A 62-year-old man was afflicted with implantable cardioverter defibrillator (ICD) shocks during sinus rhythm. Stored ICD data revealed that sensing of noise due to fracture of the ventricular lead triggered the delivery of shocks. Since the lead fracture developed suddenly, it is suggested that close, early attention should be paid to the potential of such events during follow-up of ICD leads.
In a patient with sustained ventricular tachycardia (VT), we observed two different conduction times through the reentry circuit at the critical paced cycle length. The cycle length of the VT was 420msec and overdrive pacing initially performed at a paced cycle length of 400msec and repeated at decrements of 10msec until the VT was interrupted at a paced cycle length of 320msec. During rapid pacing, constant fusion and progressive fusion were confirmed. The first post-pacing return cycle was identical to each paced cycle length. The conduction time between the stimulus artifact and the orthodromically captured electrogram at the left ventricle was constant at 350msec in each paced cycle length. However, only at a pacing cycle length of 360msec two conduction times were alternatively observed, one of 350msec and the other of 365msec. When the conduction time changed from 350msec to 365msec, morphological alternation both in the surface QRS complex and in the orthodromically captured electrogram was evident. Dual slow pathways or a single slow pathway with plural exits from the reentry circuit is a likely mechanism of the alternation.
The effects of adrenergic activity and beta-blockade were studied in a canine experimental model of type-3 long QT syndrome (LQT3) induced by application of anthopleurin-A.Boluses of epinephrine at 0.5 and/or 1.0 microg/kg were administered before and after propranolol, 0.3 mg/kg, and the distribution of the ventricular repolarization and the development of polymorphic ventricular tachyarrhythmia (VA) were assessed. Using needle electrodes, transmural unipolar electrograms were recorded across the left ventricle (LV) and right ventricle (RV). Activation-recovery interval (ARI) was measured in each electrogram to estimate local repolarization during RV pacing at the cycle length of 750 ms after the creation of complete atrioventricular block. Before propranolol, epinephrine, 0.5 microg/kg, did not induce VA in any experiment. However, a dose of 1.0 microg/kg induced polymorphic VA following multiple premature ventricular complex (PVC) in four of six experiments. Epinephrine, 0.5 microg/kg, shortened ARI at all sites and lessened LV transmural ARI dispersion. Neither ARI nor its dispersion could be determined after 1.0 microg/kg of epinephrine because of the induction of PVC, polymorphic VA, or both. Propranolol (i) prevented epinephrine-induced PVC and polymorphic VA in all experiments, (ii) slightly prolonged ARI at all sites, along with a decrease in LV transmural ARI dispersion, and (iii) reversed the epinephrine-induced shortening of ARI.In this LQT3 model, an increase in adrenergic activity by epinephrine had dose-dependent, opposite effects on ventricular electrical stability. Since beta-adrenergic blockade suppressed epinephrine-induced PVC and polymorphic VA, it might be considered for supplemental therapy to suppress VA in patients presenting with LQT3.
Ventricular fibrillation associated with coronary vasospasm developed 8 h after successful radiofrequency (RF) ablation of the right accessory pathway in an 81-year-old male. A segment of the coronary vasospasm was located close to the accessory pathway, where seven RF ablations had been applied. Although rare, physicians should carefully consider the risk of such events when an RF current is applied near a coronary artery.
We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low‐voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted >30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.
Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the J-point (ST(J)), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated ST(J) by > or = 0.1 mV. Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented ST(J) by > or = 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.
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