A 79 year old male with history of sick sinus syndrome associated with frequent syncopal events underwent dual lead pacemaker implantation with atrial and ventricular active fixation leads. Six months post implant he experienced acute inferolateral ST-segment elevation myocardial infarction complicated by cardiogenic shock and underwent successful primary percutaneous revascularization. During diagnostic coronary angiography the angiographic catheters were identified to engage the previously implanted pacemaker leads. Inadvertent positioning of the atrial and ventricular leads via the left subclavian artery to the right coronary cusp and left ventricular apex, respectively, was confirmed with detailed fluoroscopy and selective subclavian angiography. Pacemaker interrogation confirmed lack of atrial capture and normal ventricular sensing and capture thresholds. Following revascularization, the patient had an uneventful hospital course and was discharged on appropriate medical therapy including antithrombotic therapy with aspirin and thienopyridine. Warfarin was not instituted due to persistent anemia and requirement of dual antiplatelet therapy.\nGiven the high risk position of the atrial lead tip in close proximity to the right coronary artery ostium, the patient was electively admitted one month later for transarterial lead removal. Under general anesthesia and in a hybrid operating theater and catheterization laboratory, vascular access was obtained in the right and left femoral arteries and right femoral vein. Prior to systemic anticoagulation, the left subpectoral pocket was opened under sterile conditions, and the subcutaneous tissue was carefully dissected until the leads were visible and freed. Venipuncture was performed using the Seldinger technique, and the left axillary vein was accessed. Two active fixation pacemaker leads were implanted in the right ventricular outflow tract and the right atrial appendage, respectively. Fluoroscopy and aortography were performed demonstrating the dual pacemaker system (). Aortic arch angiography demonstrated a type 1 arch and no significant disease in the origin of the great vessels. Using 5-French diameter, 90 cm length guiding sheaths, the right and left common carotid arterieswere selectively engaged over a guidewire. Carotid angiography revealed nonobstructive disease in the intracranial and extracranial portions bilaterally. Unfractionated heparin was administered to achieve an activated clotting time of approximately 350 seconds. A distal embolic filter wire (Spider, EV3 Inc., Plymouth, MN)was then deployed in the distal segment of the both internal carotid arteries. Selective left subclavian angiography was then performed, confirming the pacemaker leads entry point in the subclavian artery, but no critical subclavian arterial stenosis. Unfractionated heparin was administered to achieve an activated clotting time of approximately 350 seconds.\nStylets were then advanced through the chronic transarterial leads, and after retracting the active fixation mechanism, gentle traction on the ventricular lead enabled withdrawal without requirement of laser extraction. Similarly, the atrial lead was manually withdrawn from the aortic root, and both leads were carefully pulled back until the tips were in close proximity to the insertion site of the subclavian artery. Over an antegradeguidewire, intravascular ultrasound was performed to ensure appropriate sizing for an 8mm x 60 mm self-expanding nitinol covered stent (Viabahn, W.L. Gore, Flagstaff, Arizona) placement. The stent was delivered and positioned between the proximal and distal insertion site margins and deployed immediately as the leads were withdrawn (). Angiography confirmed adequate stent expansion and no contrast extravasation. The distal embolic protection devices were subsequently withdrawn. Following the procedure, the patient remained hemodynamically stable, and recovery was uneventful without neurological or vascular 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.