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    • Early recognition of ICD lead malfunction is desirable to pr

    2019-06-29

    Early recognition of ICD lead malfunction is desirable to prevent the life-threatening consequences of lead failure. Recent reports indicate that the majority of patients with ICD lead failure experience inappropriate ICD therapies, often as the presenting problem [4,6]. GANT61 what Regular device interrogation is mandatory, but impending lead failure commonly remains undiscovered as measurements of lead impedance, sensing, and pacing threshold may be normal even in the presence of defective insulation. Inappropriate electrical discharge may be the first sign of lead failure, and therefore, ICD defibrillation events should be thoroughly evaluated. VENTAK Prizm 2 DR ICDs manufactured prior to 2002 were vulnerable to the development of a short circuit within the device header assembly itself; this was because of the deterioration of the polyimide insulation around the high-voltage ground wire connected to the external lead [11,12]. A high-voltage discharge has the potential to damage the components within the ICD generator and render the case inoperable. The problem in our case was different: the defect in the ICD lead insulation was within the pre-pectoral ICD pocket. This exposed the high-voltage conductor, thereby allowing the development of an electrical short circuit between this conductor and the ICD generator casing. Upon appropriate detection of VF, a high-voltage electrical discharge was transmitted back to the ICD generator casing via the short circuit created by the denuded lead. Fortunately, the patient\'s generator remained capable of delivering a subsequent defibrillation, presumably due to the loss of contact between the lead and the ICD generator can at that moment. Sweeney [13] in 2001 described a similar case in which a short circuit between a denuded ICD lead (Medtronic 6932 lead) and an ICD generator (Medtronic 7271 pulse generator) within a pre-pectoral pocket was revealed by a light flash above the pocket at the time of unsuccessful defibrillation threshold testing. This event was followed by the inability to deliver a further shock despite ongoing VF and the subsequent finding of reduced high-voltage lead impedance. As observed in their case, an appropriate shock unmasked an ICD lead insulation breach.
    Conflict of interest
    Case presentation A 66-year-old man, with a long history of rheumatic GANT61 what disease, valvular cardiomyopathy, and congestive heart failure, underwent a mechanical mitral and aortic valve replacement in 1995. In 2005, an implantable cardioverter defibrillator (ICD) was implanted because of nonsustained ventricular tachycardia (VT) and a reduced left ventricular function (left ventricular ejection fraction, 30%). In 2010, the patient developed a VT storm refractory to amiodarone, sotalol, lidocaine and beta-blockers, and received multiple ICD shocks. There were at least 3 clinical VTs. VT1 exhibited a right bundle-branch block (RBBB) morphology, northwest axis, and a cycle length (CL) of 560ms; VT2 exhibited an RBBB morphology, right-axis deviation, and CL of 490ms; and VT3 had a left bundle-branch block (LBBB) morphology, right-axis deviation, and CL of 430ms. During the electrophysiological study, the VTs were induced by programmed ventricular stimulation, hence bundle branch reentry was ruled out. Mapping in the coronary veins during VT suggested an epicardial circuit of the tachycardia. Electroanatomical mapping in the epicardium using a NaviStar catheter (Biosense-Webster, Diamond Bar, California) revealed the presence of a wide low-voltage area in the apical region. During the induced VT1 a presystolic potential (PP) was recorded from this area, which preceded the onset of the QRS by 60ms (Fig. 1A). Entrainment pacing with a 9.9V output (1.0ms width) was performed from this site at a CL of 500ms. The surface ECG during entrainment pacing showed some degree of fusion. The interval between the pacing stimulus and onset of the QRS complex (S-QRS) was 160ms, whilst the interval from the electrogram recorded at the pacing site to the QRS onset during the VT (Eg-QRS) was just 60ms. The post-pacing interval (PPI) was 680ms (120ms longer than the VT–CL). A radiofrequency (RF) energy application using open irrigation (30ml/min, 35W) was performed at this site. The VT was terminated 4s after initiation of RF energy delivery (Fig. 1B). During the RF energy application the VT–CL, and interval between the QRS and next PP, gradually extended, and the VT terminated by block between the QRS and PP. The recording at the same site during sinus rhythm demonstrated an isolated delayed potential (IDP) after the QRS. After several additional RF energy deliveries at adjacent sites, both VT1 and VT2 became non-inducible. What is the mechanism underlying this successful ablation at this site with manifest entrainment and a long PPI?