Right atrial substrate properties associated with age in patients with typical atrial flutter.

BACKGROUND: Data detailing the age-related difference in the atrial substrate for formation of typical atrial flutter (AFL) are sparse. OBJECTIVE: The purpose of this study was to characterize the difference in the right atrial substrate related to aging using noncontact mapping of the right atrium. METHODS: A total of 54 patients (23 young [<60 years; 45 +/- 12 years] and 31 old [>or=60 years; 74 +/- 6 years]) with typical AFL who underwent three-dimensional noncontact mapping of typical AFL were enrolled in the study. The atrial substrate was characterized according to (1) regional wavefront activation mapping, (2) regional conduction velocity, and (3) regional voltage distribution by dynamic substrate mapping. RESULTS: During activation mapping of the crista terminalis, two activation patterns were observed: (1) around the upper end of the crista terminalis (67%) and (2) through a gap in the crista terminalis. The presence of a crista terminalis gap was associated with a high incidence of induced atypical AFL/atrial fibrillation (P <.001). The conduction velocities of the medial cavotricuspid isthmus were slower in the old group than in the young group. In regional activation mapping of the AFL, the location of the slowest conduction shifted from the lateral cavotricuspid isthmus (71%) in the young group to the medial cavotricuspid isthmus (40%) in the old group. More cases with a low-voltage zone (

Azithromycin-induced torsade de pointes.

Although erythromycin frequently induces long QT interval and torsade de pointes, the newer drug, azithromycin, has rarely been reported to be associated with torsade de pointes. We report here the occurrence of a significant typical QT prolongation within a few hours after taking azithromycin which lead to torsade de pointes.

Sulpiride induced torsade de pointes.

Antipsychotic agents are known to be associated with a long QT interval and torsade de pointes. We report a 69 year old female who suffered from a syncopal attack at a psychiatric hospital and was referred to our center. Torsade de pointes with a long QT interval (QTc=680 ms) was observed on the 12 lead ECG in the emergency department and intensive care unit. A careful drug history revealed that sulpiride was the culprit agent. After stopping the medication, the QT interval returned to normal (420 ms). The patients taking sulpiride should be closely monitored, especially when it is used in combination with other antidepressant agents.

Noncontact three-dimensional mapping guides catheter ablation of difficult atrioventricular nodal reentrant tachycardia.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common supraventricular tachycardia in adulthood. Although selective ablation of the slow AV nodal pathway can cure AVNRT, accidental AV block may occur. The details on the electrophysiologic characteristics, quantitative data on the voltage inside Koch's triangle, and the use of three-dimensional noncontact mapping to facilitate the catheter ablation of AVNRT associated with a high-risk for AV block or other arrhythmias have been limited. METHODS AND RESULTS: Nine patients (M/F=5/4, 34+/-23 years, range 17-76) with clinically documented AVNRT were included. All patients had undergone previous sessions for slow AV nodal pathway ablation but they had failed, because of repetitive episodes of complete AV block during the RF energy applications. Further, one patient had a complex anatomy and 4 patients were associated with other tachycardias, respectively. The electrophysiologic studies revealed that 4 patients had the slow-fast, 4 the slow-intermediate and one the fast-intermediate form of AVNRT. Noncontact mapping demonstrated two types of antegrade AV nodal conduction, markedly differing sites of the earliest atrial activation during retrograde VA conduction, and a lower range of voltage within Koch's triangle. The lowest border of the retrograde conduction region was defined on the map, and the application of the RF energy was delivered below that border to prevent the occurrence of AV block. The distance between the successful ablation lesions and the lowest border of the retrograde conduction region was significantly shorter in the patients with the slow-intermediate form of AVNRT than in those with the slow-fast form (5.5+/-3.4 vs. 15+/-7.6 mm; p<0.05). After the ablation procedure, either rapid pacing or extrastimulation could not induce any tachycardia, and there was no recurrence during the follow-up (10.3+/-5.4, 2 to 22 months). CONCLUSIONS: Noncontact mapping could effectively demonstrate the antegrade and retrograde atrionodal conduction patterns, electrophysiologic characteristics of Koch's triangle, and guide the successful catheter ablation in difficult AVNRT cases.

