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Background The purpose of this study was to determine whether the extent of atrial electrical remodeling affects the recurrence of atrial fibrillation (AF) after cardioversion of persistent AF (PAF). Methods and Results Internal atrial cardioversion was performed in 47 patients with PAF. The right atrial monophasic action potential duration (RA-MAPD) at pacing cycle lengths (PCLs) of 800-300 ms and P wave signal-averaged electrocardiogram were recorded after cardioversion. Bepridil (150-200 mg/day) and carvedilol (10 mg/day) were administered to all patients after cardioversion. Of the 47 patients, 20 had recurrent AF within 3 months. No relation was observed between age, left atrial dimension, left ventricular ejection fraction, and AF recurrence. The AF duration was significantly longer (p

Brugada syndrome is characterized by right bundle branch block morphology and ST-segment elevation in the right precordial leads and a propensity to develop ventricular arrhythmias. Mutations in a cardiac sodium channel gene have been linked to this syndrome, and the ionic mechanisms responsible for the electrocardiographic phenotype are temperature-dependent. This case report describes a patient in whom a typical Brugada ECG pattern developed during fever and could be reproduced at normal body temperature by administration of pilsicainide.

Right atrial monophasic action potentials were recorded before and after 60 minutes of rapid atrial pacing (pacing cycle length (CL); 127 +/- 10 ms) in 12 closed-chest dogs. The right atrial (RA) monophasic action potential (MAP) duration at 90% repolarization (RAMAPD) was measured at CLs of 400 ms and 250 ms. CL-dependent changes in RAMAPD (CL 400 ms - 250 ms) before and after rapid atrial pacing were 24 +/- 1 ms and 16 +/- 5 ms, respectively (p 5 minutes) was induced in 1 of 12 dogs at a pacing CL of 130 ms before rapid atrial pacing and in 4 of 12 dogs at a pacing CL of 135 +/- 17 ms after rapid atrial pacing. Onset of AF was always preceded by the RAMAPD alternans. Sixty minutes of rapid atrial pacing leads to diminution of rate adaptation of atrial action potential duration (APD) and appearance of APD alternans of greater magnitude at longer CL, both of which may contribute to the initiation and perpetuation of AF during its early phase.

Atrioventricular nodal reentrant tachycardia (AVNRT) is a relatively common paroxysmal supraventricular tachycardia. This study investigated whether adenosine-5'-triphosphate (ATP) injection during sinus rhythm might be useful in the noninvasive diagnosis of dual AV nodal pathways. The study group consisted of 9 patients with slow/fast AVNRT and 11 control patients without antegrade dual AV nodal physiology (DAVNP). ATP (2.5 to 30 mg, in 2.5-mg increments was injected during sinus rhythm until signs of DAVNP (> or = 50 msec increase or decrease in AH or PR interval in two consecutive beats) or > or = second-degree AV block was observed. DAVNP was diagnosed by ATP test in all 9 patients with slow/fast AVNRT. DAVNP was observed by ATP test in 3 of the 11 control patients. Thus, the test had a sensitivity of 100% and specificity of 73%. ATP test given during sinus rhythm is useful for identifying patients with dual AV nodal pathways who are prone to AVNRT.

