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1/8. A typical P-wave morphology in incessant atrial tachycardia originating from the right upper pulmonary vein.

    Automatic atrial tachycardias often originate from the ostia of the pulmonary veins. P-wave morphology during tachycardia may indicate from which pulmonary vein the tachycardia originates. Two patients with pulmonary vein tachycardias demonstrating atypical P-wave morphology were investigated. One of the patients had a tachycardia with two different cycle lengths. P-wave morphology was evaluated in 12-lead ECGs from two patients with incessant atrial tachycardia, during tachycardia and sinus rhythm. Their tachycardias were successfully ablated at the mouth of the right upper pulmonary vein. Previous studies have demonstrated a positive or negative P-wave configuration in lead aVL originating from this area and a change from a biphasic P-wave in V1 during sinus rhythm to a positive P-wave configuration during tachycardia. Neither of our two patients had such a change in lead V1. One our patients had two tachycardias with different cycle lengths originating from the same area. It is concluded that if an atrial tachycardia with P-wave morphology resembling that of sinus rhythm cannot be located to the right atrium, its origin may be the right upper pulmonary vein.
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2/8. Iterative atrial tachycardia originating from the coronary sinus musculature.

    A case of iterative atrial tachycardia leading to dilated cardiomyopathy is reported. During electrophysiologic study, the tachycardia showed a markedly irregular cycle length associated with changes in atrial activation breakthrough as demonstrated by coronary sinus (CS) recordings and frequently degenerated into self-terminating atrial fibrillation. Left atrial transseptal mapping demonstrated the earliest endocardial atrial activation close to the posterolateral mitral annulus, but this was invariably later than that recorded within the CS, where low-energy radiofrequency applications eliminated the tachycardia. No acute vessel damage was observed at postablation CS angiography. In accordance with previously published experimental data, we hypothesized that the muscular sleeves surrounding the CS might be involved in the genesis of this tachycardia. During 6-month follow-up, the patient remained asymptomatic without tachycardia recurrences and with complete recovery of left ventricular function, confirming the reversible nature of the tachycardia-induced cardiomyopathy.
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3/8. Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia.

    We describe a case of post-incisional atrial tachycardia resembling typical atrial flutter on the surface ECG. Typical atrial flutter reentry was ruled out by the results of activation and entrainment mapping. Nevertheless, overdrive pacing from the lateral edge of the cavo-tricuspid isthmus produced tachycardia entrainment with concealed fusion associated with post-pacing and stimulus-to-P wave onset intervals exactly matching the tachycardia cycle length duration and the electrogram-to-P wave onset interval, respectively. Therefore, that site was firstly severed by sequential radiofrequency pulses. However, a transformation of the tachycardia P wave morphology and endocardial activation sequence, not associated with tachycardia termination or cycle length modification occurred. After additional mapping manoeuvres, a relatively small reentrant circuit was identified in the low and mid aspect of the lateral right atrium with the critical isthmus located between the lower border of a cannulation atriotomy and the crista terminalis, close to the inferior vena cava orifice. A single radiofrequency pulse at that site terminated the tachycardia. Both the electrocardiographic pattern and the endocardial mapping data obtained in our case might be explained by a split of the reentrant wavefront into a secondary wavelet which freely propagated through the cavo-tricuspid isthmus without completing the peritricuspid loop. In conclusion, bystander cavo-tricuspid isthmus activation during atrial tachycardia may simulate a typical atrial flutter pattern on the surface ECG. Further studies should evaluate the prevalence of this propagation pattern in post-incisional atrial reentry and atypical atrial flutters, and identify its implications for ablation strategy.
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4/8. A combination of two simultaneous tachycardias in the right atrium close to the atrio-ventricular node and within the coronary sinus in a post-operative cor triatriatum patient.

