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 23-year-old female with Ebstein's anomaly of tricuspid valve underwent one and half ventricular repair with tricuspid valve annuloplasty, atrial septal defect closure and cavopulmonary anastamosis of right superior venacava to the right pulmonary artery. She also needed dual chamber pacing for symptomatic bradycardia secondary to sinus nodal and atrioventricular nodal disease. There was no pre-excitation or tachyarrhythmias. Left atrial and left ventricular epicardial leads were connected to a pulse generator that was implanted in epigastric subcutaneous pocket. There was synchronous atrioventricular pacing with acceptable pacing thresholds during the time of implantation. Three months later, new onset symptomatic diaphragmatic pacing was observed from atrial lead. So the pacemaker was reprogrammed to pace ventricle alone. After another two months, diaphragmatic pacing was observed from ventricular lead too. The threshold voltage for ventricular capture was more than that of the diaphragm. The reasons for delayed onset diaphragmatic pacing through both leads almost five months after the epicardial lead placement and pacemaker implantation was not understood. Her symptoms related to bradycardia warranted permanent dual chamber pacing. Since extensive dissections will be needed through the previous surgical scars and adhesions in midline sternotomy and left thoracotomy, a second epicardial lead repositioning was not considered. A minimal incision right anterolateral thoracotomy was made and two introducer sheaths were inserted through two pursestring sutures placed on the right atrial free wall.() Two screw-in endocardial leads were inserted through the sheaths under transesophageal echocardiographic guidance into the right atrial appendage tip and right ventricular apex to achieve atrioventricular pacing. On a follow up of nine months, the patient was asymptomatic, pacing was synchronous and chest X-ray showed both the new and old leads. ()