Substrate mapping to detect abnormal atrial endocardium with slow conduction in patients with atypical right atrial flutter.

OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter. BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear. METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones. RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 +/- 0.3 cm and mean voltage at the isthmus was -0.91 +/- 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 +/- 0.18 m/s vs. 1.14 +/- 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%). CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.

Electrophysiological characteristics and catheter ablation in patients with paroxysmal right atrial fibrillation.

BACKGROUND: Catheter ablation of the right atrial (RA) substrate has had variable efficacy in curing paroxysmal atrial fibrillation (PAF), suggesting that RA substrate ablation can play an important role in the treatment of atrial fibrillation (AF) in some patients. The aim of this study was to investigate the electrophysiological characteristics and ablation strategy and its results in a specific group of patients with paroxysmal RA-AF. METHODS AND RESULTS: The study population consisted of 13 patients (8 men; age, 64+/-15 years) with drug-refractory (2+/-1 drugs), frequent episodes of PAF. Provocation maneuvers did not reveal any ectopic beat-initiating AF. However, rapid atrial pacing easily induced AF. Activation mapping during sinus rhythm, atrial pacing, and AF was visualized by using a noncontact mapping system. Noncontact mapping revealed RA reentry (6 patients with single-loop circuits and 7 with double-loop circuits) with conduction through channels between lines of block, crista terminalis gaps, and the cavotricuspid isthmus, which could be identified during sinus rhythm and atrial pacing, resulting in fibrillatory conduction in other parts of the RA. The consistency of wavefront activation was confirmed by frequency analysis from equally distributed mapping sites in the RA. Short lines of ablation lesions were aimed at the conduction channels between the lines of block, crista terminalis gaps, and the cavotricuspid isthmus, resulting in bidirectional block. AF was eliminated in 11 (85%) of 13 patients, and those 11 patients with acute success were free of AF without any antiarrhythmic drugs during the long-term follow-up period (16+/-6 months). CONCLUSIONS: RA ablation still can cure selected patients with PAF. Linear ablation of the RA substrate guided by the electrophysiological characteristics of RA-AF is an effective approach for treating this specific group of patients with AF.

A new electrocardiographic algorithm to differentiate upper loop re-entry from reverse typical atrial flutter.

OBJECTIVES: This study was performed to differentiate upper loop re-entry (ULR) from reverse typical atrial flutter (AFL). BACKGROUND: Right atrial ULR and reverse typical AFL have different mechanisms and ablation strategies, but similar electrocardiographic characteristics. METHODS: This study included 26 patients with reverse typical AFL and 20 patients with ULR. The noncontact mapping system (EnSite-3000, Endocardial Solutions, St. Paul, Minnesota) was used to confirm diagnosis and guide successful radiofrequency ablation. Flutter wave polarity and amplitude in the 12-lead surface electrocardiogram were determined by two independent electrophysiologists. RESULTS: The flutter wave polarity in leads I and aVL was significantly different between the reverse typical AFL and ULR groups (p < or = 0.001). Voltage measurement revealed significant differences between reverse typical AFL and ULR in leads I, II, aVR, aVF, V1, and V2 (p < 0.001). A new diagnostic algorithm based on negative or isoelectric/flat flutter wave polarity and amplitude < or =0.07 mV in lead I was useful for diagnosis of ULR, with an accuracy of 90% to 97%, a sensitivity of 82% to 100%, and a specificity of 95%. CONCLUSIONS: Polarity and voltage measurement of flutter wave in lead I can differentiate reverse typical AFL from ULR.

Morphology of the thoracic veins and left atrium in paroxysmal atrial fibrillation initiated by superior caval vein ectopy.

