the CARTO system. Local activation time (AT), end-of-repolarization (EOR) time, and MAP duration were calculated and three-dimensional global maps of AT, EOR, and MAP duration constructed. LV maps were obtained from all ten pigs and RV maps from three pigs. Five RV maps and five LV maps were obtained from the eight patients. (1) EOR sequence was recognizable in 12 of 13 pig maps and in all the patient maps. (2) EOR followed the sequence of activation in 12 of 13 pig maps and 8 of 10 patient maps. (3) The longest MAPs were recorded in or near the earliest activation area, and the shortest ones in or near the latest activation area in all the pig maps and in nine often and eight often patient maps, respectively. (4) In all maps, MAP duration and AT were negatively correlated, and EOR and AT positively correlated. In conclusion, repolarization gradients exist over the pig and the human ventricular endocardium. The activation sequence is a determinant for the repolarization sequence. The magnitude of the progressive MAP shortening with progressively later activation, relative to local AT, is a critical factor governing the direction and pattern of the EOR.

A computer model of human ventricular myocardium for simulation of ECG, MCG, and activation sequence including reentry rhythms.

A computer model is presented for simulation of the spread of activation and repolarization in ventricular myocardium. The program calculating the activation sequence is based on an algorithm similar to Huygen's principle of constructing wavefronts. Physiological parameters of the heart, such as areas of early activation on the endocardium, conduction velocity, anisotropy of propagation, duration of action potentials and refractory periods are taken into account. The time-course of ECG and MCG is calculated using the equations of the bidomain model. Simulation of pathologic cases of activation is performed through variation of the physiological heart parameters. The simulations presented here show good agreement of ECG and MCG with measurements in the normal case, the case of bundle branch block and abnormal repolarization. A special feature of the model is the possibility of simulating reentry rhythms following a premature stimulus in ventricular myocardium. Two kinds of reentry are simulated: reentry around an anatomical obstacle and the leading-circle model. The widespread capability for investigating not only ECG but also MCG and various kinds of pathologic activation patterns including reentry rhythms indicates that the model may be useful in studying numerous problems in cardiologic research.

Cryoablation of refractory sustained ventricular tachycardia due to coronary artery disease

Thirty-nine patients with medically refractory sustained monomorphic ventricular tachycardia (VT) due to coronary artery disease underwent map-guided cryosurgery. Locations of prior myocardial infarctions had been inferior in 22, anterior in 16 and combined in 1. Mean age was 61 ± 9 years and the mean number of drug trials per patient before surgery was 3.8 ± 1.4. Intraoperative endocardial mapping induced 67 tachycardias in 35 patients. Each patient received 6 to 18 (11 ± 3) endocardial cryothermic applications (15 mm, −60 °C, 2 minutes) at areas of earliest activation during VT. Encircling endocardial cryoablation was performed in 4 patients who had unsuccessful mapping. In addition, 11 patients had subendocardial resection of their well-demarcated septal scars as well as cryosurgery. There were 2 in-hospital deaths. At post-operative programmed ventricular stimulation, 28 of the 37 patients (76%) had no inducible or spontaneous VT before hospital discharge. Six patients (16%) with spontaneous or inducible VT had a single morphology and were controlled with antiarrhythmic drugs that had previously failed. Therefore, surgery alone or in combination with drugs was efficacious in 92% of the population surviving surgery. The remaining 3 patients (8%) received automatic implantable cardioverter defibrillators. No significant difference in surgical outcome was seen between patients who had cryosurgery alone and those who had subendocardial resection together with cryoablation. Mean left ventricular ejection fractions before and after surgery were 33 and 39%, respectively (p < 0.01). Clinical follow-up ranged from 2 to 36 months (18 ± 12). One patient died of heart failure and another underwent heart transplantation. No recurrence of sustained VT, cardiac arrest, syncope or defibrillator discharge has occurred in the remaining patients. Thus, cryoablation was highly effective and should be considered as a good alternative to subendocardial resection in patients with drug-resistant sustained VT related to coronary artery disease.