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  • At autopsy approximately cm of blood and clots


    At autopsy, approximately 180cm3 of blood and clots were found inside the pericardial cavity. Careful inspection of the AVE 0991 cost showed AVE 0991 cost a deep lesion, 2mm in length, on the antero-lateral aspect of the vessel (Fig. 1) 2cm above the valvular plane (Fig. 2). On the medial aspect of the right atrium, the lead metal extremity was implanted at the base of the auricle on the medial wall. The right atrium was very thin, with an average thickness of 2mm. Histology showed abundant adipose tissue in its context, endocardial fibrosis, and numerous foci of inflammatory infiltration by various elements including lymphocytes and monocytes as well numerous plasma cells and eosinophils, clearly indicating myocarditis that was not recent. The ascending aorta was incised and approximately 2cm above the noncoronary cusp, a pinpoint injury related to the lesion described on the aortic adventia (Fig. 2) was noted.
    Discussion The pathogenetic mechanism underlying this patient׳s death can be explained in the following manner: the active lead (Fig. 1), positioned in the right atrium medial aspect, perforated the thin atrial wall and the lateral aspect of the aortic wall. After aortic perforation, the lead initially remained inside its wall, which explains why the device interrogation revealed satisfactory R-wave sensing (>5mV) and pacing thresholds (<1.0V at 0.5-ms pulse width). The patient eventually underwent DFT to guarantee proper device function. At this point, the active lead, positioned inside the aorta like a cork, slipped out, causing cardiac tamponade. In a review of relevant literature, we identified only five cases [1–5] of atrial damage by a pacemaker lead with concomitant aortic wall perforation, as shown in Table 1. However, not all reports indicate whether the lead responsible for the cardiac laceration was active or passive.
    Conflict of interest
    Introduction Left ventricular pacing (LVP) has been recognized as a rare trigger of ventricular arrhythmias after cardiac resynchronization therapy (CRT) [1]. In general, such events arise early after implantation, while a late occurrence has been reported only once, in a patient with ischemic cardiomyopathy suffering from LVP-induced ventricular tachycardia (VT) storm 7 years after CRT initiation [2]. The pathophysiology of LVP-induced VTs remains controversial. The leading theory relies on enhanced transmural dispersion of repolarization during LVP [3]; recently, a reentrant mechanism involving an epicardial scar was demonstrated in a small group of patients with early electrical storm after CRT onset, in which catheter ablation resulted in complete resolution of the condition and safe CRT resumption [4].
    Case report The patient was affected by dilated cardiomyopathy with an apical aneurysm, severe left-ventricular (LV) systolic impairment, a complete left bundle branch block (LBBB), a chronic total occlusion of the left descending coronary artery, and severe stenosis of the right coronary artery. An atriobiventricular defibrillator had been implanted in 2006 following resuscitation from a cardiac arrest, with a passive fixation, dual-coil implantable cardioverter defibrillator (ICD) lead (Sprint Fidelis®, Medtronic Inc., Minneapolis, MN, US) positioned at the mid-apical right ventricular (RV) septum. After the initial evaluation, which excluded acute ischemia, electrolyte imbalance, and other common transient precipitating factors, stabilization was achieved with sedation and intravenous amiodarone. Subsequently, a recurrence of slower, short NSVTs occurred. Of note, each biventricular stimulation was reproducibly followed by three monomorphic ventricular complexes (Fig. 1A). A VT ablation procedure was scheduled. The procedure was conducted in a fasting state under general anesthesia with mechanical ventilation. The presence of intraventricular thrombus was excluded using echocardiography. The pre-specified procedural end-points were the non-inducibility of sustained monomorphic VTs and substrate modification by means of the elimination of late potentials (LPs). As previously described [5], an LP was defined as an isolated bipolar potential occurring after the end of the surface QRS (either spontaneous or paced), which was separated from the main ventricular potential by an isoelectric tract.