Three-dimensional high-density bipolar contact mapping of left atrial endocardial activation during sinus rhythm in patients with atrial fibrillation.

Non-contact array mapping studies have demonstrated the existence of a line of conduction block along the septopulmonary bundle area and the posterior left atrial (LA) roof during sinus rhythm (SR). However, little is known of the global LA activation pattern during SR using a high-density contact bipolar mapping system. High-density contact bipolar isochronal mapping (bipolar mapping sites: 292 [IQR 250-348] points) of the LA was performed during SR with the NavX mapping system in 20 patients with paroxysmal atrial fibrillation (AF) and 11 patients with non-paroxysmal AF. The earliest endocardial breakthrough in the the LA from the right atrium (RA) during SR occurred in the anterosuperior LA (77%) or anterior to the right pulmonary veins (23%), and the breakthrough site did not differ between patients with paroxysmal and non-paroxysmal AF. Regardless of the site of breakthrough, the LA activation pattern was homogeneous, and no line of functional block was observed in any patient. Total LA activation time was significantly longer in non-paroxysmal AF patients than in paroxysmal AF patients (95.1 ± 4.3 ms versus 78.3 ± 3.2 ms, P = 0.0040). Contact-based bipolar LA endocardial activation mapping revealed a homogeneous LA activation pattern during SR, regardless of the between-group difference in activation time and the between-patient difference in sites of earliest LA endocardial breakthrough from the RA.

Effect of catheter tip-tissue surface contact on three-dimensional left atrial and pulmonary vein geometries: potential anatomic distortion of 3D ultrasound, fast anatomical mapping, and merged 3D CT-derived images.

UNLABELLED: Anatomic Distortion of 3D Mapping. BACKGROUND: Although catheter tip-tissue contact is known as a reliable basis for mapping and ablation of atrial fibrillation (AF), the effects of different mapping methods on 3-dimensional (3D) map configuration remain unknown. METHODS AND RESULTS: Twenty AF patients underwent Carto-based 3D ultrasound (US) evaluation. Left atrium (LA)/pulmonary vein (PV) geometry was constructed with the 3D US system. The resulting geometry was compared to geometries created with a fast electroanatomical mapping (FAM) algorithm and 3D US merged with computed tomography (merged 3D US-CT). The 3D US-derived LA volumes were smaller than the FAM- and merged 3D US-CT-derived volumes (75 ± 21 cm(3) vs 120 ± 20 cm(3) and 125 ± 25 cm(3) , P < 0.0001 for both). Differences in anatomic PV orifice fiducials between 3D US- and FAM- and merged 3D US-CT-derived geometries were 6.0 (interquartile range 0-9.3) mm and 4.1 (0-7.0) mm, respectively. Extensive encircling PV isolation guided by 3D US images with real-time 2D intracardiac echocardiography-based visualization of catheter tip-tissue contact generated ablation point (n = 983) drop-out at 1.9 ± 3.8 mm beyond the surface of the 3D US-derived LA/PV geometry. However, these same points were located 1.5 ± 5.4 and 0.4 ± 4.1 mm below the FAM- and merged 3D US-CT-derived surfaces. CONCLUSIONS: Different mapping methods yield different 3D geometries. When AF ablation is guided by 3D US-derived images, ablation points fall beyond the 3D US surface but below the FAM- or merged 3D US-CT-derived surface. Our data reveal anatomic distortion of 3D images, providing important information for improving the safety and efficacy of 3D mapping-guided AF ablation. (J Cardiovasc Electrophysiol, Vol. 24, pp. 259-266, March 2013).

Linear catheter ablation of the right atrium for rapid atrial pacing-induced sustained atrial fibrillation in dogs.

Catheter ablation of persistent/long-persistent atrial fibrillation (AF) has been shown to be less effective by pulmonary vein isolation (PVI) and additional left atrial (LA) complex fractionated atrial electrograms and long linear lesions are often required. Recent reports have demonstrated right atrial (RA) ablation increases the success rate of maintaining sinus rhythm in persistent/long-persistent AF. The aim of this study was to investigate whether effective RA linear lesions can terminate AF and render it noninducible in a canine model of rapid atrial pacing-induced sustained AF. Sustained AF was induced by rapid atrial pacing in 20 dogs. AF duration was 21-126 days (median, 50 days). Four RA linear lesions (superior vena cava-inferior vena cava, septal line, transverse line, and cavo-tricuspid line) were created with the use of 1 of 3 different ablation catheters (large-tip [8-mm tip], coil-tip, and cooled-tip catheters). AF was terminated with the large-tip catheter in 4/7 dogs (1 dog died of ventricular fibrillation [VF]), with the coil-tip catheter in 3/7 dogs (1 dog died of VF), and with the cooled-tip catheter in 1/6 dogs. In 6 dogs in which AF could not be terminated acutely by RA ablation, AF terminated spontaneously at 7-78 days (median, 14 days) after ablation. RA linear ablation terminated AF with limited success in our dog model of rapid atrial pacing-induced AF, but late AF termination was noted in the surviving dogs. Therefore, RA linear lesions in addition to the PVI and LA lesions may have additional effects on the catheter ablation for the persistent AF.

