Cases reported "Tachycardia, Ventricular"

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1/44. AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias.

    An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias.
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2/44. Radiofrequency catheter ablation as primary therapy for symptomatic ventricular tachycardia.

    Most applications of radiofrequency (RF) catheter ablation for treatment of ventricular tachycardia (VT) have been as a treatment of last resort. The purpose of this study was to determine the efficacy and safety of RF catheter ablation as the primary treatment for symptomatic single morphology VT. Eleven of 81 patients (14%) with inducible sustained monomorphic VT underwent RF ablation as the primary treatment. One of these 11 patients had successful RF ablation of bundle branch reentry VT and was excluded from this series. The remaining 10 patients had a mean age of 58 /- 19 years (range 20 to 73 years), were mostly men (7 of 10 patients), and all presented with documented evidence of symptomatic sustained monomorphic VT, at a mean cycle length of 340 /- 60 milliseconds (ms) (range 250 to 430 ms). Six patients had coronary artery disease (CAD), one had surgical repair for tetralogy of fallot, one had surgical repair of a ventricular septal defect, and two had a normal cardiac substrate. The VT origin was mapped using a combination of activation mapping, mid-diastolic potentials, pace mapping, and concealed entrainment. A mean of 5 /- 3 (range 2 to 11) RF applications were administered to the putative VT foci. Eight of 10 (80%) clinical VTs were successfully ablated. There were no serious complications. patients with VT originating from the left ventricle were offered implantable cardioverter-defibrillator back-up; however, only one patient accepted this option. At a mean follow-up of 12 /- 7 months, only one patient had a possible arrhythmia recurrence.
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3/44. Transient local changes in right ventricular monophasic action potentials due to ajmaline in a patient with brugada syndrome.

    A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (maps) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial maps may demonstrate regionally different action potential changes that may contribute to the ECG changes in brugada syndrome.
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4/44. Beneficial effect of amiodarone on pacing induced terminability of reentrant ventricular tachycardia.

    A 33 year-old woman was referred to our hospital for further treatment of ventricular tachycardia (VT). During treatment with amiodarone (200 mg/day), clinical VT at the cycle length of 510 ms was induced. During the VT, rapid ventricular pacing was repeated at progressively shorter cycle lengths after a decrement of 10 ms steps. The VT was entrained by the rapid pacing and reproducibly terminated at a paced cycle length of 380 ms. Four weeks after reducing the amiodarone to 100 mg/day, programmed stimulation was repeated. The VT with the same morphology but with a slightly shorter cycle length of 480 ms was again induced. However, at this time, rapid pacing from the same site could not terminate VT and transient acceleration developed at a shorter paced cycle length of 260 ms. The QT (QTc) interval, effective refractory period at the pacing site and width of the paced QRS complex were similar before and after changing the amiodarone treatment. The most characteristic change of VT in the second study was a widening of the entrainment zone, which was calculated as the difference between VT cycle length and the longest pacing cycle length which interrupts VT during the entrainment (from 130 to > 220 ms), and it may be explained by the preferential shortening of the action potential duration and/or facilitation of the depressed cell to cell conduction within the reentry circuit. amiodarone must exert a preferential action in the reentry circuit and modulate the conduction property as well as the effective refractory period. We should pay close attention to the efficacy of antitachycardia pacing during the modification of amiodarone treatment.
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5/44. Sustained ventricular tachycardia and its successful prophylaxis during high-dose bolus interleukin-2 therapy for metastatic renal cell carcinoma.

    In the setting of interleukin-2 (IL-2) administration, tachycardias of ventricular origin are classified as serious, grade IV toxicities, necessitating the discontinuation of therapy. In this report, we describe a patient with renal cell carcinoma who experienced ventricular tachycardia while undergoing treatment with high-dose bolus IL-2. Prophylaxis with sotalol permitted the successful completion of his first cycle of treatment, without any recurrent rhythm disturbances.
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6/44. Simultaneous alterations of QRS configuration and tachycardia cycle length during radiofrequency ablation of idiopathic left ventricular tachycardia.