Right bundle branch block and ST segment elevation (RBBB-STE) in the right precordial leads have been reported as a distinct clinical and electrocardiographic syndrome in patients prone to ventricular fibrillation (VF) in the absence of structural heart disease (Brugada syndrome). The purpose of the study was to investigate the role of signal averaged electrocardiogram (SAECG) in identifying patients at high risk among asymptomatic RBBB-STE patients. Thirteen patients with the RBBB-STE ECG were identified. Symptoms were: syncope (n=3, cases 1, 3, and 11), atypical chest pain (n=3, cases 4, 10, and 12) and palpitations (n=2, cases 6, and 7). The other 5 patients were asymptomatic. SAECG and programmed electrical stimulation (PES) were conducted in all patients. Body surface late potentials (LPs) were present in 7 of 13 patients before PES. Vf was induced in 6 of 7 LP positive patients. Vf was induced in 3 of 6 LP negative patients, but LP became positive in 2 of 3 patients in whom Vf was induced. One patient with syncope due to VF (case 1), 1 patient without symptoms who died suddenly during follow up (case 2), and 1 asymptomatic patient (case 9) showed reproducibly positive LP. In a patient (case 9) with positive LP at baseline, LP transiently became negative during follow up. In RBBB-STE patients, reproducibly positive LP is at risk for malignant ventricular arrhythmias and sudden death. Repeated SAECG recording may be useful for screening high-risk patients who should receive electrophysiological study among asymptomatic RBBB-STE patients.

Background: The relation between ECG and activation patterns within atria in typical atrial flutter (AFL) patients (pts) has not been defined due to the lack of simultaneous multisite right and left atrial mapping.

Since myocardial lesion size during radio-frequency (RF) ablation is limited at high power by impedance rise when electrode tip temperature exceed 100 °C, controlling tip temperature by continuous intraelectrode saline infusion could permit generation of larger lesion. (1) Two dogs randomly received either standard or cooled tip RF ablation at 4 to 6 separate LV sites. Power output of 30 W was delivered via modified 7 Fr deflectable catheter with 4 mm tip for up to 120 sec or until impedance rise occurred. (2) Six dogs randomly received cooled tip RF ablation at power output of 20, 30, 40 W for 120 sec. (3) Three dogs randomly received cooled tip RF ablation using room temperature saline (21–25 °C) or chilled saline (1–4 °C) infusion.

To compare the effects of class Ic and III antiarrhythmic agents on the termination and prevention of atrial fibrillation, the present study investigated the use-dependent electrophysiological effects of flecainide, nifekalant and d,l-sotalol on the human atrium. Flecainide significantly prolonged effective refractory period (ERP), intra-atrial conduction time (IACT) and monophasic action potential duration (MAPD), and its effects on ERP and IACT were use-dependent. Nifekalalant significantly prolonged ERP and MAPD, and these effects were reverse use-dependent; however, there was no significant change in IACT. d,l-Sotalol significantly prolonged MAPD and the effect was reverse use-dependent. It significantly prolonged ERP, but the effect was not reverse use-dependent. d,l-Sotalol increased IACT in a use-dependent manner. Thus, for atrial fibrillation, class Ic antiarrhythmic agents might be more effective in termination and class III antiarrhythmic agents might be more effective in prevention. (Jpn Circ J 2001; 65: 1 - 6)

Most of the class III antiarrhythmic agents developed in recent years blocks the rapid component of delayed rectifier potassium current (IKr). IKr blocker shows reverse use-dependency and also may cause torsades de pointes at slower heart rate. Ibutilide fumarate, a novel class III antiarrhythmic agent, increases window Na+ current at the action potential plateau phase. We studied the rate-dependent effect of ibutilide on the electrophysiological parameters of human atrium and ventricle. Franz catheter and a pacing catheter were placed closely in the high right atrium and right ventricular apex to record monophasic action potentials (MAP) during pacing at cycle length (PCL) of 600[emsp4 ]ms and 350[emsp4 ]ms in eight patients who underwent electrophysiological study. MAP duration of right atrium (RA-MAPD) and right ventricle (RV-MAPD), effective refractory period of RA and RV (RA-ERP and RV-ERP), intra-atrial conduction time (IACT) and intra-ventricular conduction time (IVCT) were measured before and after intravenous administration of ibutilide (0.01[emsp4 ]mg/kg up to 1[emsp4 ]mg). A conduction time from RA pacing spike to distal coronary sinus potential was used to measure IACT, while QRS duration of surface ECG during RV pacing was used to measure IVCT. Ibutilide prolonged RA-MAPD by 60[emsp4 ]ms at PCL 600[emsp4 ]ms and by 53[emsp4 ]ms at PCL 350[emsp4 ]ms; RV-MAPD by 48[emsp4 ]ms at PCL 600[emsp4 ]ms and by 55[emsp4 ]ms at PCL 350[emsp4 ]ms. Ibutilide did not affected RA and RV-ERP/MAPD ratio, IACT, and IVCT. Ibutilide prolongs MAPD and ERP of human atrium and ventricle without reverse use-dependency.

