Ablation of premature ventricular contraction triggering ventricular fibrillation in a patient with early repolarization syndrome

Early repolarization syndrome is associated with an increased risk of arrhythmic death caused by ventricular fibrillation (VF). VF is usually initiated by premature ventricular contractions (PVCs), and PVCs commonly arise from Purkinje system, the ventricular outflow tract, and papillary muscles. We report the case of a patient with J wave syndromes and recurrent VF, triggered by PVCs originating from the tricuspid annular region. VF was successfully suppressed by catheter ablation of the triggering PVCs, and there has been no recurrence of VF during a follow-up period of 6 months.     

预激综合征合并心房颤动伴快速心室反应蜕变为心室颤动一例

患者男性 ,32岁 ,预激综合征伴阵发性心动过速 10年 (图 1Ａ)。本次发作持续 2ｈ不缓解就诊。急诊体格检查 :血压 80 / 6 0ｍｍＨｇ (1ｍｍＨｇ =0 133ｋＰａ) ,心率 2 4 0次 /ｍｉｎ ,心律绝对不齐 ,心音强弱不等。心电图示ＲＲ间距不等 ,ＱＲＳ波宽大畸形 ,起始部粗钝 ,有δ波 ,ＱＲＳ波形态多变 ,宽窄不一 ,时限最宽 0 2 8ｓ ,心电图诊断为预激综合征合并心房颤动 (房颤 )伴快速心室反应 (图 1Ｂ) ,立即吸氧 ,静脉注射普罗帕酮 70ｍｇ ,2 0ｍｉｎ后房颤未能转复。心室率减慢至 2 10次 /ｍｉｎ ,10ｍｉｎ后心室率达 2 30次 /ｍｉｎ ,患…     

Ventricular fibrillation associated with early repolarization in a patient with thyroid storm

We present a case of a 69-year-old male who was hospitalized for the treatment of thyroid storm due to Grave’s disease, who presented with unexpected ventricular fibrillation (VF). The possible etiology was early repolarization (ER), characterized by J-point elevation in inferior and posterolateral leads, unmasked by the attenuation of beta-adrenergic effect with normalization of thyroid hormones and following the administration of a beta-blocker. Our case focuses attention on the occurrence of VF in a patient with ER during the treatment of hyperthyroidism, which to our knowledge is the first such report.     

Vagal response is involved in the occurrence of ventricular fibrillation in patients with early repolarization syndrome

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Idiopathic ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Ventricular fibrillation in a patient with ventricular preexcitation is usually due to atrial fibrillation with an extremely rapid ventricular rate from which it degenerates. We present a case with Wolff-Parkinson-White syndrome and coexistent idiopathic ventricular fibrillation. The patient, a 23-year-old male, had had a cardiac arrest four years earlier. In electrophysiological study, the accessory pathway was located in the left posteroseptal region and successfully eliminated with radiofrequency catheter ablation. After the ablation procedure, ventricular fibrillation was induced with programmed ventricular stimulation. A dual chamber implantable cardioverter defibrillator was implanted in the patient.     

Onset of atrial fibrillation during antidromic tachycardia: Association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic evaluation in an 18 year old youth with the Wolff-Parkinson-White syndrome who had a sudden cardiac arrest while playing racquetball revealed two types of paroxysmal reciprocating tachycardia: (1) A normal QRS tachycardia with a short ventriculoatrial (V-A) interval fulfilled the criteria for reentry within the atrioventricular (A-V) node; and (2) a wide QRS tachycardia with a QRS configuration of maximal preexcitation was demonstrated to be the result of an antidromic mechanism.During laboratory study, the wide QRS tachycardia spontaneously degenerated into atrial fibrillation. In the basal state, the shortest R-R interval between preexcited QRS complexes was 270 ms, but after infusion of isoproterenol (1.6 μg/min intravenously), the shortest R-R interval became 180 ms. Consequently, this electrophysiologic study suggested that evolution of antidromic reciprocating tachycardia into atrial fibrillation with a rapid ventricular response during exercise-induced catecholamine release may have been the mechanism for ventricular fibrillation in this patient.     

Several aspects of early ventricular repolarization syndrome

An epidemiological study was undertaken to examine the prevalence of the early ventricular repolarization syndrome (EVRS) among 3,105 subjects. An analysis was made of 796 ECG showing EVRS. The genesis of EVRS was interpreted in terms of vector-scalar and chronotopographic analyses of myocardial de- and repolarization. The syndrome was also characterized from clinical and electrophysiological points of view.     

Sotalol prevents atrio-ventricular tachycardia but not atrial fibrillation with rapid ventricular response in a patient wiht WPW syndrome

We present a case of 23-year-old male with the Marfan syndrome multiple accessory pathways and atrio-ventricular reentry ant tachycardia (AVRT) as well as atrial fibrillation (AF). Sotalol was partially effective for AVRT, however, it did not prevent AF, RF ablation cured all arrythmias. This case shows that sotalol can attenuate AVRT recurrences, however, it does not prevent rapid conduction via accessory pathways during AF.     

Swallowing induced atrial tachycardia and fibrillation in a patient with a Wolf-Parkinson-White syndrome

A 56-year-old man with the Wolf-Parkinson-White (WPW) syndrome (type A) is described. His presenting signs were paroxysmal atrial tachycardia and fibrillation induced by swallowing. This supraventricular tachyarrhythmia (SVT) could be abolished by performing the valsalva maneuver or carotid stimulation, and prevented only by treatment with amiodarone.     

Double tachyarrhythmia: left anterior fascicular ventricular tachycardia associated with atrial flutter and fibrillation. Report of a case

A patient with episodes of palpitation in whom the electrocardiogram showed a right bundle branch (RBBB) configuration and right axis deviation underwent electrophysiologic study and radiofrequency ablation. Left ventricular endocardial mapping during ventricular tachycardia (VT) identified the earliest ventricular activation in the anterolateral wall of the left ventricle. The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 47 mseg, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. The stimulus to QRS time was equal to the Purkinje potential-QRS time. Several radiofrequency lesions were applied in this region, one of them resulted with termination of the tachycardia. Following delivery of this lesion the ventricular tachycardia couldn't be induced either at baseline or during isoproterenol infusion. During VT, atrial fibrillation and atrial flutter were observed, cardioversion was performed reverting to sinus rhythm.     

Spontaneous right ventricular outflow tract tachycardia in a patient with Brugada syndrome

We report the case of a 28-year-old man with no structural heart disease, who exhibited clearly augmented ST segment elevation in the right precordial leads, followed by induction of spontaneous right ventricular outflow tract tachycardia with intravenous administration of Class IA antiarrhythmic drugs. The electrophysiologic mechanism of this tachycardia was thought to be triggered activity due to delayed afterdepolarizations. Due to the existence of substrates that were similar to Brugada syndrome combined with right ventricular outflow tract tachycardia, this case may represent a subtype of Brugada syndrome.