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.

Usefulness of the polarity in high-density wide range-filtered bipolar mapping to detect isthmus block during radiofrequency ablation of typical atrial flutter.

BACKGROUND: The atrial activation sequence around the tricuspid annulus (TA) cannot always be used to establish whether complete block has been achieved across the cavotricuspid isthmus (CTI) during radiofrequency ablation (RFCA) for typical counterclockwise atrial flutter (CCW-AFL). AIM: We examined whether a change in the polarity of the atrial high-density wide range-filtered bipolar electrograms recorded near the ablation line is an accurate indicator of complete CTI block. METHODS: Nineteen patients with CCW-AFL underwent RFCA. Electrograms were recorded around the TA with duodecapolar conventional (2mm x 8mm x 2mm spacing) and high-density (2-mm spacing) Halo catheters. The bipolar electrograms on the high-density Halo catheter recorded from a series of adjacent electrode pairs positioned just lateral to the ablation line were filtered at a bandpass setting of 0.05-500 Hz. The activation sequence on the conventional Halo catheter during coronary sinus pacing (CSp) and inferolateral TA pacing, and the bipolar electrograms on the high-density Halo catheter during CSp were determined before and after RFCA. The final complete CTI block was verified by the presence of widely split double electrograms > or =100 msec along the ablation line. RESULTS: The final complete CTI block was achieved in all the 19 patients. Before RFCA, the polarity of bipolar electrograms was predominantly negative during CCW-AFL and positive during CSp. In 18 of the 19 patients, the bipolar electrograms exhibited the CCW activation and a negative polarity during CSp only after complete CTI block. In one of those 18 patients, additional applications of RFCA changed the polarity of bipolar electrograms positive to negative although the conventional Halo electrogram activation sequence suggested complete CTI block during CSp. In seven patients, who had transverse conduction across the crista terminalis during CSp, the conventional Halo electrogram activation sequence suggested an incomplete CTI block. However, in six of those seven patients, the CCW activation had a predominantly negative polarity of the bipolar electrograms. In one of those seven patients, complete CTI block was unable to be detected even using the high-density Halo catheter. CONCLUSIONS: These data demonstrate that the high-density wide range-filtered mapping can identify the CTI block in undetectable cases of complete CTI block or incomplete CTI block by the conventional method. The polarity of the bipolar electrograms recorded just lateral to the ablation line during CSp after RFCA of AFL may be used as a simple and an accurate indicator of complete CTI block.