INTRODUCTION: The structural changes of the superior caval vein, pulmonary veins, and left atrium in atrial fibrillation initiated by superior caval vein ectopy have not been reported. METHODS AND RESULTS: Nine patients with atrial fibrillation initiated by superior caval vein ectopic beats (male = 5, 54 +/- 10 years) and 15 control (n = 15, male = 10, 52 +/- 8 years) without any cardiac arrhythmias were included in this study. Using gadolinium-enhanced magnetic resonant angiography with three-dimensional reconstruction, the parameters of the superior caval vein morphology (length, various diameters, area, eccentricity, and volume) were measured. The morphological parameters of the four pulmonary veins (diameter, ostial area, and eccentricity) were also measured at the pulmonary vein-left atrial junction in an oblique sagittal section from the multiple-plane reconstruction images. The left atrial diameters and volume were measured. The different morphological parameters were compared between the two groups. The patients with atrial fibrillation initiated by superior caval vein ectopic beats exhibited a more eccentric structure of the second part of the superior caval vein as compared to the control group. All the ectopic beats initiating atrial fibrillation were located in the second part of the superior caval vein. Furthermore, the patients with atrial fibrillation initiated by superior caval vein ectopic beats had a larger superior caval vein volume, left atrial volume, and pulmonary vein size, and more eccentric pulmonary vein ostia than the controls. CONCLUSION: Structural changes of the superior caval vein were demonstrated in the patients with atrial fibrillation initiated by superior caval vein ectopic beats. These findings might explain the arrhythmogenic mechanism of atrial fibrillation initiated by superior caval vein ectopy.

Effects of right bundle branch block during atrioventricular nodal reentrant tachycardia.

BACKGROUND: The significant role of bundle branch block during atrioventricular nodal reentrant tachycardia (AVNRT) is not clear. The purposes of this study were to study the effects of complete right bundle branch block (RBBB) on electrophysiological parameters during AVNRT and to define the significance of complete RBBB during AVNRT. METHODS AND RESULTS: According to characteristics of electrocardiogram during sinus rhythm and AVNRT, 50 patients who underwent catheter ablation for slow-fast AVNRT were divided into three groups. Group I included 20 patients who had narrow QRS (< or = 110 ms) during sinus rhythm and AVNRT. Group II included 18 patients who had persistent RBBB (< or = 120 ms) during sinus rhythm and AVNRT. Group III included 12 patients who had narrow QRS during sinus rhythm, but they had narrow QRS and transient RBBB during AVNRT. The atrio-His (AH) interval (296+/-60 vs. 288+/-75 ms), His-ventricular (HV) interval (36+/-11 vs. 35+/-11 ms), His-atrial (HA) interval (72+/-24 vs. 71+/-28 ms), VA(HRA) interval (defined as the interval between the onset of ventricular depolarization and the onset of atrial activity of right high atrium; 34+/-24 vs. 37+/-25 ms), VA(CSO) interval (defined as the interval between the onset of ventricular depolarization and the onset of atrial activity of coronary sinus ostium; 13+/-28 vs. 26+/-23 ms) and tachycardia cycle length (TCL; 368+/-67 vs. 359+/-73 ms) during AVNRT were similar between group I and group II (all P > 0.05). In group III, the AH interval (255+/-81 vs. 246+/-83 ms), HV interval (44+/-5 vs. 42+/-11 ms), HA interval (66+/-19 vs. 70+/-15 ms), VA(HRA) interval (27+/-15 vs. 29+/-16 ms), VA(CSO) interval (23+/-25 vs. 21+/-25 ms) and TCL (322+/-76 vs. 316+/-77 ms) were not significantly different between AVNRT with narrow QRS and those with transient RBBB (all P > 0.05). CONCLUSIONS: Persistent RBBB and transient RBBB have no significant effects on the electrophysiological parameters during AVNRT. These findings suggest that RBBB might not influence the conduction of lower common pathway or the circuit of AVNRT.

Morphologic remodeling of pulmonary veins and left atrium after catheter ablation of atrial fibrillation: insight from long-term follow-up of three-dimensional magnetic resonance imaging.

