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Although diagnostically indispensable, magnetic resonance imaging (MRI) has been, until recently, contraindicated in patients with an implantable cardiac device. MR conditional cardiac devices are now widely used, but the mode programming needed for safe MRI has yet to be established. We reviewed the details of 41 MRI examinations of patients with a MR conditional device. There were no associated adverse events. However, in 3 cases, paced beats competed with the patient's own beats during the MRI examination. We describe 2 of the 3 specific cases because they illustrate these potentially risky situations: a case in which the intrinsic heart rate increased and another in which atrial fibrillation occurred. Safe MRI in patients with an MR conditional device necessitates detailed MRI mode programming. The MRI pacing mode should be carefully and individually selected.

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.

Background: On a cellular level, Brugada syndrome has been attributed to a deep phase 1 notch and subsequent shallow and prolonged repolarization in the right ventricular outflow tract (RVOT). A sodium channel mutation that leads to early inactivation of the late sodium current has been identified in some patients. Thus, drugs that inhibit the transient outward current (Ito) responsible for the phase 1 notch and/or enhance the late sodium current might suppress arrhythmic events in patients with Brugada syndrome. The effects of quinidine gluconate, a potent inhibitor of Ito, on RVOT action potential duration (APD) restitution kinetics in patients with Brugada syndrome were evaluated. Methods and Results: Programmed ventricular stimulation was performed in 9 Brugada syndrome patients by delivering up to 3 extrastimuli from the right ventricular apex and RVOT. RVOT monophasic action potentials (MAPs) were recorded before and after intravenous administration of quinidine (n=6) or ibutilide (n=3). All patients had inducible ventricular fibrillation (VF) before drug administration. Both quinidine and ibutilide increased steady-state and minimum RVOT MAP duration during programmed stimulation. Quinidine decreased the maximum slope of the RVOT APD restitution curve and VF could not be induced after administration of quinidine in 5 of the 6 patients. Conclusions: Quinidine appears to suppress the induction of VF by increasing RVOT MAP duration and decreasing the maximum slope of the restitution curve. (Circ J 2011; 75: 2080-2086)

The type 1 (coved) ECG pattern is diagnostic for Brugada syndrome; types 2 and 3 require antiarrhythmic drug challenge to confirm its presence. We evaluated a 12-lead ECG-based criterion to differentiate between ordinary incomplete right bundle branch block (iRBBB) and true type 2 and 3 patterns that evolve toward type 1 during drug challenge. The subjects were 22 patients (21 men, 1 woman; mean age, 46.8 ± 13.2 years) referred for drug challenge (1 mg/kg pilsicainide, iv). In magnified ECG lead V1 and/or V2 with an iRBBB pattern, the baseline angle defined as the cross section of the upslope of the r' wave with the downslope of the r' wave was measured and compared between patients responding negatively versus positively to drug challenge, and was found to be significantly smaller in patients responding negatively (20.9 ± 12.9°, n = 6, versus 38.7 ± 16.5°, n = 13; P = 0.009). This ECG-based method successfully discriminates between the ordinary iRBBB pattern and drug-induced evolution toward a type 1 Brugada ECG.

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.

Background: Although patients with Brugada syndrome (BS) are at risk of ventricular fibrillation (VF) and ensuing death, the action potential duration (APD) restitution properties of the right ventricular outflow tract (RVOT) in patients with BS remain undetermined. Methods and Results: Endocardial monophasic action potentials (MAPs) were obtained from 16 patients with BS and 17 control patients. MAPs were recorded from the RVOT in all patients. The MAP duration at 90% repolarization (MAPD90), effective refractory period (ERP), and maximum slope of the APD restitution curve were obtained. VF was induced with up to 3 extrastimuli from the RV apex or RVOT. There was no difference in MAPD90 between the 2 groups, but the ERP was significantly shorter in patients with BS than in control patients (210.7±10.5 vs 223.8±13.4 ms, P=0.008). MAPD at the shortest diastolic interval was significantly shorter in patients with BS than in control patients (149.9±19.9 vs 179.8±13.7 ms, P

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 MAPD80 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 afterdepolarization 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.

