Cases reported "Ventricular Fibrillation"

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1/77. Development of ventricular fibrillations with different characteristics in the local electrocardiogram: large and small amplitude of activation, and its implication for implantable cardioverter defibrillator treatment.

    An implantable cardioverter defibrillator (ICD) was implanted in 2 patients with ventricular tachyarrhythmia related to old myocardial infarction, and defibrillation tests were attempted at the time of ICD implantation and at 2 or 4 weeks after the operation. ventricular fibrillation (VF) was induced by T-wave shocks, but the amplitude of the ventricular electrogram was different in each VF. In most of the VFs with large ventricular electrograms, the local activity was appropriately detected. However, many undersensed beats were observed in other VFs that had fine ventricular electrograms and a longer time was needed before delivering the shock. The amplitude of the ventricular electrogram might be small in some cases of VF and this might result in undersensing and/or unsuccessful defibrillation. Close attention must be paid to the amplitude of ventricular activation in each VF to avoid possible difficulty in ICD therapy.
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2/77. ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a brugada syndrome variant?

    Recurrent ventricular fibrillation was observed in a 29-year-old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate-dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high-risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice.
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3/77. brugada syndrome characterized by the appearance of J waves.

    We describe a patient with brugada syndrome. The ST-segment elevation in precordial leads was revealed during admission, but the appearance of J waves was characteristic before ventricular fibrillation (VF), rather than ST-segment elevation. J waves have been reported to be associated with the presence of an Ito-mediated prominent action potential notch in the epicardium. It is considered that one of the mechanisms of this VF is due to heterogeneous distribution of the refractory period according to changes in K channels including Ito.
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4/77. ST segment and T wave alternans in a patient with brugada syndrome.

    We describe a patient with brugada syndrome in whom J point and ST-segment elevation in leads V1 and V2 were augmented by atrial pacing and intravenous administration of propranolol or cibenzoline. Significant T wave alternans with a 2:1 appearance of terminal negative T wave was observed in the absence and presence of atrial pacing after the administration of cibenzoline. The cellular mechanism responsible for T wave alternans, beat-to-beat appearance of terminal negative T wave and augmented J point and ST-segment elevation is discussed.
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5/77. Dangerous impact--commotio cordis.

    Sudden death following blunt chest trauma is a frightening occurrence known as 'commotio cordis' or 'concussion of the heart'. It is speculated that commotio cordis could be caused by ventricular fibrillation secondary to an impact-induced energy that was transmitted via the chest wall to the myocardium during its vulnerable repolarization period. We describe a survivor of commotio cordis caused by a baseball. In this patient, an initial ventricular fibrillation was documented and converted by direct current defibrillation. Serial electrocardiographic changes (bifascicular conduction block and T wave inversion in precordial leads) were noticed in this patient. Our case suggested that coronary vasospasm might also play a role in commotio cordis.
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6/77. Clinical characteristics of patients with spontaneous or inducible ventricular fibrillation without apparent heart disease presenting with J wave and ST segment elevation in inferior leads.

    INTRODUCTION: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. methods AND RESULTS: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. CONCLUSION: These characteristics were very similar to those of patients with brugada syndrome. These three patients with these specific features might have a variant of brugada syndrome.
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7/77. 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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8/77. syncope in pharmacologically unmasked brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

    A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.
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9/77. catheter ablation of a monofocal premature ventricular complex triggering idiopathic ventricular fibrillation.

    A 62 year old man was admitted for evaluation of recurrent episodes of syncope. A surface ECG showed frequent repetitive premature ventricular complexes of right ventricular outflow tract origin. ventricular fibrillation was inducible by programmed electrical stimulation but otherwise cardiac evaluation was unremarkable. A diagnosis of idiopathic ventricular fibrillation was made and an implantable cardioverter-defibrillator (ICD) was installed. However, spontaneous ventricular fibrillation recurred, requiring repeated ICD discharges. The ventricular fibrillation was reproducibly triggered by a single premature ventricular complex with a specific QRS morphology. Radiofrequency catheter ablation was carried out to eradicate this complex. No ventricular fibrillation has developed after this procedure, and the patient does not require drug treatment.
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keywords = frequency
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10/77. Inappropriate discharges from an intravenous implantable cardioverter defibrillator due to T-wave oversensing.

    This report describes the clinical management of 2 patients with ventricular fibrillation (VF) who received inappropriate shocks from an implantable cardioverter defibrillator (ICD) due to T-wave oversensing. Cardiac sarcoidosis was confirmed as the underlying heart disease in 1 patient and idiopathic dilated cardiomyopathy in the other. Within 2 months after ICD implantation, both patients received several inappropriate shocks during sinus rhythm. Stored electrograms showed decreased R-wave amplitudes and increased T-wave amplitudes. The ICD sensed both R- and T-waves as ventricular activation, which met the rate criteria for VF treatment. Reprogramming the sensing threshold in association with administration of a drug to slow the heart rate decreased the incidence of the inappropriate shocks in both patients, but these palliative measures did not completely suppress the inappropriate shocks. To avoid T-wave oversensing, the repositioning or adding of a sensing lead is required. The potential risk of T-wave oversensing in ICD patients who have small R-wave amplitudes should be recognized.
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