A 63 year old male with history of ischemic cardiomyopathy and single chamber ICD with a dual coil active fixation lead implanted twelve months prior to presentation, underwent routine echocardiography identifying the lead localized in the aortic root and crossing the aortic valve. The proximal coil was adjacent to the right coronary cusp. The patient had recurrent gastrointestinal bleeding prohibiting long term anticoagulation therapy. Considering the thromboembolic risk of arterial lead placement and concern for adhesion near the ostium of the right coronary artery, we opted to proceed with transarterial lead extraction. Under general anesthesia and in the hybrid operating room, the subpectoral pocket was exposed. Thoracic aortic arch and carotid angiography was performed, and distal embolic filter wires were deployed in the right and left internal carotid arteries following anticoagulation with unfractionated heparin. Intravascular ultrasound of the left subclavian artery was performed to localize the lead entry point at the left subclavian artery and determine appropriate reference vessel sizing for stent graft placement. As the lead was withdrawn, a covered stent was deployed at the entry site as described previously. There were no neurological or vascular complications following the procedure. Reimplantation of a cardiac resynchronization device was performed electively via the left subclavian vein without any complications.
A 78 year-old man with a history of paroxysmal atrial fibrillation (AF) presented with syncope and underwent implantation of a dual-chamber Medtronic KDR703 pacemaker while in AF. A Medtronic 4068 ventricular lead was implanted and found to have a threshold of 1.2 Volts (V) at 0.5 ms, a current of 1.8 milliamps and an impedance of 887 ohms. R-wave sensing was noted to be 16.6 mV. A Medtronic 4568 atrial lead was implanted but threshold testing was not performed and sensing was not reported. The pacemaker was programmed to VVIR 60-120.\nTwo months later, the patient developed left upper extremity weakness and a computed-tomography (CT) scan confirmed the clinical diagnosis of a right parietal cerebrovascular accident (CVA). The CVA was attributed to thromboembolism secondary to AF and the patient was initiated on warfarin therapy with a target INR of 2.0-3.0.\nThe patient was referred to our clinic after his ventricular lead was noted to have low impedance and a decrease in sensed R wave amplitude on routine interrogation. The patient's ECG is shown (). The diagnosis of inappropriate lead placement in the LV was suspected on the basis of the paced right bundle branch block (RBBB) pattern noted on this ECG. The diagnosis was confirmed by anterior and lateral chest radiography (). A non-contrast chest CT scan shows the ventricular lead coursing from the right atrium into the left atrium (LA) through an atrial septum defect (ASD) ().\nDevice interrogation revealed a ventricular lead threshold of 1.25 V at 0.4 ms, R wave sensing of 2.8-4.0 mV and a lead impedence of 248 ohms. The patient was in AF during interrogation with a slow, irregular ventricular response. No atrial capture could be demonstrated and no P waves were sensed.\nDue to suspected ventricular lead dysfunction and concern that sudden loss of ventricular pacing would lead to a recurrence of syncope, the patient underwent lead revision. A St. Jude 1688 lead was inserted into the right ventricle under fluoroscopic guidance using anterior and lateral views and the existing atrial lead and LV lead were capped. The patient's warfarin dose was increased to achieve a target INR of 2.5-3.5. The patient was discharged home without event. At the time of this report submission, the patient has had no further TE complications. Given the patient's age and comorbidities, should he experience further TE complications despite appropriate anticoagulation or if he develops an absolute contraindication to warfarin, we would consider percutaneous LV lead extraction with on-site cardiothoracic surgery back-up.