Does location of epicardial adipose tissue correspond to endocardial high dominant frequency or complex fractionated atrial electrogram sites during atrial fibrillation?

BACKGROUND: Although increased epicardial adipose tissue (EAT) volume is known to be associated with increased prevalence of atrial fibrillation (AF), the exact mechanisms are unclear. Therefore, we investigated whether EAT locations were associated with high dominant frequency (DF) sites or complicated fractionated atrial electrogram sites during AF. METHODS AND RESULTS: Three-dimensional reconstruction computed tomography images depicting EAT volumes (obtained by 320-detector-row multislice computed tomography) were merged with NavX-based DF and complicated fractionated atrial electrogram maps obtained during AF for 16 patients with paroxysmal AF and for 18 patients with persistent AF. Agreement between locations of the EAT, especially EAT surrounding the left atrium, and of high DF or complicated fractionated atrial electrogram sites was quantified. In addition, serum biomarker levels were determined. EAT surrounding the left atrium volumes was significantly greater in patients with persistent AF than in patients with paroxysmal AF (52.9 cm(3) [95% CI, 44.2-61.5] versus 34.8 cm(3) [95% CI, 26.6-43.0]; P=0.007). Serum high-sensitivity C-reactive protein and interleukin-6 levels were significantly higher in persistent AF patients than in paroxysmal AF patients (median high-sensitivity C-reactive protein, 969 ng/mL [interquartile range, 307-1678] versus 320 ng/mL [interquartile range, 120-660]; P=0.008; median interleukin-6, 2.4 pg/mL [interquartile range, 1.7-3.2] versus 1.3 [interquartile range, 0.8-2.4] pg/mL; P=0.017). EAT locations were in excellent agreement with high DF sites (κ=0.77 [95% CI, 0.71-0.82]) but in poor agreement with complicated fractionated atrial electrogram sites (κ=0.22 [95% CI, 0.13-0.31]). CONCLUSIONS: Increased EAT volume and elevation of inflammatory biomarkers are noted in persistent AF rather than paroxysmal AF patients. High DF sites are located adjacent to EAT sites. Thus, EAT may be involved in the maintenance of AF.

Characteristics and distribution of complex fractionated atrial electrograms and the dominant frequency during atrial fibrillation: relationship to the response and outcome of circumferential pulmonary vein isolation.

BACKGROUND: Although sites of complex fractionated electrograms (CFAEs) and dominant frequency (DF) are known to be critical for the maintenance of atrial fibrillation (AF), spatial distribution of CFAEs and DF and their impact on the outcome of AF ablation remain unclear. METHODS: We created CFAE and DF maps of the left atrium (LA), right atrium, and pulmonary veins (PVs) with a NavX mapping system and simultaneously calculated the DF values with a Bard LabSystem Pro in 40 patients with AF (nonparoxysmal, n = 16). RESULTS: In 19 patients in whom circumferential PV isolation (CPVI) terminated AF, there was a high DF in the PVs (Bard-based DF value, 6.70 ± 1.01 Hz), low DF in the LA body (5.94 ± 0.75 Hz), and a significant PV-to-LA body DF gradient (0.76 ± 0.65 Hz), and the CFAEs were located mainly in the PV antrum. In the 21 patients not responding to CPVI, a high DF was located in both the PVs (7.04 ± 0.81 Hz) and LA body (6.75 ± 0.81 Hz), and therefore, the PV-to-LA body DF gradient was smaller than that in the CPVI responders (0.29 ± 0.52 Hz, P = 0.0160), and the CFAEs extended to the LA body. The higher DF in the LA body, nonparoxysmal AF, and longer AF duration remained as independent predictors of a post-ablation AF recurrence by using a multivariate analysis. CONCLUSIONS: A higher LA-DF value, smaller PV-to-LA DF gradient, and wider LA-CFAE distribution were noted more often in the nonresponders to CPVI than in the responders. This suggested the presence of an arrhythmogenic substrate in the LA beyond the PVs in patients whose AF persisted after CPVI, which was further associated with post-ablation AF recurrence.

Clarifying the arrhythmogenic substrate for Brugada syndrome.

The right ventricular outflow tract (RVOT) is considered the arrhythmogenic region that gives rise to Brugada syndrome. To obtain a better understanding of this substrate, we performed electroanatomic mapping of the right ventricle (RV) in patients with Brugada syndrome. The RV was mapped electroanatomically with the CARTO system in 11 patients with asymptomatic Brugada syndrome but in whom ventricular fibrillation was induced by programmed ventricular stimulation, and in 5 control patients. The low voltage zone area (< 1.5 mV) was larger (16.1% versus 7.8%, P < 0.01) and the bipolar electrogram duration was greater (81.6 ± 7.8 ms versus 53.4 ± 5.6 ms, P < 0.01) in the patients with Brugada syndrome versus the control patients; the bipolar electrogram duration was greater in the septal portion and free wall of the RVOT. Our data suggest that regional endocardial conduction slowing based on structural abnormalities exists at the RVOT in Brugada syndrome.

