Cases reported "Bundle-Branch Block"

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1/54. Intermittent bundle branch blocks in a patient with uncommon-type atrioventricular nodal reentrant tachycardia and enhanced atrioventricular nodal conduction.

    We report on a patient with uncommon-type atrioventricular (AV) nodal reentrant tachycardia with a short tachycardia cycle length (235-270 ms), in whom transient wide QRS tachycardia with both left bundle branch block and right bundle branch block aberrancy were followed by narrow QRS complexes. In addition, His-ventricular (H-V) block and a sudden prolongation of the H-V interval occurred during the tachycardia. As the determinant of these unusual findings, the possibility that the anterograde limb of the reentry circuit has an enhanced AV nodal conduction property is discussed, as is the clinical significance of this type of tachycardia.
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2/54. 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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3/54. Electrophysiologic characteristics and radiofrequency ablation of concealed nodofascicular and left anterograde atriofascicular pathways.

    INTRODUCTION: True nodoventricular or nodofascicular pathways and left-sided anterograde decremental accessory pathways (APs) are considered rare findings. methods AND RESULTS: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His-bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid-septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus. CONCLUSION: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.
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4/54. Intravenous administration of class I antiarrhythmic drugs induced T wave alternans in a patient with brugada syndrome.

    A 71-year-old man who experienced aborted sudden death was referred to our hospital. coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V1 to V3. Double ventricular extrastimuli at coupling intervals >180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V1 to V3, and visible T wave alternans was induced in leads V2 and V3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V2 and V3. Class I antiarrhythmic drug-related T wave alternans has been reported rarely in brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in brugada syndrome.
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5/54. Facilitation of atrioventricular reentrant tachycardia by iatrogenic right bundle branch block.

    The present case report describes the diagnosis of a concealed bypass tract in the right lateral wall revealed by electrophysiologic evaluation performed in a patient with rare palpitations. A iatrogenic right bundle branch block (RBBB) caused the occurrence of an incessant atrioventricular reentrant tachycardia. The disappearance of the RBBB determined a very difficult induction of the tachycardia that, when induced, showed a shorter cycle length and ventriculoatrial interval than those observed during RBBB tachycardia. The presence of a RBBB ipsilateral to the right free wall accessory pathway provided a critical delay within the circuit thus allowing the bypass tract to recover excitability. This relevant delay also allows the sinus beat to initiate and stabilize the tachycardia thus rendering it incessant.
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6/54. A case of secondary myocardial lymphoma presenting with ventricular tachycardia.

    Malignant lymphoma can involve the cardiac cavity or myocardium as a mass. Clinical symptoms of its cardiac involvement are usually absent or nonspecific, making the diagnosis of the cardiac involvement very difficult before death. We experienced a patient with secondary myocardial non-Hodgkin's lymphoma presenting with sustained ventricular tachycardia (VT) as a primary clinical problem. A 39-yr-old woman visited our hospital because of dyspnea and palpitation for 7 days. physical examination revealed rapid heart beat with variable intensity of the first heart sound and soft mass in the lower abdomen. VT with a cycle length of 480 msec was recorded in resting 12-lead electrocardiogram. Two well-circumscribed hypo-echogenic round masses were demonstrated in the interventricular septum and left ventricular posterior wall. Cytological examination of aspirated pericardial fluid and percutaneous needle biopsy of the abdominal mass revealed a diffuse large cell type non-Hodgkin's lymphoma. Myocardial masses and ventricular tachycardia resolved with chemotherapy using cyclophosphamide, adriamycin, vincristine and prednisone regimen. To our best knowledge, the same case as ours has not been reported previously.
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7/54. Entrainment of ventricular tachycardia with a permanent biventricular pacemaker.