Steam pop and intramural charring have been reported during cooled-tip radiofrequency catheter ablation (RFCA). We studied the feasibility of temperature-controlled cooled-tip RFCA in the canine heart.An internally cooled ablation catheter was inserted into the left ventricle. A custom-made radiofrequency (RF) generator capable of controlling the tip-temperature at the preset level by slow increases in the power was used. Temperature-controlled cooled-tip RF applications were performed at a target temperature of 40 degrees C for 90 seconds. Acute study: Intramyocardial temperature was measured at the ablation site in 10 dogs by inserting a fluoroptic probe. Chronic study: Lesion depth and volume were measured in 5 dogs after 3 weeks of survival. In the acute study, no pop or abrupt impedance rise was observed. Maximum intramyocardial temperature was 72.4 + or - 14.4 degrees C at 2-4 mm above the endocardium. No coagulum formation, craters, or intramural charring were observed. Maximum lesion depth was 6.7 + or - 1.5 mm, and lesion volume was 404 + or - 219 mm3. In the chronic study, maximum lesion depth was 5.9 + or - 1.1 mm, and lesion volume was 281 + or - 210 mm(3).Temperature controlled RFCA is feasible with a cooled-tip catheter and an RF generator that slowly increases the RF power until the preset catheter-tip temperature is reached.

This case report describes a left bundle branch block (LBBB)-type ventricular tachycardia (VT) with a unique reentrant circuit in a patient with cardiac sarcoidosis. The VT morphology and pace mapping supported an exit site of the VT from the basal posterior right ventricle (RV) septum. Nonetheless, concealed entrainment was established by pacing from a septal left ventricular (LV) site recording a diastolic potential, opposite site to the RV site. A point ablation at that LV site could successfully terminate the VT, suggesting that a critical isthmus was located on the LV side of the interventricular septum despite the demonstration of an LBBB-type VT.

要旨 背景：致死的な心室性不整脈は Brugada 症候群の特徴であるが，その不整脈発生基盤は心室のみにとどまらず，心房においても同様の変化がみられ，上室性不整脈の基盤を形成していると考えられている．しかしながら，上室性不整脈の電気生理学的背景はあまり知られていない．そこで我々は Brugada 症候群と対照群での心房筋の脱分極と再分極の電気生理学的指標について比較検討した．対象：全例 pilsicainide 負荷試験陽性であったBrugada 症候群 18 症例で，心房細動 (AF) の既往は認めなかった．対照群として，房室結節回帰性頻拍，WPW症候群，右室流出路起源心室頻拍にて心臓電気生理学的検査，カテーテルアブレーションを施行した 11 症例で比較検討した．方法：右心耳よりプログラム刺激を基本刺激周期 600 ms および 400 ms で 2 連早期刺激まで施行した．次に単相性活動電位 (MAP) を高位右房側壁より記録した．心房内伝導時間 (IACT) は刺激スパイクから遠位冠静脈洞内電位で計測した． 結果：対照群では全例 AF は誘発されず，Brugada 症候群では全例 AF が誘発された．対照群と Brugada 症候群間で，基本刺激時における MAP 持続時間 (MAPD) および IACT に有意差はなく，また右房有効不応期にも有意差は認めなかった．最短拡張期における MAPD は，Brugada 症候群で短縮しており，IACT 延長率は Brugada 症候群で有意に延長していた．Brugada 症候群間で MAPD の回復曲線における最大スロープは有意に大きかった．結語：我々の検討では，BS において，最短拡張期における MAPD の短縮，MAPD の回復曲線の最大スロープの増大および，IACTの延長が AF の易誘発性に関与していると考えられた．

