Target Sites For Catheter Ablation Research Articles

Local Variation and Age-Related Change in Atrial and Ventricular Myocardial Contiguity at the Atrioventricular Junction in Human Hearts

Background: We explored the histologic patterns of and age-related changes in atrial and ventricular myocardial contiguity at the left and right atrioventricular (AV) junction that could be a target site for catheter ablation.Methods and Results: Twenty-three structurally normal adult hearts obtained at autopsy were studied. The 2 AV annuli were divided into 13 clinically recognized portions in which we measured distance between the atrial and ventricular myocardium at the AV junction. Overall, measured distance was less on the right than left side (mean [±SD] 0.74±0.59 vs. 1.15±0.78 mm, respectively), and distance increased gradually with age. The gap was smallest at the anterolateral portion on the right side and posterolateral portion on the left side. Three specific features were noted, namely extension of the ventricular myocardium (coarse trabeculae) towards the atrium on the right side of the AV junction, extension of the atrial myocardium onto the AV valve leaflets, and a collection of small myocardial cells, perhaps including specialized cells, in the right anterolateral portion. No concealed AV muscular connections were found.Conclusions: Contiguity and separation of the myocardium at the AV junction have specific patterns, and myocardial proximity is influenced by age. These histologic features of the AV junction may prove to be informative for catheter ablation of tachyarrhythmias related to the AV junction.

Association of the Clinical and Genetic Factors With Superior Vena Cava Arrhythmogenicity in Atrial Fibrillation.

Atrial fibrillation (AF) can be initiated from arrhythmogenic foci within the muscular sleeves that extend not only into the pulmonary veins but also into both vena cavae. The superior vena cava (SVC) is a key target site for catheter ablation. Patients with SVC-derived AF often lack the clinical risk factors of AF.Methods and Results:We conducted a meta-analysis of the clinical and genetic factors of 2,170 AF patients with and without SVC arrhythmogenicity. In agreement with previous reports, the left atrial diameter was smaller in AF patients with SVC arrhythmogenicity. Among 6 variants identified in a previous genome-wide association study in Japanese patients, rs2634073 and rs6584555 were associated with SVC arrhythmogenicity. This finding was confirmed in our meta-analysis using independent cohorts. We also found that SVC arrhythmogenicity was conditionally dependent on age, body mass index, and left ventricular ejection fraction. Both clinical and genetic factors are associated with SVC arrhythmogenicity.

Injection of cold saline for diagnosis of intramural ventricular arrhythmias

The failure to identify a successful target site for catheter ablation despite extensive endocardial and epicardial mapping is a common feature for an intramural site of origin of a ventricular arrhythmia. The purpose of this study was to assess whether transient suppression of premature ventricular complexes (PVCs) by injection of cold saline into the distal coronary venous system can identify an intramural focus. Cold saline (room temperature) was injected through an irrigated-tip catheter into the distal coronary venous system in a consecutive series of 26 patients with frequent PVCs referred for catheter ablation. PVCs were temporarily suppressed in 11 of 26 patients during injection of cold saline. Extensive mapping suggested the presence of an intramural site of origin in 9 of 11 patients with PVC suppression by cold saline but in only 1 of 15 patients in whom PVCs were not suppressed. The suppression of PVCs by cold saline was associated with the presence of an intramural PVC focus with an accuracy of 88% (sensitivity 90%, specificity 88%, positive predictive value 82%, negative predictive value 93%, P = .0002). Temporary suppression of PVCs by cold saline infused into the distal coronary venous system and the perforator veins strongly suggests the presence of an intramural septal focus of the PVCs.

Prevention of Ventricular Fibrillation Episodes in Brugada Syndrome by Catheter Ablation Over the Anterior Right Ventricular Outflow Tract Epicardium

