Cases reported "Tachycardia, Paroxysmal"

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1/77. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of brugada syndrome.

    We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to brugada syndrome even in patients without any history of syncope or ventricular fibrillation.
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2/77. Arrhythmias in the coronary-care unit. IV. Physiologic bases of paroxysmal tachycardia-dependent bundle branch block.

    Paroxysmal BBB may be either tachycardia-dependent which is referred to as "phase 3 block" or bradycardia-dependent, referred to as "phase 4 block." tachycardia-dependent BBB is related to prolonged recovery. bradycardia-dependent BBB is related to hypopolarization and SDD. These fundamental electrophysiological properties aid in understanding of transient BBB occurring during an acute MI.
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3/77. Unusual induction of slow-fast atrioventricular nodal reentrant tachycardia. Report of two cases.

    INTRODUCTION: Generally, the induction of typical atrioventricular nodal reentrant tachycardia (AVNRT) occurs with a premature atrial stimulus that blocks in the fast pathway and proceeds down the slow pathway slowly enough to allow the refractory fast pathway time to recover. We describe two cases in which a typical AVNRT was induced in an unusual fashion. RESULTS: The first case is a 41-year-old man with paroxysmal supraventricular tachycardia. During the electrophysiology study, the atrial extrastimulus inducing the typical AVNRT was conducted simultaneously over the fast (AH) and the slow pathway (AH'). A successful ablation of the slow pathway was performed. During the follow-up no recurrence was noted. The second case is a 52-year-old woman with a wolff-parkinson-white syndrome due to a left posterior accessory pathway. After 5 minutes of atrioventricular reentrant tachycardia (AVRT) induced by a ventricular extrastimulus, a variability of the antegrade conduction was noted in presence of the same VA conduction. In fact, a short AH interval (fast pathway) alternated with a more prolonged AH intervals (slow pathway) that progressively lengthened until a typical AVNRT was induced. The ablation of the accessory pathway eliminated both tachycardias. DISCUSSION: A rare manifestation of dual atrioventricular nodal pathways is a double ventricular response to an atrial impulse that may cause a tachycardia with an atrioventricular conduction of 1:2. In our first case, an atrial extrastimulus was simultaneously conducted over the fast and the slow pathway inducing an AVNRT. This nodal reentry implies two different mechanisms: 1) a retrograde block on the slow pathway impeding the activation of the slow pathway from the impulse coming down the fast pathway, and 2) a critical slowing of conduction in the slow pathway to allow the recovery of excitability of the fast pathway. Interestingly, in the second case, during an AVRT the atrial impulse suddenly proceeded alternately over the fast and the slow pathway. The progressive slowing of conduction over the slow pathway until a certain point which allows the recovery of excitability of the fast pathway determines the AVNRT. This is a case of "tachycardia-induced tachycardia" as confirmed by the fact that the ablation of the accessory pathway eliminated both tachycardias.
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4/77. Transient QT prolongation with torsades de pointes tachycardia after ablation of permanent junctional reciprocating tachycardia.

    INTRODUCTION: catheter ablation with radiofrequency energy is a curative therapy in patients with permanent junctional reciprocating tachycardia (PJRT). methods AND RESULTS: For the first time, we report a case of transient QT prolongation with torsades de pointes tachycardia 18 hours after successful radiofrequency energy ablation of PJRT in a 25-year-old woman with tachycardia-induced cardiomyopathy. Of note, the torsades de pointes occurred in the absence of bradycardia, electrolyte disturbances, or QT-prolonging drugs. This patient initially was thought to have a hereditary long qt syndrome that was unmasked by PJRT ablation. Therefore, the patient received an implantable defibrillator in addition to beta-blocker therapy, which was discontinued 6 months later. Surprisingly, the QT interval completely normalized within 1 week after PJRT ablation, and the patient remained free of arrhythmias during a follow-up period of 4.5 years. CONCLUSION: patients with incessant tachyarrhythmias should undergo ECG monitoring for at least 24 hours following successful radiofrequency catheter ablation because transient QT prolongation with torsades de pointes may occur even in the absence of bradycardia, QT-prolonging drugs, or electrolyte disturbances.
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5/77. Shortening of conduction time over arborized atrioventricular accessory pathway with Mahaim fibers physiology just before interruption during radiofrequency ablation.

    A 21-year-old woman had paroxysmal wide QRS tachycardia with a left bundle branch block configuration and a retrograde conducted P wave just behind the QRS complex. An electrophysiological study revealed antidromic atrioventricular tachycardia involving an atrioventricular connection with decremental conduction as the anterograde limb and normal atrioventricular node as the retrograde limb. During constant pacing from the high right atrium (HRA) at the cycle length (CL) of 600 ms, the QRS configurations were not identical to those during the wide QRS tachycardia or constant pacing at the CL of less than 500 ms. The process by which this arborized atrioventricular accessory pathway with the Mahaim fibers physiology was interrupted by radiofrequency catheter ablation is described. Radiofrequency energy was delivered to the site recording a Mahaim potential at the tricuspid annulus during constant pacing from the HRA at the CL of 429 ms. The stimulus-QRS interval gradually shortened as it reached the power plateau without changing the preexcited QRS configuration. Shortening of the conduction time over the Mahiam pathway might have resulted in changing of the propagation from a slow to fast conduction zone or acceleration in response to thermal effect in a node-like structure on the atrial insertion site.
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6/77. Exit block of focal repetitive activity in the superior vena cava masquerading as a high right atrial tachycardia.