Background:The pulmonary veins (PVs) are topographically complex and motile, so angiographic visualization of the PVs anatomy is limited. An imaging technique that accurately portrays the pulmonary vein (PV) anatomy would be valuable during and after catheter ablation procedures. Purpose:We investigated whether three-dimensional (3D) intracardiac echocardiography (ICE) can visualize radiofrequency (RF)-induced tissue changes after PV isolation. Methods:We performed 3D ICE studies with a 9F, 9-MHz ICE catheter after segmental or extended PV isolation. The ICE catheter was placed 3–4 cm inside the PV ostium and mounted onto a pullback device. Sequential two-dimensional (2D) images of the full length of the vein were obtained in 0.3 mm steps with cardiac and respiratory cycle gating. Each image was fed into a computer, and the aggregate data set was reconstructed into a 3D, full-motion image. RF lesion location and lesion size were studied on 67 pullback images from 29 patients. Results:The 2D and 3D reconstruction was possible for 27 left superior PVs, 13 left inferior PVs, 26 right superior PVs, and one right inferior PV. The ablation site was identified 3–7 mm inside the PV ostium, and a 1/2 – 4/5 circumferential area was ablated with no clinically relevant stenosis. No significant differences were found on the ablated area or ablation site between segmental and extensive PV isolation. Conclusion:The 2D and 3D ICE of the PVs provides detailed anatomical information of the proximal PVs, and RF-induced tissue changes in the PV wall can be visualized by ICE.

ブルガダ症候群 (BS) における心室細動 (VF) の発生機序として，右室流出路心筋活動電位波形の第 1 相の増強とそれに続く活動電位ドームの減高，消失に基 づく phase 2 reentry が注目されている．我々は BS と対照群に対し右室流出路 (RVOT) で単相性活動電位を記 録し，有効不応期 (ERP) および心筋活動電位持続時間 (MAPD) の回復特性について検討を行った．対象は電気生理学的検査で 3 連早期刺激までで VF が誘発された BS 9 例および対照群 8 例．基本周期刺激時における MAPDは 2 群間で有意差がなかった．しかし ERP および最短拡張期間隔における MAPD は BS で有意に短縮していた．また MAPD 回復曲線より算出された最大の傾き (slope max) は BS の方が急峻の傾向を示した．以上より，RVOT における心室早期刺激時の MAPD の短縮および slope max の急峻化が BS の VF 発生に関与していると考えられた．

The cavotricuspid isthmus (CTI) is crucial in the ablation of typical atrial flutter (AFL), and consequently the CTI anatomy and/or its relation to resistant ablation cases have been widely described in human angiographic studies. Intracardiac echocardiography (ICE) has been shown to be a useful tool for determining detailed anatomical information. Thus, this technology may also allow the visualization of the anatomical characteristics of the CTI, providing an opportunity to further understand the anatomy.We conducted a study to compare the anatomy of the CTI between the patients with and without AFL and to characterize the anatomy of the CTI in the patients with AFL resistant to ablation.Twelve patients with typical AFL and 20 without AFL were enrolled in the study. Two-dimensional (2D) intracardiac echocardiography (ICE) was performed. The recordings were obtained with a 9F, 9-MHz ICE catheter from the right ventricular outflow tract to the inferior vena cava by pulling the catheter back 0.3 mm at a time under guidance with echocardiographic imaging in a respiration-gated manner. Three-dimensional (3D) reconstruction of the images of the CTI were made with a 3D reconstruction system. After the acquisition of the ICE, the CTI ablation was performed in the patients with AFL.The 2D and 3D images provided clear visualization of the tricuspid valve, coronary sinus ostium, fossa ovalis and Eustachian valve/ridge (EVR). The CTI was significantly longer in the patients with AFL than in those without AFL (median length 24.6 mm (range 17.0-39.1 mm) versus median length 20.6 mm (range 12.5-28.0 mm), respectively, P0.05). However, a deep recess due to a prominent EVR was observed in 9 of 12 (75%) patients with AFL and in 12 of 20 (60%) patients without AFL (N.S.). A deep recess and the relatively long CTI were related to aging in all the study patients, and that relationship was similar in a limited number of patients without AFL. In five patients with AFL resistant to ablation, a deep recess and prominent EVR were observed.The 2D and 3D ICE were useful for visualizing the complex anatomy of the CTI and identifying the anatomical characteristics of the CTIs refractory to ablation therapy. The anatomical changes observed in the CTI region may simply be the result of aging and may partially be involved in the development of AFL.