The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (Vt/VF) in patients with the Brugada syndrome (BrS) remains unelucidated. However, several studies have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electrophysiological substrate. We hypothesized that in patients with BrS who have frequent recurrent VF episodes, the substrate site is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified at this location, which would serve as the target site for catheter ablation. We studied 9 symptomatic patients with the BrS (all men; median age 38 years) who had recurrent VF episodes (median 4 episodes) per month, necessitating implantable cardioverter defibrillator discharge. Electroanatomic mapping of the right ventricle, both endocardially and epicardially, and epicardial mapping of the left ventricle were performed in all patients during sinus rhythm. All patients had typical type 1 Brugada ECG pattern and inducible Vt/VF; they were found to have unique abnormal low voltage (0.94±0.79 mV), prolonged duration (132±48 ms), and fractionated late potentials (96±47 ms beyond QRS complex) clustering exclusively in the anterior aspect of the RVOT epicardium. Ablation at these sites rendered Vt/VF noninducible (7 of 9 patients [78%]; 95% confidence interval, 0.40 to 0.97, P=0.015) and normalization of the Brugada ECG pattern in 89% (95% confidence interval, 0.52 to 0.99; P=0.008). Long-term outcomes (20±6 months) were excellent, with no recurrent Vt/VF in all patients off medication (except 1 patient on amiodarone). The underlying electrophysiological mechanism in patients with BrS is delayed depolarization over the anterior aspect of the RVOT epicardium. Catheter ablation over this abnormal area results in normalization of the Brugada ECG pattern and prevents Vt/VF, both during electrophysiological studies as well as spontaneous recurrent Vt/VF episodes in patients with BrS.

Mechanisms of Wave Fractionation at Boundaries of High-Frequency Excitation in the Posterior Left Atrium of the Isolated Sheep Heart During Atrial Fibrillation

High-frequency fractionated electrograms recorded during atrial fibrillation (AF) in the posterior left atrium (PLA) and elsewhere are being used as target sites for catheter ablation. We tested the hypothesis that highly periodic electric waves emerging from AF sources at or near the PLA give rise to the most fractionated activity in adjacent locations. Sustained AF was induced in 8 isolated sheep hearts (0.5 micromol/L acetylcholine). Endocardial videoimaging (DI-4-ANEPPS) and electric mapping of the PLA enabled spatial characterization of dominant frequencies (DFs) and a regularity index (ratio of DF to total power). Regularity index showed that fractionation was lowest within the area with the maximal DF (DFmax domain; 0.19+/-0.02) and highest within a band of &3 mm (0.16+/-0.02; P=0.047) at boundaries with lower-frequency domains. The numbers of spatiotemporal periodic episodes (25.9+/-2.3) and rotors per experiment (1.9+/-0.7) were also highest within the DFmax domain. Most commonly, breakthrough waves at the PLA traveled toward the rest of the atria (76.8+/-8.1% outward versus 23.2+/-8.1% inward; P<0.01). In both experiments and simulations with an atrial ionic model, fractionation at DFmax boundaries was associated with increased beat-to-beat variability of conduction velocity and directionality with wavebreak formation. During stable AF, the PLA harbors regular, fast, and highly organized activity; the outer limit of the DFmax domain is the area where the most propagation pattern variability and fractionated activity occur. These new concepts introduce a new perspective in the clinical use of high-frequency fractionated electrograms to localize sources of AF precisely at the PLA and elsewhere.

A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate

ObjectivesWe sought to test the hypothesis that complex fractionated electrograms (CFAEs) recorded during atrial fibrillation (AF) could be used as target sites for catheter ablation of AF. BackgroundMapping of AF in humans has shown that areas of CFAEs correlate with areas of slowed conduction and pivot points of reentrant wavelets. We hypothesized that such areas of CFAEs could be identified in patients with AF and might serve as target sites for catheter ablation to maintain sinus rhythm. MethodsThe study population included 121 patients (29 females; mean age, 63 years) with refractory AF (57 paroxysmal, 64 chronic). All patients underwent nonfluoroscopic electroanatomic mapping (CARTO) during AF. Using CARTO, the biatrial replica, displayed in a three-dimensional color-coded voltage map, was created during AF, and areas associated with CFAEs were identified. Radiofrequency ablation of the area with CFAEs was performed, aiming to eliminate CFAE and/or convert to sinus rhythm. ResultsComplex fractionated atrial electrograms were found in seven of nine regions of both atria, but were mainly confined to the interatrial septum, pulmonary veins, roof of left atrium, and left posteroseptal mitral annulus and coronary sinus ostium. Ablations of the areas associated with CFAEs resulted in termination of AF without external cardioversion in 115 of the 121 patients (95%); 32 (28%) required concomitant ibutilide treatment. At the one-year follow-up, 110 (91%) patients were free of arrhythmia and symptoms, 92 after one ablation and 18 after two. ConclusionsAreas with CFAEs represent a defined electrophysiologic substrate and are ideal target sites for ablations to eliminate AF and maintain normal sinus rhythm.

Three-dimensional distribution of bipolar atrial electrogram voltages in patients with congenital heart disease.

