Polyurethane (PU55D) and copolymer materials have low thermal stability and are highly susceptible to thermal damage during cautery. Implanting physicians should be aware of the lead insulation materials being used during implant procedures and their properties. The use of direct contact cautery on transvenous leads should be minimized to avoid damage to the lead, especially on leads with polyurethane or copolymer outer insulations.

Patients with hypertrophic cardiomyopathy (HCM) and left ventricular (LV) apical aneurysm represent a previously under-recognized but important subgroup within this heterogeneous disease spectrum. Apical aneurysms and the contiguous areas of myocardial fibrosis have been associated with monomorphic ventricular tachycardia (VT) and increased risk for adverse clinical events including sudden cardiac death, prioritizing the application of primary prevention implantable defibrillators. However, VT may be repetitive, thereby raising considerations for additional treatment strategies such as radiofrequency ablation. In this report, we describe such a patient with HCM and apical aneurysm in whom the mapping and ablation procedure was effective in identifying and abolishing the VT focus.

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A 47-year-old man with a past medical history significant for mitral stenosis, status post mitral valve replacement, and intraoperative Maze procedure for paroxysmal atrial fibrillation presented to our institution for heart failure management. He had a nonischemic dilated cardiomyopathy with an ejection fraction of 15%, New York Heart Association class III symptoms, and a left bundle branch block. Subsequently, he underwent implantation of Cardiac Resynchronization Therapy-Defibrillator (CRT-D) system (Guidant Contak Renewal 3 HE, model H177; Boston Scientific) in May 2005. Device interrogations during follow-up revealed thousands of atrial tachycardia response (ATR) episodes secondary to recurrent paroxysmal atrial fibrillation and atypical atrial flutter (AFL). Noncompliant with medical therapy, the patient received an inappropriate shock for an episode of atrial fibrillation with a rapid ventricular response. Atrioventricular (AV) node ablation was performed to avoid further inappropriate shocks and to ensure biventricular pacing. Three months later, the patient received another shock, at which time 69783 ATR episodes had been recorded. The device intracardiac event sequence is shown in Figure 1. Is the event associated with normal device function? DiscussionThe figure shows the stored intracardiac electrograms (EGMs) retrieved after the patient received a defibrillator shock. The three panels are continuous. Panel A shows an AFL with a CL of 220 msec, which is dissociated from a regular ventricular rhythm that has a cycle length (CL) of approximately 700 msec. This rhythm is consistent with the patient's documented clinical AFL with complete heart block and either ventricular pacing or a ventricular escape rhythm. In addition, it should be noted that there is evidence of atrial EGM dropout. Toward the end of panel A, a polymorphic ventricular tachycardia (VT) is initiated. The VT becomes regular and monomorphic in panel B with a CL of approximately 250 msec. During the VT, the CL of the AFL remains unchanged at 220 msec. The rhythm in panel B is consistent with a double tachycardia consisting of both an AFL and a VT. In panel C, it appears that a shock is delivered. The shock converts both the AFL and the VT to sinus tachycardia and a competing, irregular, slow VT. Toward the end of panel C, atrial sensing-ventricular pacing is delivered. The strips appear to be consistent with an appropriate defibrillator shock for VT.However, the confidence of the interpreting physician is challenged when the marker annotations are reviewed in context with the EGMs. The marker annotations in Panel A indicate a ventricular event detected in the VF zone with a cycle length of approximately 250 msec, while the ventricular EGM demonstrates a regular ventricular rhythm with a cycle length of 700 msec. This finding raises the question of whether this recording represents oversensing on the ventricular channel and thus, an inappropriately detected event. In addition, the interval annotation channel in Panel B indicates ventricula...

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For every minute of cardiac arrest, mortality increases by 10%. Still, the variablity of meaningful neurologic survival suggests multiple factors involved in the hypoxia and encephalopathy of cardiac arrest (CA). We studied the cardiac chamber environment during ventricular fibrillation and asystole using direct ultrasound visualization using real-time intracardiac echocardiography (ICE). Four pigs were studied under general anesthesia per protocol. Venous access was obtained for catheter placement within the right heart. A bipolar paciing wire was placed into the right ventricle. A 10 French Acuson ICE catheter was placed into the right atrium using fluoroscopy. Baseline images were obtained. Ventricular fibrillation was induced using direct current energy. 30 minutes of ventricular fibrillation and terminal asystole was observed. Chest compressions were delivered intermittently with direct visualization of effects. Intra-chamber thrombus was quantified by chamber and by arrhythmia. All subjects began to form intracardiac thrombus within 1 minute of ventricular fibrillation. The persistence of sinus rhythm during fibrillation prevented thrombus formation in the atria and the basal portions of both ventricles. The thrombus was predominantly in the right heart within the first 4 minutes of CA. ICE documents that chest compressions completely clear the thrombus when delivered within the first five minutes of CA. Asystole led to more solidified thrombus that was more difficult to clear. Thrombus formation during CA is marked and may be a predominant reason for neurologic damage post resuscitation. Asystole was associated with complete chamber thrombus in comparison to ventricular fibrillation.