Background The study examined the electrocardiographic and electrophysiologic characteristics in relation to programmed ventricular stimulation (PVS)-induced ventricular fibrillation (VF) in patients with Brugada syndrome. Methods and Results Thirty-four patients with a Brugada-type electrocardiogram (ECG) were enrolled. Twelve patients had a type 1 ECG, 12 had a type 2 ECG, and 10 had a type 3 ECG. PVS was performed with up to 2 ventricular premature beats from the right ventricular apex and outflow tract at 2 basic cycle lengths (600 and 400 ms). VF was induced in 17 of 23 (74%) asymptomatic patients and 10 of 11 (91%) symptomatic patients (p

Background: Symptomatic prolonged sinus pauses upon termination of atrial fibrillation (AF) are an indication for pacemaker implantation. Methods and Results: We evaluated the clinical outcomes of 4 patients who showed prolonged sinus pauses (> 2 seconds) upon termination of AF and thus underwent ablation. The ablative procedure included pulmonary vein isolation, superior vena cava isolation, and cavo-tricuspid isthmus ablation. Twenty-four-hour ambulatory electro-cardiogram monitoring was performed before and 1 month after ablation. The maximum sinus pause decreased from 4.5 ± 2.1 seconds before ablation to 1.7 ± 0.2 seconds after ablation. Sinus pauses > 2.0 seconds disappeared after ablation in all 4 patients. Minimum heart rate increased from 35.0 ± 8.1 beats/minute before ablation to 52 ± 6.7 beats/minute after ablation. The number of heart beats in 24 hours did not change significantly after ablation. Conclusion: Prolonged sinus pauses after paroxysmal AF may result from depressed sinus node function, which can be eliminated by curative ablation of AF.

Background: Brain natriuretic peptide (BNP) level has been shown to increase in patients with chronic atrial fibrillation (CAF) without overt heart failure (HF). Although atrial electrical remodeling associated with CAF has been described, little is known about the effects of the BNP level on the electrophysiological properties in CAF patients. Methods and results: In 42 CAF patients without overt HF, the atrial monophasic action potential duration (MAPD) at pacing cycle lengths (CLs) of 300-800 msec and P-wave signal-averaged electrograms were recorded after cardioversion. The MAPDs for all CLs were significantly longer in patients with a BNP concentration greater than the 50th percentile (group 1, BNP = 215 ± 118.2 pg/mL) than in patients with a concentration less than the 50th percentile (group 2, BNP = 68.3 ± 20.9 pg/mL), resulting in a similar value in the MAPDs at CLs of 350 and 600 msec for group 1 and the control patients (n = 8). The slope value of the MAPDs between CLs of 350 and 600 msec was normal in group 1, but slightly lower in group 2 than in group 1 and control patients. The filtered P-wave duration did not differ between the two groups. Conclusions: These electrophysiological characteristics related to the BNP level suggest that the atrial repolarization may be affected by a latent ventricular dysfunction.

Background The posterior right atrial transverse conduction capability during typical atrial flutter (AFL) is well known, but its relationship to the anatomical characteristics remains controversial. Methods and Results Thirty-four AFL and 16 controls underwent intracardiac echocardiography after placement of a 20-polar catheter at the posterior block site during AFL or pacing. In 31 patients, the effective refractory period (ERP) at the block site was determined as the longest coupling interval that resulted in double potentials during extrastimuli from the mid-septal (SW) and free (FW) walls. The block site was located 3.0-29.0 mm posterior to the crista terminalis (CT) in each AFL and control patient. The CT area indexed to the body surface area was larger in AFL patients than in control patients (16.4±6.5 mm2/m2 vs 11.3±6.4 mm2/m2, p=0.01), and was positively correlated to age (r=0.34, p=0.02). The ERP was longer in the AFL patients than in controls (SW: median value 600 [270-725] ms vs 220 [200-253] ms; FW: 280 [230-675] ms vs 215 [188-260] ms, p

