A new approach for the comparison of conduction abnormality between arrhythmogenic right ventricular cardiomyopathy/dysplasia and Brugada syndrome.

BACKGROUND: Right ventricular outflow tract ventricular tachycardia (RVOT-VT), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), and Brugada syndrome (BrS) were characterized by arrhythmias originating in the right ventricle, and the pathophysiologic mechanism underlying these arrhythmias has not been fully understood. METHODS: This study consisted of 40 subjects, including 20 patients with RVOT-VT, 10 patients with BrS, and 10 ARVD patients. The parameters on the signal-averaged electrocardiography (ECG) and the frequency components recorded from the wavelet-transformed ECG were compared between the three groups. Late potentials were positive in none of the patients with RVOT-VT, seven of the patients with BrS, and all of ARVD patients. RESULTS: In Brugada and ARVD patients, the power of high-frequency components (80-150 Hz) was developed to a greater extent than in RVOT-VT patients. In the power analysis of the high-frequency components between BrS and ARVD, the frequency showing the greatest power was significantly higher in ARVD patients than that in BrS patients (145.4 ± 27.9 Hz vs 81.7 ± 19.9 Hz, P < 0.01). CONCLUSIONS: High-frequency components were developed in ARVD and BrS, but not in RVOT-VT. The frequency levels showing high power by wavelet analysis obviously differ between ARVD and BrS. Wavelet analysis may provide new insight into unsolved mechanisms in arrhythmogenic right heart disease.

The VA relationship after differential atrial overdrive pacing: a novel tool for the diagnosis of atrial tachycardia in the electrophysiologic laboratory.

INTRODUCTION: Despite recent advances in clinical electrophysiology, diagnosis of atrial tachycardia (AT) originating near Koch's triangle remains challenging. We sought a novel technique for rapid and accurate diagnosis of AT in the electrophysiologic laboratory. METHODS: Sixty-two supraventricular tachycardias including 18 ATs (10 ATs arising from near Koch's triangle), 32 atrioventricular nodal reentrant tachycardias (AVNRTs), and 12 orthodromic reciprocating tachycardias (ORTs) were studied. Overdrive pacing during the tachycardia from different atrial sites was performed, and the maximal difference in the postpacing VA intervals (last captured ventricular electrogram to the earliest atrial electrogram of the initial beat after pacing) among the different pacing sites was calculated (delta-VA interval). RESULTS: The delta-VA intervals were >14 ms in all AT patients and <14 ms in all AVNRT/ORT patients, and thus, the delta-VA interval was diagnostic for AT with the sensitivity, specificity, and positive and negative predictive values all being 100%. When the diagnostic value of the delta-VA interval and conventional maneuvers were compared for differentiating AT from atypical AVNRT, both a delta-VA interval >14 ms and "atrial-atrial-ventricular" response after overdrive ventricular pacing during the tachycardia were diagnostic. However, the "atrial-atrial-ventricular" response criterion was available in only 52% of the patients because of poor ventriculoatrial conduction. CONCLUSIONS: The delta-VA interval was useful for diagnosing AT irrespective of patient conditions such as ventriculoatrial conduction.

Adenosine-sensitive atrial tachycardia originating from the proximal coronary sinus.

BACKGROUND: Atrial tachycardia (AT) can originate from the proximal coronary sinus (CS). However, detailed electrophysiologic characteristics of the tachycardia are not available. OBJECTIVES: We describe the electrophysiologic characteristics, response to adenosine 5'-triphosphate, and results of radiofrequency ablation of AT with the earliest activation in the proximal CS. METHODS: In 7 of 54 patients (age 57 +/- 18 years) with nonmacroreentrant "focal" AT undergoing electrophysiologic study and radiofrequency ablation, the earliest atrial activation site was located in the proximal CS. RESULTS: The earliest activation site was inside the CS 13 +/- 3 mm from the ostium. The AT could be induced and terminated by atrial extrastimuli or burst pacing. In all patients, the AT was also terminated by a very small dose of adenosine 5'-triphosphate (4.2 +/- 1.1 mg). Rapid ventricular pacing during the tachycardia produced ventriculoatrial dissociation. Radiofrequency ablation directed at the earliest atrial activation site was effective in only three patients (group A). In the remaining four patients (group B), after the radiofrequency energy deliveries, the earliest activation site shifted to an adjacent site with a small increase in the cycle length. Three group B patients underwent successful ablation in the slow pathway region. No recurrence was observed over a follow-up period of 22 +/- 5 months. CONCLUSION: AT with earliest activation in the proximal CS is sensitive to a small dose of adenosine 5'-triphosphate. In some patients, radiofrequency applications in the slow pathway region are effective even if the local activation is not early.

Electrocardiographic and electrophysiological characteristics of atrial fibrillation organized into atrial flutter by oral administration of class I antiarrhythmic agents.

The aim of this study was to evaluate the electrocardiographic (ECG) and electrophysiological characteristics of atrial fibrillation (AF) that organized into atrial flutter during oral administration of class I antiarrhythmic agents. The former clinical study included 72 consecutive patients (58 paroxysmal AF, 14 persistent AF) in whom class I antiarrhythmic agents were orally administered in the outpatient clinic for termination or prophylaxis of AF. The clinical background and ECG variables were compared between the patients with and without atrial flutter during class I antiarrhythmic agents therapy. An electrophysiological study was performed in ten patients with paroxysmal AF (five with [group A] and five without atrial flutter [group B] during oral class I antiarrhythmic agents therapy. Local electrograms from five different atrial sites (high and low right free wall, high and low septum, and distal coronary sinus) were analyzed during induced AF. The activation pattern of the right free wall during AF was also analyzed using a Halo catheter. Atrial flutter was documented during class I antiarrhythmic agents therapy in 14 (24%) patients with paroxysmal AF, whereas in none with persistent AF. The mean cycle length (f-f interval) and amplitude of the fibrillation waves in leads II and V1 from the surface ECG were significantly greater in the patients with than in those without atrial flutter. In the electrophysiological study, the mean cycle lengths for the low and high right free wall were significantly longer in group A than in group B, whereas those for the low septums and distal coronary sinus did not differ between the two groups. During the induced AF, the ratio of time exhibiting a consistent activation pattern (cranio-caudal, caudo-cranial, or undetermined) along the right free wall was significantly greater in group A than in group B. Atrial flutter newly developed during class I antiarrhythmic agents therapy in patients with coarse AF on the surface ECG and a relatively organized activation in the right atrial free wall. The observation of these findings may facilitate the identification of candidates for hybrid pharmacologic and ablative therapies.