Ventricular tachycardia (VT) in coronary artery disease arises mostly from endocardial sites. However, little is known about the site of origin in other diseases. We report two patients who had VT originating from an anterior aspect of the left ventricle just below the mitral annulus, adjacent to the left ventricular outflow tract. The QRS configuration of VT showed an inferior axis and monophasic R waves in all the precordial leads. Radiofrequency current delivered to this site from the endocardial site successfully ablated the tachycardia in both.

Beraprost sodium (BPS, an analogue of prostacyclin) and telmisartan (TS, an angiotensin receptor blocker) have been reported to have a preventive effect on arterial stiffness in patients with cardiovascular diseases. The purpose of this study was to estimate the effects of a combined therapy using BPS and TS on arterial pulse wave velocity (PWV) values in elderly patients with hypertension and cerebral infarction. Over a 3-month period, 80 subjects with hypertension and histories of cerebral infarction received BPS only (120 microg/day p.o.), TS only (40 mg/day p.o.), both BPS and TS, or no medication at all (control). Arterial PWV and ankle brachial indices (ABI) were determined prior to and after 3 months of drug administration. During the follow-up, there were no significant changes in any of the parameters monitored with the exception of a significant decrease in systolic blood pressure in the BPS only, TS only, and BPS plus TS groups when compared to controls. The difference values for PWV in the control group, BPS only group, TS only group, and BPS plus TS group were +232.5, -114.6, -151.5, and -248.1 cm/s, respectively. The reduction values were significantly more pronounced in the BPS plus TS group than in the BPS only (P=0.037) and the TS only (P=0.022) groups. When BPS is combined with TS, an overall additive effect is seen in the improvement of PWV in Japanese patients with hypertension and cerebral infarction. This combination therapy is more beneficial than the corresponding monotherapies.

The purpose of this study was to determine whether the extent of atrial electrical remodeling affects the recurrence of atrial fibrillation (AF) after cardioversion of persistent AF (PAF).Internal atrial cardioversion was performed in 47 patients with PAF. The right atrial monophasic action potential duration (RA-MAPD) at pacing cycle lengths (PCLs) of 800-300 ms and P wave signal-averaged electrocardiogram were recorded after cardioversion. Bepridil (150-200 mg/day) and carvedilol (10 mg/day) were administered to all patients after cardioversion. Of the 47 patients, 20 had recurrent AF within 3 months. No relation was observed between age, left atrial dimension, left ventricular ejection fraction, and AF recurrence. The AF duration was significantly longer (p0.05) and RA-MAPD at PCLs of 800 to 300 ms were significantly shorter (p0.05) in patients with AF recurrence than in those without recurrence. The mean slope of the RA-MAPD for PCLs between 600 and 300 ms did not differ between the patients with and without AF recurrence. The filtered P-wave duration (FPD) was significantly longer in the patients with AF recurrence than in those without (p0.05). Multivariate analysis also showed that the RA-MAPD at a PCL of 300 ms and FPD were predictors of AF recurrence (RAMAPD: p=0.038; FPD: p=0.052).These results suggest that electrical remodeling related to the repolarization and depolarization may be the main contributors to early AF recurrence after cardioversion under the administration of bepridil and carvedilol.