Defibrillation threshold (DFT) testing is performed routinely in patients undergoing implantable cardioverter-defibrillator (ICD) implantation to verify the ability of the ICD to terminate ventricular fibrillation (VF). However, neither the efficacy nor the safety of DFT testing has been proven; thus, the necessity of such testing is controversial. We conducted a retrospective study of the efficacy of DFT testing, particularly with respect to long-term outcomes of ICD implantation.The study included 150 patients (125 men, 25 women, aged 59.0 ± 17.6 years) who underwent ICD or cardiac resynchronization therapy defibrillator implantation, with (n = 73) or without (n = 77) intraoperative DFT testing, between June 1996 and September 2007. VF was induced by delivery of a T-wave shock, and a 20-25-J shock was then delivered. If the 20-25-J shock failed to terminate VF, 30 J was delivered. We assessed whether undersensed VF events occurred during DFT testing and/or during patient follow-up and checked for any association between undersensing and delayed shock delivery. During DFT testing, fine VF was sensed, and shocks were delivered in a timely manner. Nevertheless, 2 patients in the DFT testing group died from VF within 3 years after device implantation.DFT testing, in comparison to non-DFT testing, appeared to have no influence on the long-term outcomes of our patients, suggesting that DFT testing at the time of ICD implantation is limited.

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 × 8mm × 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 ≥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.

Atrial premature depolarizations (APDs) triggering atrial fibrillation (AF) originate from mainly the pulmonary veins (PVs), but, in some cases, atrial ectopic beats (AEBs) triggering AF originate from the right atrium (RA) or the superior vena cava. Accurate identification of the origin of APDs in the PVs by means of RA and coronary sinus mapping is difficult. Purpose: The aim of this study was to identify the origin of AEBs triggering AF before transseptal catheterization. Electrode catheters were placed in the posteroseptal RA (PSRA), right pulmonary artery (RPA), left pulmonary artery (LPA), and esophagus in 10 patients with paroxysmal AF. We analyzed endocardial electrograms from the PSRA, RPA and LPA, and epicardial electrograms from the esophagus. The origin of the AEBs in the PVs was determined before PV ablation by mapping 4 PVs simultaneously. Four AEBs originated from the left superior PV (LSPV), 2 from the left inferior PV (LIPV), 4 from the right superior PV (RSPV), 2 from the RA or superior vena cava. In AEBs originating from the RA, the PSRA activation was the earliest and it proceeded in a cranial to caudal direction. In AEBs originating from the RUPV, RPA was the earliest. The esophageal activation sequence was in a cranial to caudal direction. In AEBs from the LSPV, LPA was the earliest and the esophageal activation sequence proceeded in a cranial to caudal direction. In AEDs from LIPV, LPA was the earliest, and the esophageal activation sequence was nearly simultaneous. Atrial activation sequences from the PSRA, RPA, LPA, and esophageal catheters can accurately identify the location of the initiating foci of AF before a transseptal procedure.

Left atrial tachycardia (AT) has been reported to occur after pulmonary vein isolation (PVI) for the treatment of atrial fibrillation (AF). We treated 3 patients who developed AT of different mechanisms following PVI. In case 1, focal AT originating at the ostium of the left superior PV was demonstrated and focal radiofrequency ablation was performed at the breakthrough point at the ostium of the left superior PV terminated the AT. In case 2, AT was shown to be counterclockwise macroreentrant AT around the left inferior PV through the conduction gap of the left sided posterior wall for which linear ablation was performed between left superior and inferior PVs. Focal ablation at the conduction gap terminated the AT. In case 3, a macroreentrant AT propagating around the mitral annulus was demonstrated and linear ablation between left inferior pulmonary vein and mitral annulus (mitral isthmus) terminated the AT.

Brugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome.

Due to the difficulty in producing a transmural linear lesion and the possibility of complications such as thrombus formation leading to thromboembolism, the catheter-based maze procedure remains problematic. We tested, in pigs, the possibility of using a temperature-controlled cooled-tip radiofrequency (RF) ablation system together with a realtime position management (RPM) system to create a transmural linear lesion uncomplicated by thrombus formation.Nine pigs underwent insertion of two electrode catheters (each with two ultrasound electrodes), one into the coronary sinus (CS) and one into the right ventricular apex (references for ultrasound-based non-fluoroscopic three-dimensional mapping). A cooled-tip catheter (with two ultrasound electrodes) was introduced into the right atrium. Linear right atrial ablation was performed with a custom radiofrequency (RF) generator. The catheter was perfused with 0.66 mL/second of saline. RF was delivered for 60 seconds at a target temperature of 40°C. A linear ablation line was created between the superior vena cava and inferior vena cava. Three-dimensional isochronal maps were created during CS pacing before and after ablation. In 4 of the 9 pigs, a transmural linear ablation line was confirmed by three-dimensional mapping and postmortem macroscopic examination. No endocardial thrombus formation was noted. Temperature-controlled cooled-tip RF linear ablation guided by an RPM system appears to have potential for creating linear lesions in the atria. Further studies are needed to determine whether such an ablation technique and the parameters used will facilitate successful completion of the catheter-based maze procedure.