    Idiopathic left ventricular tachycardia is characterized by a QRS morphology of right bundle branch block pattern and left axis deviation. Alterations in the QRS configuration and tachycardia cycle length, as well as shifting of the earliest activation site occurred after eliminating the original tachycardia by radiofrequency current in an 18-year-old man with idiopathic left ventricular tachycardia. Activation mapping and entrainment mapping during tachycardia identified 2 putative tachycardia exits, 15 mm apart. Elimination of both tachycardias was accomplished after applying radiofrequency current to each exit separately. We proposed that the first radiofrequency application might have altered the exit site and the zone of slow conduction adjacent to the exit site, such that the ventricular tachycardia had a different QRS morphology and became slower in this patient.
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7/44. A case of primary cardiac B cell lymphoma associated with ventricular tachycardia, successfully treated with systemic chemotherapy and radiotherapy: a long-term survival case.

    We experienced a long-term survival case of primary cardiac lymphoma (PCL) demonstrating ventricular tachycardia (VT) as an initial sign, which was related to localized myocardial damage by lymphoma cells. A 70-year-old woman with sustained VT was admitted to the Kofu Municipal Hospital. VT ceased with the administration of disopyramide intravenously. The origin of the VT was the free wall of the right ventricular outflow tract (RVOT) as observed by electrocardiography on admission. A solitary mass in the free wall of the RVOT was found by echocardiography, chest computed tomographic scanning and magnetic resonance imaging. There was no evidence of extracardiac involvement. The patient was histologically diagnosed as PCL by endomyocardial biopsy. Chemotherapy started immediately after the diagnosis and the mass showed a marked reduction in size. After 8 cycles of chemotherapy, radiotherapy was performed. Pericardial thickness in the free wall of the RVOT developed without severe side effects. Complete remission has been maintained for 30 months after the initial diagnosis, and no recurrence and arrhythmias have been detected during the follow-up period. It was demonstrated that rapid diagnosis and chemotherapy followed by radiotherapy for PCL achieved better survival.
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8/44. Both low and high energy cardioversion induced accelerated ventricular tachycardia in a patient treated with an implantable cardioverter defibrillator.

    A 72-year old male with an old myocardial infarction who had drug-refractory ventricular tachyarrhythmias received an implantable cardioverter-defibrillator (ICD). The patient did not take his prescribed beta-blocking agent for two days, following which he experienced six discrete shocks for spontaneous VT while riding his bicycle. Both 5J and 30J cardioversions were ineffective at terminating the VT and accelerated VT developed following the shocks. After admission, an electrophysiological study was performed while he was taking the beta-blocking agent, both low and high energy cardioversions reproducibly terminated the clinical VT without showing any accelerated rhythm. These findings suggest that the increase in sympathetic discharge may enhance the proarrhythmic potential of ICDs.
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9/44. Double ventricular response by a single ventricular extrastimulus to the inner loop of reentry in a patient without apparent heart disease.

    In a patient without apparent heart disease, a ventricular extrastimulus delivered from the left ventricular apex where the electrogram was recorded 30 ms after the onset of the QRS complex during VT advanced the second QRS complex, but not the first QRS complex. The morphology of the second QRS complex was the same as that of VT. The postpacing interval was the same as the cycle length of the VT. These findings indicated that the site of stimulation was at the inner loop of the reentry circuit of the VT. A ventricular extrastimulus with a shorter coupling interval advanced the first and second QRS complexes, indicating that the ventricle was activated by antidromic and orthodromic activation from the extrastimulus. Radiofrequency ablation at that site of stimulation terminated the VT and no further VT could be induced.
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10/44. Demonstration of the reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia: direct evidence for macroreentry as the underlying mechanism.

    The exact reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) remains unclear. This case report demonstrates the reentrant circuit of ILVT. A 20-pole electrode catheter was placed along the left posterior fascicle during electrophysiologic study. ILVT was reproducibly induced by programmed ventricular stimulation. During the tachycardia, sequential diastolic potentials bridging the entire diastolic period were observed in the recordings from the electrodes positioned from left ventricular mid-septum to inferoapical septum. The slow conduction zone appeared to be composed of a false tendon in this patient. Entrainment of the ILVT from the right ventricular outflow tract at a different pacing cycle length revealed that a dominant conduction delay occurred at the proximal site of the slow conduction zone. Entrainment studies from several sites on the left ventricular septum confirmed that these sites where sequential electrical activity was recorded were included within the reentrant circuit. However, the left posterior fascicle itself seemed to be a bystander. This report provides the direct evidence of macroreentry as the underlying mechanism of this ILVT, adjacent to the left posterior fascicle.
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