Background: Chronic atrial fibrillation (AF) is characterized by a marked decrease in the atrial effective refractory period (ERP) and in the ERP adaptation to rate as well as a decrease in the atrial conduction velocity. Little information is available about the ionic mechanisms underlying AF in humans. Materials and Methods: We studied the effect of IKr blocker nifekalant on the rate-dependent changes in atrial action potential duration in 11 patients after successful internal cardioversion of chronic AF of >2 months duration and in 7 patients without AF. In AF patients, right atrial (RA) monophasic action potential (MAP) was recorded at pacing cycle lengths (CLs) of 800–250 ms before and after administration of nifekalant. In control patients, RAMAP was recorded at CLs of 600 and 350 ms before and after administration of nifekalant. Results: Nifekalant significantly increased RAMAPD at 90% repolarization (RAMAPD90) at CLs of 800–300 ms in the AF patients. The increase in RAMAPD90 by nifekalant became significantly smaller at shorter CLs (42.5 ± 12.4 ms at a CL of 600 ms vs 32.8 ± 14.5 ms at a CL of 350 ms, P < 0.05). Effect of nifekalant on RAPMAPD was attenuated at CL of 600 ms in AF patients in comparison to control patients (increase in RAMAPD in control; 73.0 ± 36.6 ms vs increase in RAMAPD in AF; 42.5 ± 12.4 ms, P < 0.05); however, it was similar at a CL of 350 ms between control and AF patients. Conclusions: Electrophysiological effects of nifekalant are significantly attenuated in the chronically remodeled human atrium at slower heart rates, but the beneficial effect of RAMAPD prolongation by IKr blocker was well-preserved even at shorter CLs after chronic AF.

Introduction: Dual AV nodal physiology is the electrophysiologic substrate for AV nodal reentrant tachycardia (AVNRT), but the anatomic basis for this arrhythmia remains to be elucidated. Atrial flutter (AFL) has been shown to be more frequently inducible in patients with AVNRT. Methods and Results: A 3.2-French, 20-MHz intracardiac ultrasound (ICUS) catheter was introduced into the coronary sinus (CS), and two-dimensional ICUS images were recorded during transducer pullback in 21 patients with AVNRT and 18 control patients. Three-dimensional reconstruction of the CS was created using the TomTec Imaging system. The area of the CS lumen at 15 mm within the CS ostium (os) was not significantly different in patients with and without AVNRT (54.4 ± 34.7 mm2 vs 39.1 ± 28.5 mm2). However, the area of the CS os was significantly larger in patients with AVNRT than in those without (112.1 ± 60.9 mm2 vs 71.7 ± 44.4 mm2, P < 0.05). Three-dimensional morphology of the CS os revealed flaring in patients with AVNRT, giving it a “windsock” appearance. Sustained AFL was induced in 10 of 21 patients with AVNRT, but in none of 18 control patients (P < 0.005). Conclusion: The CS os was significantly wider in patients with AVNRT than in those without. These findings may have important implications for arrhythmia pathogenesis in AVNRT as well as AFL. (J Cardiovasc Electrophysiol, Vol. 15, pp. 269-273, March 2004)

A 29-year-old man was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation over 2 years. A 12-lead electrocardiogram during sinus rhythm showed manifest Wolff-Parkinson-White syndrome and during palpitation showed narrow QRS tachycardia at a rate of 213 beats/min. Following successful radiofrequency ablation of the left anterolateral accessory pathway, sustained atrial fibrillation was induced by atrial extrastimulation. Cibenzoline (2 mg/kg body weight) was injected to terminate atrial fibrillation. ST-T segment elevation in the right precordial leads was observed following cibenzoline administration. Ventricular fibrillation was reproducibly induced by ventricular extrastimuli (S1: 600 ms, S2: 220 ms, S3: 210 ms). (PACE 2004; 27:109–111)

A 29-year-old woman was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation of a 8-year duration. The 12-lead ECG during palpitations showed narrow QRS tachycardia at a rate of 160 beats/min. Dual AVN physiology according to electrophysiological criteria was not shown by single atrial extrastimulation and the tachycardia could not be induced. Slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) was induced once by double atrial extrastimuli, but it was not reproducible. However, intravenous bolus injection of adenosine triphosphate (12.5 mg) during sinus rhythm led to reproducible initiation of slow/fast AVNRT.