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. AF5 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.

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.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.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.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.

This study was conducted to examine the virtual unipolar electrogram configuration of right/left outflow tract (OT) premature ventricular contraction (PVC)/ventricular tachycardia (VT) origins obtained from a non-contact mapping system (NCMS).The subjects consisted of 30 patients with OT-PVCs/VT who underwent NCMS-guided ablation. We evaluated the virtual unipolar electrograms of the origin on 3D right ventricular (RV)-OT isochronal maps.Successful ablation was achieved from the RV in 20 patients (RVOT group), and it failed in 10 (non-RVOT group: including left-sided/pulmonary artery/deep RVOT foci). On the virtual unipolar electrograms, the earliest activation (EA) preceded the QRS onset by 11.2 ± 2.6 ms in the RVOT group and by 7.4 ± 10.5 ms in the non-RVOT group (P = 0.138). The negative slope of the electrogram at the EA site (EA slope(5)), quantified by the virtual unipolar voltage amplitude 5 ms after the EA onset, was significantly steeper in the RVOT group than in the non-RVOT group (0.66 ± 0.52 mV vs. 0.14 ± 0.17 mV, P = 0.005). Cutoff values for the EA-to-QRS onset time and EA slope(5) of ≥ 8 ms and0.3 mV, respectively, completely differentiated the RVOT group from the non-RVOT group. A lesser EA slope(5) was associated with a greater radiofrequency energy delivery required to terminate RVOT-PVCs/VT.These demonstrate the importance of the virtual unipolar electrograms from OT-PVC/VT origins obtained with the NCMS. The virtual EA predicts both successful and potentially difficult ablation sites from the RV side.

Steam pop and intramural charring have been reported during cooled-tip radiofrequency catheter ablation (RFCA). We studied the feasibility of temperature-controlled cooled-tip RFCA in the canine heart.An internally cooled ablation catheter was inserted into the left ventricle. A custom-made radiofrequency (RF) generator capable of controlling the tip-temperature at the preset level by slow increases in the power was used. Temperature-controlled cooled-tip RF applications were performed at a target temperature of 40 degrees C for 90 seconds. Acute study: Intramyocardial temperature was measured at the ablation site in 10 dogs by inserting a fluoroptic probe. Chronic study: Lesion depth and volume were measured in 5 dogs after 3 weeks of survival. In the acute study, no pop or abrupt impedance rise was observed. Maximum intramyocardial temperature was 72.4 + or - 14.4 degrees C at 2-4 mm above the endocardium. No coagulum formation, craters, or intramural charring were observed. Maximum lesion depth was 6.7 + or - 1.5 mm, and lesion volume was 404 + or - 219 mm3. In the chronic study, maximum lesion depth was 5.9 + or - 1.1 mm, and lesion volume was 281 + or - 210 mm(3).Temperature controlled RFCA is feasible with a cooled-tip catheter and an RF generator that slowly increases the RF power until the preset catheter-tip temperature is reached.

Brugada syndrome is often accompanied by atrial tachyarrhythmia, such as atrial fibrillation (AF). The aim of this study was to examine atrial vulnerability in patients with Brugada syndrome. Two groups of patients were compared: 18 patients with Brugada syndrome (Brugada syndrome group) and 11 age-matched patients with neither organic heart disease nor AF episodes (control group). Programmed electrical stimulation was performed from the right atrium (RA), and the effective refractory period of the right atrium (ERP-RA), interatrial conduction time (IACT), monophasic action potentials (MAPs) at the high RA, and the inducibility of AF lasting > 30 seconds were studied. MAP duration at 80% repolarization (MAPD(80)) was calculated. AF was induced with a single extrastimulus or double extrastimuli in all patients with Brugada syndrome but in none of the control patients. The ERP-RA did not differ between the groups. IACT at the shortest diastolic interval was significantly increased in the Brugada syndrome group compared to that in the control group. The maximum slope of the MAPD(80) restitution curve was significantly steeper in the Brugada syndrome group than in the control group (2.4 + or - 2.0 versus 0.82 + or - 0.36, P < 0.02). Ventricular fibrillation was induced with ventricular programmed stimulation in all Brugada syndrome patients. Both abnormal interatrial conduction and steep restitution of action potential duration may contribute to the atrial arrhythmogenicity in Brugada syndrome.

The reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT.

BACKGROUND The efficacy of transcatheter cryoablation for ventricular tachycardia (VT) remains controversial because of the limited size of the lesion produced. An increased lesion size if the cryoablation catheter profile and catheter tip length were increased was hypothesized. METHODS AND RESULTS Closed-chest transcatheter cryoablation was applied with 7F, 6-mm tip (n=11, 7F group) and 9F, 8-mm tip (n=8, 9F group) catheters to the left ventricular (LV) endocardium and epicardium. Catheter-tip temperature was set to -70 to -80 degrees C, and cryoablation duration was set to 240 s. In acute experiments in the 7F group, endocardial lesion volume was 144.1 +/-86.0 mm(3) and lesion depth was 5.1 +/-1.6 mm, and epicardial lesion volume was 205.6 +/-157.8 mm(3) and lesion depth was 4.7 +/-2.2 mm. In the 9F group, endocardial lesion volume was 301.5 +/-177.4 mm(3) (P

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.

Ablation catheters with multiple electrodes are effective for the creation of linear atrial lesions but are associated with an increased risk of coagulum formation. In an animal study, we used a novel 9Fr deflectable ablation catheter with two saline/foam electrode pocket covered with 20 mm tubing. Each pocket contained six 2-mm long electrodes with a 1-mm interelectrode distance. Bipolar electrograms between the 3 distal and 3 proximal composite electrodes were recorded, and the pacing threshold was determined before and after radiofrequency (RF) ablation. Long linear lesions were created by applying RF energy for 90 seconds at 50 W during saline irrigation (0.4 mL/sec) between 1) the superior vena cava (SVC) and inferior vena cava (IVC), 2) SVC, fossa ovalis, and IVC, 3) transverse loop from the crista terminalis to the tricuspid valve (TV), and 4) TV and the IVC. Continuous transmural lesions were created only in a minority of cases, and lesion gaps were noted in the free wall lesions. No coagulum formation was observed after RF energy delivery. A long lesion can be created in the right atrium by using an irrigated balloon catheter, but continuous lesion formation was achieved only in a minority of animals.

A 72-year-old man who suffered dizziness and syncope was referred to the Division of Cardiology Division, Nihon University Hospital in 2006. A 12-lead electrocardiogram recorded at the outpatient clinic showed complete atrioventricular block with a ventricular escape rhythm of 26 bpm. In 1997, he had been as referred to the Department of Neurosurgery for implantation of bilateral deep brain stimulators (DBSs) to treat advanced Parkinson's disease refractory to medical treatment. Six days after admission to our department, a permanent cardiac pacemaker was implanted to …

This study was designed to determine whether endocardial high-frequency stimulation at the pulmonary vein (PV) antrums can localize cardiac autonomic ganglionated plexi (GP) and whether ablation at these sites can evoke a vagal response and provide a long-term benefit after PV isolation (PVI) for atrial fibrillation (AF). Radiofrequency ablation of each PV antrum was performed in 21 patients with paroxysmal AF (n = 17) or persistent (n = 4) AF. In 8 patients with paroxysmal AF, a ring electrode catheter was placed at each PV antrum. High-frequency stimulation prolonged the R-R interval in 6 of 8 patients at the left superior (LS) PV, in 3 of 8 patients at the left inferior (LI) PV, in 3 of 8 patients at the right superior (RS) PV, and in 3 of 8 patients at the right inferior (RI) PV. A decrease in sinus rate > 20% was observed in 4 of 21 patients during LS PVI, in 2 of 21 patients during RS PVI, and in 1 of 2 patients during RI PVI. Atrioventricular block or a > 5 second pause was observed in 5 of 21 patients during LS PVI. AF recurred during the follow-up period in 5 of the 16 patients (31%) who had no atrioventricular block or > 5 second pause during PVI but did not recur in 5 patients in whom atrioventricular block or a > 5 second pause developed during PVI. GP can be identified by endocardial stimulation. The AF recurrence rate is decreased when a vagal response is achieved by radiofrequency ablation.