    Biventricular pacing has been introduced as a treatment for congestive heart failure. These devices presently pace and sense from two disparate ventricular sites. Antitachycardia pacing (ATP) is used for termination of sustained monomorphic ventricular tachycardia (VT) and has been incorporated with simultaneous dual site ventricular pacing for treatment of VT. We report a case of entrainment of sustained monomorphic VT in a 62-year-old female with an ischemic cardiomyopathy and VT, who received a biventricular pacemaker-implantable cardioverter defibrillator, Contak CD (Guidant, St. Paul, MN). Biventricular pacing sites were at the right ventricular apex and the middle of the anterior cardiac vein on the left ventricle. The entrained VT has a left bundle branch block and left axis deviation morphology with a cycle length of 350 msec. ATP at 270 msec produced concealed entrainment of an induced VT. Only one pacing site demonstrated capture. The inability to capture both pacing sites simultaneously was the result of ventricular refractoriness at one of the sites during ATP of the VT. The entrance and exit points of the loop for VT appeared to rest between the two pacing sites in the intraventricular septum. This case illustrates one of the sensing limitations of today's biventricular pacing defibrillator systems.
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8/54. Retrograde His bundle deflection in bundle-branch re-entry.

    Atrial echo beats resulting from a reciprocating mechanism involving the bundle-branches were produced by premature atrial impulses in a patient with an A-V nodal bypass tract. The mechanism of the arrhythmia was suggested by the presence of a retrograde His bundle deflection which appeared 'sandwiched' in between a QRS complex with complete right bundle-branch morphology and a negative P wave. Though at a shorter cycle length the His bundle was still activated retrogradely echo beats were not seen because the retrograde H deflection occurred too early, when both bypass tract and A-V node were still effectively refractory. At the faster driven rate concealed retrograde activation of the right branch (by the premature impulse) was responsible for the right bundle-branch block patterns shown by the post-premature driven beat.
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9/54. An underrecognized subepicardial reentrant ventricular tachycardia attributable to left ventricular aneurysm in patients with normal coronary arteriograms.

    BACKGROUND: In patients with apparently normal hearts, ventricular tachycardia (VT) may only involve the subepicardial myocardium. methods AND RESULTS: Four patients with exercise-induced fast VT with right bundle branch block morphology were investigated. ECG showed a small q wave in leads II, III, and aVF during sinus rhythm (SR) in all 4 patients. Left ventricular angiography showed small inferolateral aneurysms in all patients. Coronary arteriograms were normal in all 4 patients. Six unstable VTs (cycle length, 200 to 305 ms) and 1 stable VT (cycle length 370 ms) were reproducibly induced in the 4 patients. During SR, endocardial mapping was normal in all 4 patients, and epicardial mapping showed fragmented and late potentials in the left inferolateral wall anatomically consistent with the left ventricle aneurysm. During tachycardia, epicardial mapping showed a macroreentrant VT with focal endocardial activation in the patient with stable VT, whereas in 2 patients with unstable VT, a diastolic potential was only recorded and coincided with the late potential in the same area. Epicardial ablation was performed in 3 patients and successfully abolished those VTs. No VT recurred in 2 patients during follow-up of 2 and 9 months. Clinical VT recurred 6 months after the ablation and was successfully ablated in a repeated epicardial ablation in 1 patient. In the remaining patient without epicardial ablation, an implantable cardiac defibrillator was implanted. There were multiple shocks during a follow-up of 31 months. CONCLUSIONS: In patients with normal coronary arteriograms and left ventricle aneurysm, exercise-induced VT with right bundle branch block morphology may have a subepicardial arrhythmogenic substrate, which may be amenable to epicardial ablation.
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10/54. Propagated responses produced by pacemaker stimuli falling within the QRS complex.

    In a patient with idiopathic hypertrophic subaortic stenosis, propagated responses followed testing stimuli (St2) delivered within the wide QRS complexes elicited by driving stimuli (St1). This phenomenon was not seen at all St1-St2 which produced the minimal V1-V2 interval. It appeared at St1-St2 intervals which resulted in the largest difference between St1-St2 intervals, probably because of the marked asymmetry of propagation occurring very early in the cycle. More studies are required to determine whether this was due to a shift of the vulnerable period toward early systole (suigenesis to idiopathic hypertrophic subaortic stenosis) or to more complex types of intraventricular reentry. In other clinical conditions a similar mechanism could explain the multiple responses produced by pacemaker stimuli falling at the end of ventricular depolarization and also by "properly synchronized' low intensity transthoracic electrical discharges.
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