A 53-year-old man with an abnormal ECG was referred to the Nihon University School of Medicine. The 12-lead ECG showed right bundle branch block and saddleback-type ST elevation in leads V1-V3 (Brugada-type ECG). Signal-averaged ECG showed positive late potentials. Double ventricular extrastimuli (S1: 500 ms, S2: 250 ms, S3: 210 ms) induced VF. Amiodarone (200 mg/day) was administered for 6 months and programmed ventricular stimulation was repeated. VF was induced again by double ventricular stimuli (S1: 600 ms, S2: 240 ms, S3: 170 ms). Intravenous administration of class Ic antiarrhythmic drug, pilsicainide (1 mg/kg), augmented ST-T elevation in leads V1-V3, and visible ST-T alternans that was enhanced by atrial pacing was observed in leads V2 and V3. Visible ST-T wave alternans disappeared in 15 minutes. However, microvolt T wave alternans was present during atrial pacing at a rate of 70/min without visible ST-T alternans.

A 32-year-old man with a 20-year history of palpitation showed a short PQ interval and delta wave on 12-lead ECG. An electrophysiological study showed that the atrio-His (AH) and His-ventricular intervals were not influenced by rapid right atrial pacing or by bolus injection of adenosine triphosphate (ATP). The AH interval was shortened by coronary sinus ostium (CSos) pacing. Ventricular stimulus to the atrial activation interval was not affected by ATP but shortened by para-Hisian pacing and orthodromic His bundle activation was followed by atrial activation. The tricuspid - inferior vena cava isthmus was blocked by CSos pacing, but Ith conduction existed during low lateral right atrial pacing. (Circ J 2003; 67: 715 - 717)

Right atrial monophasic action potentials were recorded before and after 60 minutes of rapid atrial pacing (pacing cycle length (CL); 127 +/- 10 ms) in 12 closed-chest dogs. The right atrial (RA) monophasic action potential (MAP) duration at 90% repolarization (RAMAPD) was measured at CLs of 400 ms and 250 ms. CL-dependent changes in RAMAPD (CL 400 ms - 250 ms) before and after rapid atrial pacing were 24 +/- 1 ms and 16 +/- 5 ms, respectively (p0.02). RAMAP was recorded at each atrial pacing CL starting at 240 ms decreasing by 10-ms increments. RAMAPD alternans was observed in 10 of 12 dogs at a CL of 163 +/- 17 ms before and in 10 of 12 dogs at s CL of 198 +/- 29 ms (p0.01) after rapid atrial pacing. Sustained atrial fibrillation (AF) (5 minutes) was induced in 1 of 12 dogs at a pacing CL of 130 ms before rapid atrial pacing and in 4 of 12 dogs at a pacing CL of 135 +/- 17 ms after rapid atrial pacing. Onset of AF was always preceded by the RAMAPD alternans. Sixty minutes of rapid atrial pacing leads to diminution of rate adaptation of atrial action potential duration (APD) and appearance of APD alternans of greater magnitude at longer CL, both of which may contribute to the initiation and perpetuation of AF during its early phase.