    A 71-year-old male was referred to another hospital for dizziness. A bradycardia -tachycardia syndrome and cor triatriatum were detected, and an operation to resect the membrane in the left atrium and implant a pacemaker epicardially was performed. However, no suitable site could be found on either atria and therefore, a single chamber ventricular pacemaker was implanted. In the electrophysiological study performed in our hospital, we could not detect any atrial potentials in either atria, excluding the region close to the His bundle (HB) and within coronary sinus (CS), in spite of extensive catheter mapping. A regular atrial rhythm with a cycle length of 820 ms, which was synchronous with the rate of the QRS complex on the surface ECG, was recorded only at the HB. Meanwhile, the CS catheter recording exhibited regular focal activity with a cycle length of 150 ms, and this focal activity did not conduct to the atrium close to the HB. Furthermore, this activity was dissociated from the ventricular activity recorded from the CS catheter. During an isoproterenol infusion, an atrial tachycardia with a cycle length of 380 ms was recorded only at the HB, and the twelve-lead ECG exhibited a regular tachycardia with the same cycle length as this tachycardia. Meanwhile, the focal activity within the CS persisted without any change in the cycle length. These findings suggested that there was dissociation between the right atrium (RA) and CS. Furthermore, partial atrial standstill was observed in both atria, excluding the RA close to the atrio-ventricular (AV) node and area within the CS. These rare electrophysiological features were considered to play an important role in the genesis of a simultaneous combination of the two tachycardias at their respective sites.
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5/8. Modulation of atrioventricular junctional parasystole during atrial pacing.

    In this report we describe a case of a 68-year-old man with atrioventricular junctional parasystole in whom atrial pacing caused marked changes in the arrhythmic pattern. During atrial pacing at a cycle length of 960 ms, the duration of the ectopic cycle length was influenced by the interval between the parasystolic and nonparasystolic beat. A shorter interval from nonparasystolic to ectopic beat prolonged the ectopic cycle length and a longer one shortened it. Pacing at a cycle length of 900 ms completely suppressed the parasystole. Both of these changes are most likely due to modulation and entrainment of the parasystolic rhythm. During spontaneous variation of the sinus cycle length over 24 hours of ambulatory ECG recording, modulation could not be confirmed; however, there was parallel variation of the ectopic and sinus cycle lengths which suggests that both pacemakers were under the influence of the autonomic nervous system.
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6/8. accelerated idioventricular rhythm complicating atrioventricular junction ablation for automatic atrial tachycardia.

    A 13-year-old male with histologic evidence of cardiomyopathy, drug-refractory primary atrial tachycardias, and deteriorating left ventricular function underwent transcatheter His bundle ablation to control ventricular rate. Following an initial successful ablation at the level of the atrioventricular node, the patient exhibited an accelerated escape rhythm of apparent junctional origin (ventricular cycle length = 470 msec, HV = 100 msec) with complete heart block. A second ablation procedure was undertaken, following which an accelerated idioventricular rhythm (cycle length = 500 msec) became apparent and has persisted (follow-up 15 months). Thus, findings in this patient suggest that attempts to control refractory rapid ventricular responses in cardiomyopathy patients with primary atrial tachycardias may be complicated by the potential for junctional and idioventricular sites to exhibit similar abnormally accelerated subsidiary pacemaker function.
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7/8. Ineffective diastolic filling in tachycardia-induced cardiomyopathy with total pulsus alternans.

    We report a case of total pulse alternans in a patient with paroxysmal ectopic atrial tachycardia and echocardiographic findings obtained before and after radiofrequency catheter ablation (RFCA) that terminated the arrhythmia. The patient was a 27-year-old man with history of paroxysmal palpitations with worsening episodic dizziness, chest tightness, and dyspnea. electrocardiography (ECG) showed atrial tachycardia at 160 to 170 beats/min while the simultaneous pulse was in the 80s beats/min. Echocardiogram showed that aortic and mitral valves opened with alternating excursions and outflow velocities. Furthermore, despite similar ventricular wall thickening during systole of consecutive cardiac cycles, there was alternating mitral valve opening during diastole of the same cycles, providing direct evidence that ineffective diastolic filling and mitral valve opening may play a role in the pathogenesis of pulse alternans. Repeat ECG and echocardiography after the successful RFCA showed normal sinus rhythm and normal opening excursion and the velocity across the aortic and mitral valves.
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8/8. Paroxysmal atrial tachycardia with second-degree atrioventricular block.

    Paroxysmal atrial tachycardia with atrioventricular block usually indicates potentially dangerous overdigitalization, and serious heart disease is almost universally present. In this report, we describe a patient with a structurally normal heart who manifested spontaneously intra-atrial reentrant tachycardia with Wenckebach atrioventricular block in the absence of medications. In this patient, the longest atrial paced cycle length that induced atrioventricular nodal block was 390 ms, and the atrial cycle length during tachycardia ranged from 360 to 400 ms. The electrophysiologic study in our patient demonstrated that second-degree atrioventricular block during atrial tachycardia may occur in patients without structural heart diseases or taking any medication.
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