Voltage differences might be used to distinguish normal atrial tissue from abnormal atrial tissue. This study was aimed at identifying lowest voltage areas in patients with atrial tachycardia after surgical correction of congenital heart disease and to evaluate if identification of these areas in diseased hearts facilitates selection of critical conduction pathways in reentrant circuits as target sites for catheter ablation. Ten patients (four men, age 39 +/- 15 years) with normal sized atria and atrioventricular reciprocating tachycardia (control group) and ten patients (5 men, 32 +/- 7 years) with congenital heart disease and postoperative atrial tachycardia (CL 281 +/- 79 ms) referred for radiofrequency catheter ablation were studied. Mapping and ablation was guided by a three-dimensional electroanatomic mapping system (CARTO) in all patients. In the control group, voltage maps were constructed during sinus rhythm and during tachycardia to evaluate the voltage distribution. The amplitude of bipolar signals was 1.90 +/- 1.45 mV (0.11-8.12 mV, n = 660) during sinus rhythm and 1.45 +/- 1.66 mV (0.12-5.83 mV, n = 440, P < 0.05) during atrioventricular reciprocating tachycardia. In the study group, the amplitude of 1,962 bipolar signals during tachycardia was 1.01 +/- 1.19 mV (0.04-9.40 mV), which differed significantly from the control group during tachycardia (P < 0.0001). No significant difference in the tachycardia cycle length was found (P < 0.05) between the control and study groups. As the lowest voltage measured in normal hearts was 0.1 mV, this value was used as the upper limit of the lowest voltage areas in the patients with congenital heart disease. These areas were identified by detailed voltage mapping and represented by a gray color. Activation and propagation maps were then used to select critical conduction pathways as target sites for ablation. These sites were characterized by fragmented signals in all patients. Ablation resulted in termination of the tachycardia in eight (80%) of ten patients. Complications were not observed. Identification of the lowest voltage areas using a cut-off value of 0.1 mV in congenital heart disease patients with postoperative atrial reentrant tachycardia facilitated the selection of critical conduction pathways as target sites for ablation.

Idiopathic Left Ventricular Tachycardia: New Insights, into Electrophysiological Characteristics and Radiofrequency Catheter Ablation

This study was performed to investigate the electrophysiological characteristics of idiopathic left ventricular tachycardia and to determine the feasibility of radiofrequency catheter ablation for nonpharmacological cure. The underlying electrophysiological mechanism of idiopathic left ventricular tachycardia with right bundle branch block morphology and left-axis deviation is presently not known. Additionally, only limited data describing the results of radiofrequency catheter ablation for treatment of idiopathic left ventricular tachycardia so far exist. Electrophysiological studies and radiofrequency catheter ablation were performed in 5 patients (3 male and 2 female, mean age 31 +/- 10 years) with idiopathic left ventricular tachycardia (cycle length 376 +/- 72 msec). The patients had a history of recurrent palpitations of 4 +/- 1 years and had been treated unsuccessfully with 2 +/- 1 antiarrhythmic drugs. Sustained ventricular tachycardia with right bundle branch block morphology and left- or right-axis deviation was documented in all patients. Inducibility with critically timed ventricular extrastimuli, inverse relationships of the coupling interval of the initiating extrastimulus and the interval to the first beat of the tachycardia, continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia, and fragmented late potentials during sinus rhythm suggested reentrant activation as the underlying mechanism in three patients. On the other hand, induction dependent on isoproterenol infusion and rapid ventricular pacing and exercise inducibility indicated different electrophysiological characteristics in the remaining two patients. During electrophysiological study, intravenous verapamil terminated ventricular tachycardia in all patients, whereas ventricular tachycardia did not respond to intravenous adenosine, autonomic maneuvers, or intravenous beta-blocking agent esmolol. Catheter mapping revealed earliest endocardial activation during ventricular tachycardia in different areas of the left ventricular septum being distributed from the base to the mid-apical portion of the septum in all patients. In 4 of 5 patients, radiofrequency catheter ablation (median number of pulses 4, range 1-9) resulted in complete abolition of idiopathic left ventricular tachycardia during a follow-up of 4-43 months (median 10) without antiarrhythmic drugs. Successful target sites for catheter ablation included continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia and late potentials during sinus rhythm (2 patients), polyphasic fragmented presystolic potentials during ventricular tachycardia (1 patient), and pace mapping with identical QRS morphology compared to the ventricular tachycardia and "earliest" detectable activity during tachycardia (1 patient). No procedure related complications occurred. Two different patterns of electrophysiological properties of idiopathic left ventricular tachycardia were observed, indicating that this arrhythmia entity does not represent a homogeneous group. The "origin" of the tachycardias as identified by successful radiofrequency catheter ablation was located in different areas of the left ventricular septum and was distributed from the base to the mid-apical region. Radiofrequency catheter ablation was an effective and safe treatment modality in most of these patients. Distinct target site characteristics for successful catheter ablation including polyphasic diastolic activity during tachycardia and fragmented late potentials during sinus rhythm could be identified.