The relation between ECG and activation patterns within atria in typical atrial flutter (AFL) patients (pts) has not been defined due to the lack of simultaneous multisite right and left atrial mapping.In 13 pts with AFL, a Halo catheter was positioned along tricuspid annulus and multipolar catheters were placed in right atrial appendage, His bundle region, coronary sinus (CS), proximal portion of right pulmonary artery (Bachmann's bundle region, BB) and esophagus (Eso) to record right and left atrial activation simultaneously.In counterclockwise (CCW) AFL (11 pts), 9 showed negative flutter wave (F) and 2 positive F in the inferior leads. CCW/negative F; CS electrograms (EGs) were proximal to distal, Eso EGs were inferior to superior and BB activation was later than CS and Eso. positive F; BB activation was earlier than CS. Eso EGs were superior to inferior or simultaneous. In clockwise (CW) AFL (7 pts), 5 showed positive F and 2 negative F. CW/positive F; BB activation preceded Eso and CS. Eso EGs were superior to inferior. CS EGs were proximal to distal (1), middle to proximal, distal (3) or proximal, distal to middle (1). negative F; CS EGs were proximal to distal. CS activation was earlier than BB or CS and BB activation were simultaneous. Eso EGs were inferior to superior.Impulse conduction to the left atrial free wall through either lower or upper interatrial connection is a major determinant of ECG morphology in AFL.

OHKUBO, K., et al.: Ectopic Atrial Rhythm with Exit Block Following Catheter Ablation for Focal Atrial Tachycardias in a Patient with Prior Surgery for Atrial Septal Defect. The patient was a 40-year-old woman with a history of surgery for atrial septal defect and catheter ablation for typical atrial flutter. An electrophysiological study was performed because she had palpitation and syncope. She had ectopic atrial rhythm originating from low lateral RA. Two focal atrial tachycardias ([1] superior vena cava-RA junction and [2] a low posteroseptal RA) were successfully ablated. Following catheter ablation for the second atrial tachycardia, she developed junctional rhythm because ectopic atrial rhythm showed exit block. However, atrial activation of junctional rhythm could conduct into the ectopic atrial rhythm focus and reset the rhythm when atrial activation of junctional rhythm reached the blocked line after atrial refractoriness by preceding ectopic atrial rhythm.

Since myocardial lesion size during radio-frequency (RF) ablation is limited at high power by impedance rise when electrode tip temperature exceed 100 degrees C, controlling tip temperature by continuous intraelectrode saline infusion could permit generation of larger lesion. (1) Two dogs randomly received either standard or cooled tip RF ablation at 4 to 6 separate LV sites. Power output of 30 W was delivered via modified 7 Fr deflectable catheter with 4 mm tip for up to 120 sec or until impedance rise occurred. (2) Six dogs randomly received cooled tip RF ablation at power output of 20, 30, 40 W for 120 sec. (3) Three dogs randomly received cooled tip RF ablation using room temperature saline (21-25 degrees C) or chilled saline (1-4 degrees C) infusion.Overall, peak tip temperature was lower for cooled vs standard RF deliveries (97 +/- 17 degrees C vs. 42 +/- 8 degrees C). Lesion depth and volume were significantly larger for cooled burns. Lesion depth and volume and the incidence of abrupt impedance rise/popping did not differ between room temperature saline and chilled saline infusion. The catheter-tip temperature at the onset of popping and abrupt impedance rise was 54 +/- 5 degrees C (48-60 degrees C) and 59 +/- 10 degrees C (50-75 degrees C).Cooled tip RF current delivery at high power is associated with increased myocardial lesion size which may facilitate successful ablation of ventricular tachycardia associated with acquired structural heart disease. Catheter-tip temperature should be maintained below 45 degrees C to prevent popping and abrupt impedance rise during RF energy delivery.

The effect of rapid atrial pacing on the rate adaptation of the atrial action potential duration was studied in humans. The right atrial monophasic action potential (RAMAP) of 5 patients was recorded before and after 30 min of rapid atrial pacing. The pacing cycle length (CL) was 146±9 ms, the shortest duration at which 1:1 capture was possible. The RAMAP duration at 90% repolarization (RMAPD) was measured. CL-dependent changes in RAMAPD (CL 600 ms - CL 300 ms) before and after rapid atrial pacing were 51.8±10.7 ms and 30.8±7.6 ms (p