    An unusual case of atrial tachycardia (AT) originating from the superior vena cava (SVC) is reported. A 34-year-old man without structural heart disease underwent catheter ablation for drug-resistant AT. During the tachycardia, low-amplitude spiky electrograms with a cycle length of 120 to 175 msec were recorded in the SVC and exhibited 2:1 exit block to the atria, masquerading as the atrial activation observed with high right AT. These spiky electrograms also were observed during sinus rhythm, but they appeared immediately after the local atrial electrograms. The spikes were traced to a point 3 cm above the junction of the right atrium. Radiofrequency ablation at the site of the earliest appearance of the spike in the SVC successfully eliminated the tachycardia. During the following 15 months, no clinically significant atrial arrhythmias, including atrial fibrillation, occurred. This report indicates that careful mapping, including inside the SVC, will be a requisite in patients with high right atrial tachyarrhythmias.
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7/77. Orthostatic hypotension associated with paroxysmal ventricular tachycardia.

    Two patients (aged 46 and 49 years) are presented who gave a history of several years' duration of unsteadiness, dizziness, and syncopal attacks on standing. Both had orthostatic hypotension which was associated with the development of a unifocal paroxysmal ventricular tachycardia. There was no evidence of organic heart disease. In one of the patients the symptoms usually developed when standing after working in a crouched position. He responded to treatment with beta-adrenergic blockade. The other patient developed her symptoms on standing, after exercise or other stress. The paroxysmal ventricular tachycardia, which occurred in the upright position only, was accompanied by a marked rise in plasma adrenaline. In this patient one contributory factor was a low blood volume and she responded to plasma volume expansion. We wish to draw attention to the common neurological symptoms with which paroxysmal ventricular tachycardia may present. We suggest that paroxysmal ventricular tachycardia may result from ventricular sensitivity to circulating adrenaline and not due to aberrant innervation of the heart as has been suggested previously.
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8/77. Demonstration of dual atrioventricular nodal pathways utilizing a ventricular extrastimulus in patients with atrioventricular nodal re-entrant paroxysmal supraventricular tachycardia.

    In patients with atrioventricular (A-V) nodal re-entrant paroxysmal supraventricular tachycardia (PSVT), atrial extrastimulus technique frequently reveals discontinuous A1-A2, H1-H2 curves suggestive of dual A-V nodal pathways. To further test the hypothesis that these curves in fact reflect dual A-V nodal pathways, a ventricular extrastimulus (VS) was coupled either to A2 at a fixed A1-A2 interval which reliably produced an A-V nodal re-entrant atrial echo (E) with a constant A2-E interval in two patients, or to QRS complex (V) during sustained PSVT with a constant E-E interval in one patient. Three response zones were defined: at longer A2-VS or V-VS coupling interval, VS manifested no effect on the timing of E (Zone 1). At closer A2-VS or V-VS coupling interval, VS conducted to the atrium, shortening the apparent A2-E or E-E interval (Zone 2). At shortest A2-VS or V-VS coupling interval, VS was blocked retrogradely, and no E was induced (Zone 3). The ability of VS to preempt control of the atria (Zone 2 response) strongly suggests the presence of dual A-V nodal pathways in these PSVT patients. If only a single pathway were present, VS would of necessity collide with the antegrade impulse and could not reach the atria. The Zone 3 response occurs because of retrograde refractoriness of the fast pathway. Failure of the echo during Zone 3 probably reflects concealed conduction to the fast pathway, or possibly interference in the slow pathway.
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9/77. Transvenous cryothermal catheter ablation of a right anteroseptal accessory pathway.

    In patients with wolff-parkinson-white syndrome, right anteroseptal accessory pathways are uncommon and run from the atrium to the ventricle in close anatomic proximity to the normal AV conduction system. Radiofrequency catheter ablation is the first-line therapy for elimination of these accessory pathways. Although the initial success rate is high, there is a potential risk of inadvertent development of complete heart block, and the recurrence rate is relatively high. The capability of cryothermal energy to create reversible lesions (ice mapping) at less severe temperatures provides a potential benefit in ablation of pathways located in a complex anatomic area, such as the mid-septum and anteroseptum.
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10/77. Anterograde block in accessory pathways with retrograde conduction in reciprocating tachycardia.

    3 patients with reciprocating tachycardia are described. In all 3, tachycardia was due to a reentrant mechanism. Anterograde conduction was via the AV node while retrograde conduction was over an accessory (Kent) pathway. In none of the 3 patients did this pathway sustain anterograde conduction despite pacing the atrium close to its location. With the advent of surgical modes of therapy, it is important to recognize such 'silent' bypasses. The observations which allow this diagnosis of unidirectional anterograde block in an accessory pathway and the exclusion of AV nodal reentry, the main differential diagnostic possibility, are discussed.
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