Effect of accessory pathway location on the efficiency of heating during radiofrequency catheter ablation

During radiofrequency catheter ablation of accessory pathways there is a poor correlation between applied power and temperature at target sites for catheter ablation. This study was designed to examine the relation between power and temperature during radiofrequency catheter ablation in patients with accessory pathways and to identify the factors that affect the efficiency of heating, defined as the ratio of applied power and temperature. Twenty-nine patients underwent radiofrequency catheter ablation of an accessory pathway. Among 257 energy applications, 108 were applied for ablation of a right-sided accessory pathway, 105 for a left-sided accessory pathway, and 44 for a posteroseptal accessory pathway. During each application of radiofrequency energy, temperature was continually monitored by use of an ablation catheter with a thermistor embedded in the tip of the distal electrode. During some applications of energy, fluctuations in temperature were observed. The average power, impedance, temperature, and efficiency of heating for all applications of radiofrequency energy was 37 ± 11 W, 100 ± 9 ohms, 53 ± 9° C, and 1.7 ± 0.8° C W (range 0.9° to 6.6° C W ), respectively. The efficiency of heating varied by location ( p < 0.0001), with the greatest efficiency of heating for posteroseptal energy applications (2.3 ± 1.2° C W , which were significantly greater than for left-sided (1.8 ± 0.8° C W ; p < 0.01) or right-sided (1.2 ± 0.4° C W ; p < 0.0001) applications. Phasic fluctuation in temperature was observed during 127 (49%) energy applications, and the efficiency of heating was 1.5 ± 0.7° C W . For the 130 applications with a stable temperature curve, the efficiency was 1.8 ± 0.9° C W ( p < 0.02). The mean impedance during energy applications correlated weakly with efficiency ( r = 0.2, p = 0.0012). In conclusion, the efficiency of heating varies according to the location of the application of radiofrequency energy. Inadequate contact, as manifested by fluctuating temperature during ablation, results in less efficient heating.

Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush-injury model.

During atrial flutter, double potentials may be recorded at specific sites in the atria. It has been suggested that double potentials represent sequential activations at the center of the reentrant circuit. An alternative hypothesis is that double potentials represent electrical activity in an area of slow conduction. Understanding their mechanism is important because double potentials have been considered a possible indicator of target sites for catheter ablation. We systematically studied double potentials in our canine model of atrial flutter produced by right atrial crush injury using a 64-channel computerized mapping system with 56 electrodes on the right atrium in seven mongrel dogs under general anesthesia. Activation maps were recorded during sinus rhythm before and after crush injury, during rapid pacing above and below the crush injury, and during sustained atrial flutter, entrainment of atrial flutter, and termination of atrial flutter induced with D-sotalol (2 mg/kg). During sinus rhythm before crush injury, activation was uniform, and double potentials were not recorded in any dog. After crush injury, activation proceeded up to and around the crush injury, and narrowly split double potentials were recorded in two of seven dogs. During rapid pacing above and below the crush injury, double potentials were recorded in five dogs. During 14 episodes of atrial flutter (mean cycle length, 140 +/- 16 msec), double potentials were recorded at electrodes along the crush injury. The activation time of the early x component of the double potentials (25 +/- 13 msec) was similar to that of adjacent electrodes above the crush injury (24 +/- 11 msec), and the activation time of the late y component (89 +/- 13 msec) was similar to that of adjacent electrodes below the crush injury (91 +/- 14 msec). The timing of the x and y components was dependent on the location of the recording electrode, with x and y widely spaced at the end of the crush injury near the area of earliest atrial activation during atrial flutter, more equally timed at the center of the crush injury, and more closely timed at the end of the crush injury opposite the area of earliest activation. During transient entrainment, double potentials were accelerated to the pacing rate, but their activation time relative to adjacent electrodes was maintained. During abrupt termination of atrial flutter, the early x component of the double potential was always recorded, but the late y component was not, because of conduction block below the posterior end of the crush injury. This study has shown in our canine model of atrial flutter that double potentials are recorded from the center of the reentrant circuit and that they represent sequential activations as the reentrant wave front passes on either side of the crush injury.