INTRODUCTION: Understanding the structural remodeling and reverse remodeling of the left atrium (LA) and pulmonary vein (PV) after radiofrequency ablation of atrial fibrillation (AF) may provide important insights into the mechanism and management of AF. This study used magnetic resonance angiographic (MRA) images to investigate changes in PV and LA morphologies before and more than 1 year after ablation. METHOD AND RESULTS: Forty-five patients (36 men and 9 women, mean age 60 +/- 13 years) who underwent MRA before and more than 12 months (mean 21 +/- 11) after ablation of paroxysmal AF were included in the study. The patients were divided into two groups: group I included 35 patients without AF recurrence, and group II included 10 patients with late (>1 month postablation) recurrence of AF. The sizes of the LA and nonablated PV were compared before and after ablation. In group I, significant reduction of ostial area of both superior PVs was noted (left superior PV: from 2.85 +/- 0.67 to 2.59 +/- 0.73 cm2; right superior PV: from 2.89 +/- 0.85 to 2.60 +/- 0.73 cm2, both P <0.001). Geometric alteration toward a round shape was noted in the ostia of superior PVs during follow-up (eccentricity of right superior PV and left superior PV decreased from 0.31 +/- 0.10 to 0.22 +/- 0.13 and from 0.27 +/- 0.11 to 0.19 +/- 0.13, respectively, both P <0.01). However, LA volume showed only borderline reduction (from 61.52 +/- 19.06 to 56.64 +/- 17.13 mL, P=0.05). In group II, significant dilation of the LA (from 61.14 +/- 17.54 to 78.73 +/- 25.27 mL, P=0.004) and right superior PV (from 3.41 +/- 1.12 to 4.08 +/- 1.31 cm2, P=0.016) was noted during follow-up. Ostial area and eccentricity of the left superior, left inferior, and right inferior PVs and LA were similar before and after ablation. CONCLUSION: Structural remodeling of the superior PVs and LA can be reversible after successful ablation without AF recurrence; however, late recurrence of AF is associated with progressive LA dilation.

Mechanism of repolarization change during initiation of supraventricular tachycardia.

INTRODUCTION: Previous literature has documented the association between narrow QRS supraventricular tachycardia (SVT) and pronounced ST-T segment change. The aim of this study was to evaluate repolarization changes during SVT initiation and demonstrate the possible mechanism. METHODS AND RESULTS: Fifty-one consecutive patients (20 men and 31 women; mean age 46.1 +/- 16.4 years) with narrow QRS SVT (32 patients with AV nodal reentrant tachycardia and 19 patients with AV reentrant tachycardia) were included. We retrospectively analyzed the intracardiac recordings and ST-T segment changes on 12-lead surface ECGs during SVT initiation. Twenty-six (51%) patients developed ST segment repolarization changes during SVT initiation. Patients with shorter baseline sinus cycle length, shorter tachycardia cycle length, elevated systolic blood pressure before tachycardia induction, and greater reduction of systolic blood pressure had a higher incidence of repolarization changes. However, multivariate analysis showed that reduction of systolic blood pressure after SVT induction was the only independent predictor of repolarization changes. Furthermore, the maximal degree of ST segment depression during SVT correlated with the reduction of systolic blood pressure (r = 0.75, P < 0.001). CONCLUSION: Repolarization changes during SVT initiation were caused mainly by concurrent hemodynamic change after SVT initiation with abrupt cycle length shortening.

Mechanism of adenosine-induced termination of focal atrial tachycardia.

INTRODUCTION: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. METHODS AND RESULTS: The study consisted of 7 patients (4 men and 3 women; age 44 +/- 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3-12 mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 +/- 11.7 msec vs 4.7 +/- 4.5 msec, P < 0.001) and standard deviation of normalized AT cycle length (0.033 +/- 0.014 vs 0.011 +/- 0.005, P < 0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (-27.2 +/- 15.3%, P < 0.01), preferential conduction (proximal: -32.1 +/- 18.7, mid: -28.4 +/- 22.8, distal portion: -29.6 +/- 21.4%, P < 0.01), and breakout (-31.4 +/- 12.5%, P < 0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 +/- 1.5 (range 1-4), with maximum shifting distance of 15.0 +/- 3.1 (range 10-19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. CONCLUSION: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

Electrophysiological mechanisms and catheter ablation of complex atrial arrhythmias from crista terminalis:.