A 44-year-old man who had suffered multiple episodes of syncope presented with ventricular fibrillation (VF). Structural heart disease was ruled out. Programmed stimulation induced VF at the right ventricular apex (RVA) but not at the outflow tract (RVOT). Monophasic action potential duration (MAPD) at a basic cycle length of 400 msec was shorter at the RVA than at the RVOT (208 versus 231 ms). The maximum slope of the MAPD restitution curve at the 400-msec cycle length was much steeper at the RVA than at the RVOT (1.4 versus 1.0). Such spatial heterogeneity of the MAPD and of its restitution may facilitate wavebreak and functional reentry, predisposing to VF.

A 71-year-old man with frequent ventricular premature contractions after right hip joint surgery was referred to the Cardiology Division. Twelve-lead ECG showed type II Brugada-type ECG and signal-averaged ECG showed positive ventricular late potentials. The 12-lead ECG changed to type I Brugada-type after administration of the class Ic antiarrhythmic drug, pilsicainide. Ventricular fibrillation (VF) was reproducibly induced with double premature stimuli from the right ventricular outflow tract (RVOT) at a basic cycle length (BCL) of 400 ms. Monophasic action potentials (MAPs) recorded from the RVOT at a BCL of 400 ms showed MAP alternans and VF was only induced when extrastimuli were applied after a shorter MAP of the alternans. (Circ J 2009; 73: 580 - 583)

Background It was hypothesized that atrial premature contractions (APCs) originating in the pulmonary veins (PVs) or superior vena cava (SVC) can be localized by evaluating characteristics of the P wave. Methods and Results Thirty-eight patients with paroxysmal atrial fibrillation were studied. P wave polarity and morphology of the ECGs during pacing from PVs were analyzed and compared to those of APCs originating from PVs. The P wave angle and notch in lead II during pacing from the right superior (RS) PV and SVC was compared to those of spontaneous APCs originating from those veins. A positive P wave in lead I was helpful in predicting right PV origin. A positive P wave in lead II distinguished superior PV origin. A notched P wave was helpful in predicting left PV origin. P wave polarity in lead II was positive during RSPV and SVC pacing. P waves in lead II during RSPV pacing had notching in 80%, but all P waves were smooth during SVC pacing. A P wave angle of >40° and notching in lead II showed RSPV origin. Conclusions These criteria are helpful in selecting which of the 4 PVs should be isolated when APCs cannot be recorded after transseptal puncture. (Circ J 2008; 72: 1650 - 1657)

Background: It remains unknown why atrial flutter (AFL) occurs as either a chronic or paroxysmal arrhythmia. Purpose: The aim of the study was to compare intracardiac echocardiographic (ICE) images of the crista terminalis (CT) and transverse conduction properties of the CT between chronic and paroxysmal forms of common AFL. Methods: Chronic AFL (n = 7) was defined as non-self-terminating AFL lasting >1 month, and paroxysmal AFL (n = 8) was defined as an intermittent arrhythmia with symptomatic episodes of 24 hours maximum duration. ICE images of the right atrium were recorded with a 9 F 9-MHz intracardiac ultrasound catheter during pullback at 0.5-mm intervals from the superior vena cava to the inferior vena cava triggered by electrocardiogram and respiration. The two-dimensional image of the right atrium was reconstructed into a three-dimensional (3-D) image. Results: Three-dimensional images from patients with chronic AFL showed the CT to be thick and continuous, and conduction across the CT was blocked at a pacing rate just above sinus rhythm in all seven patients. In contrast, 3D images from paroxysmal AFL showed the CT to be thin and discontinuous, and conduction across the CT during midseptal pacing was observed in five of the eight patients. Conclusion: The nature of AFL is determined, at least in part, by anatomic and electrophysiologic characteristics of the CT.