Functional atrioventricular conduction block in an elderly patient with acquired long QT syndrome: elucidation of the mechanism of block.

The long QT syndrome (LQTS) is occasionally complicated by impaired atrioventricular (AV) conduction. This form of LQTS can manifest before birth or during neonatal life, and no previous report has demonstrated LQTS complicated by impaired AV conduction in elderly patient. This case report describes an elderly patient with an acquired form of LQTS who developed ventricular fibrillation that was successfully defibrillated during admission to the hospital. Electrophysiologic study demonstrated that HV interval was 38 milliseconds and QT interval was 635 milliseconds during sinus rhythm cycle length of 1167 milliseconds. 1:1 AV conduction was maintained to a pacing cycle length of 545 milliseconds with an AH interval of 144 milliseconds, HV interval of 44 milliseconds, and right ventricular monophasic action potential duration of 360 milliseconds. However, 2:1 HV block developed at a pacing cycle length of 500 milliseconds. Intravenous administration of mexiletine decreased the cycle length of developing HV block to 360 milliseconds.

Upper turnaround point of the reentry circuit of common atrial flutter--three-dimensional mapping and entrainment study.

BACKGROUND: Although the anterior and posterior boundaries of cavotricuspid isthmus-dependent atrial flutter (AFL) are reported to be located at the tricuspid annulus and sinus venosa region or crista terminalis, the exact upper turnaround point of the AFL circuit remains unclear. The aim of this study was to determine the upper turnaround site of the AFL circuit by means of three-dimensional (3D) mapping and entrainment pacing. METHODS: Subjects were 21 patients with counter-clockwise AFL in whom high-density mapping of the high right atrium (RA) and superior vena cava (SVC) orifice was performed with an electroanatomical or non-contact mapping system. Entrainment pacing was performed around the SVC-RA junction. RESULTS: In 20 of the 21 patients, the wavefront from the septal RA split into two wavefronts: one that traveled anterior to the SVC and another that traveled to the posterior RA where it was blocked. In the remaining patient, the wavefront from the septal RA split into two wavefronts: one that propagated through the anterior portion of the SVC orifice and another that propagated transversely across the posterior portion of the SVC orifice. The two wavefronts joined in the lateral RA. Entrainment pacing from the SVC-RA junction demonstrated that the anterior boundary was within the circuit in all patients, but the posterior boundary also constituted a circuit in four patients. CONCLUSIONS: We surmise that the upper turnaround site of the AFL circuit is located in the anterior portion of the SVC-RA junction in the majority of patients with AFL.

Electrical remodeling in fibrillating canine atrium: action potential alternans during rapid atrial pacing and late phase 3 early afterdepolarization after cessation of rapid atrial pacing.

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD(80) of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early after depolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.

Surface ECG characteristics of ventricular tachyarrhythmias before degeneration into ventricular fibrillation in patients with Brugada-type ECG.

This study was designed to evaluate whether the right ventricular outflow tract (RVOT) is the arrhythmogenic focus in Brugada syndrome. We enrolled 45 patients with Brugada-type ECG who underwent programmed ventricular stimulation and inducible ventricular fibrillation (VF). In 25 of these 32 patients, repetitive VT was observed before degeneration into VF. The QRS morphology of surface ECG and intracardiac electrograms were evaluated to determine the origin of the ventricular tachycardia (VT) that degenerated into VF. The VT morphology was a left bundle branch block pattern with an inferior axis in 22 of 28 VTs and the intracardiac conduction sequence during VT revealed activation from the RVOT to the RV apex in these 22 VTs. The majority of the patients with Brugada syndrome showed repetitive VT originating from the RVOT that degenerated into VF. The RVOT may be an arrhythmogenic focus in patients with Brugada syndrome.

Idiopathic left ventricular tachycardia with a change from left to right axis deviation during radiofrequency catheter ablation.

A 62 year-old-woman presented with a right bundle branch block (RBBB) and left axis deviation (LAD) tachycardia. Radiofrequency (RF) energy was delivered to the left posterior fascicle (LPF) where 2 presystolic Purkinje potentials (P1 and P2) preceding onset of the QRS complex were recorded. During RF energy applications, the QRS morphology of the tachycardia changed from RBBB and LAD to RBBB and right axis deviation without termination of the tachycardia. The Purkinje potential was observed following the QRS complex during the tachycardia because of conduction block of the LPF distal to the reentry circuit due to RF catheter ablation.