Paroxysmal atrial fibrillation (PAF) can be initiated by ectopic activation from the crista terminalis. The crista terminalis conduction gap is also a critical isthmus in atrial reentrant arrhythmias like upper and lower loop reentry. The aim of this study was to investigate the mechanism and results of catheter ablation for complex atrial arrhythmias originating from the crista terminalis using the noncontact mapping system (NCM). The study population consisted of six patients (5 men, 1 woman; 70 +/- 9 years) with drug refractory PAF and typical/atypical atrial flutter. NCM identified the earliest ectopic activation originating from the crista terminalis in these six patients. The reentry circuit of atypical atrial flutter propagated around the upper crista terminalis in five patients, and lower crista terminalis in one patient. The reentry circuit of atypical atrial flutter and the initial reentry circuit of AF conducted through the crista terminalis gap in all patients. Radiofrequency applications were delivered on the sites of ectopy, which initiated AF. Substrate modification was also performed over the crista terminalis gap (six patients) and cavotricuspid isthmus (three patients) responsible for the reentry. During a mean follow-up of 9 +/- 5 months (range 5-18 months), five patients were free of AF without antiarrhythmic drugs, and one patient did not have AF or atrial flutter using propafenone. NCM demonstrated the mechanism of crista terminalis ectopy-initiating AF and associated typical/atypical atrial flutter. Catheter ablation of crista terminalis ectopy and substrate for the reentry guided by NCM successfully eliminated these atrial arrhythmias.

Functional characterization of the crista terminalis in patients with atrial flutter: implications for radiofrequency ablation.

OBJECTIVES: The aim of the study was to investigate the conduction properties and anisotropy of the crista terminalis (CT) in patients with atrial flutter (AFL) using non-contact mapping. BACKGROUND: The CT is a posterior barrier during typical AFL. However, the CT has transverse conduction capabilities in patients with upper loop re-entry (ULR). METHODS: Twenty-two patients (16 males, 63 +/- 15 years) with typical AFL and ULR were included. Non-contact mapping of the right atrium during AFL and pacing from coronary sinus (CS) and low anterolateral right atrium (LARA) was performed to evaluate transverse conduction across the CT. During ULR, the longitudinal (CV(L)) and transverse (CV(T)) conduction velocity along and across the CT were measured. The width of the CT conduction gap was evaluated to guide radiofrequency ablation (RFA). RESULTS: No transverse CT gap conduction was found during typical AFL. Transverse CT gap conduction was found in three patients during CS pacing and in three patients during LARA pacing. During ULR, CV(L) was greater than CV(T) (1.28 +/- 0.43 vs. 0.73 +/- 0.30 m/s, p < 0.001). The CV(L)/CV(T) ratio was 1.95 +/- 0.77, which was inversely related to the CT gap width (15.7 +/- 6.8 mm) (p < 0.001). The RFA of the CT gap was successful in 18 patients. Four patients had recurrence of arrhythmias during the follow-up of 11 +/- 3 months. CONCLUSIONS: Most of the CT conduction gaps were functional and only appeared during ULR. The width of the CT gap was inversely related to the anisotropic ratio of the CT. The RFA of the CT gap was effective in eliminating ULR.

Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation.

BACKGROUND: This study investigated the electrophysiologic characteristics, atrial activation pattern, and effects of radiofrequency (RF) catheter ablation guided by noncontact mapping system in patients with focal atrial tachycardia (AT). METHODS AND RESULTS: In 13 patients with 14 focal ATs, noncontact mapping system was used to map and guide ablation of AT. AT origins were in the crista terminalis (n=8), right atrial (RA) free wall (n=3), Koch triangle (n=1), anterior portion of RA-inferior vena cava junction (n=1), and superior portion of tricuspid annulus (n=1); breakout sites were in the crista terminalis (n=5), RA free wall (n=5), middle cavotricuspid isthmus (n=2), and RA-superior vena cava junction (n=2). ATs arose from the focal origins (11 ATs inside or at the border of low-voltage zone), with preferential conduction, breakout, and spread to the whole atrium. After applications of RF energy on the earliest activation site or the proximal portion of preferential conduction from AT origin, 13 ATs were eliminated without complication. During the follow-up period (8+/-5 months), 11 (91.7%) of the 12 patients with successful ablation were free of focal ATs. CONCLUSIONS: Focal AT originates from a small area and spreads out to the whole atrium through a preferential conduction. Application of RF energy guided by noncontact mapping system was effective and safe in eliminating focal AT.