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 64-year-old female, with multiple previous hospitalizations for acute heart failure, was admitted for shortness of breath, peripheral edema, and increasing abdominal size in her local hospital emergency department with subsequent hospitalization. She had a history of idiopathic dilated cardiomyopathy with severe biventricular systolic dysfunction, secondary severe mitral and tricuspid regurgitation, and permanent atrial fibrillation. As part of the sequence of heart failure therapies, the patient also had a previous implant of an ICD for primary prevention 5 years before.\nDuring hospitalization, the patient developed diverse infectious complications which contributed to a slow resolution of acute heart failure, with the need of many days of inotropic and vasopressor support and subsequent suboptimization of heart failure therapy. As the patient was recognized as having criteria for advanced heart failure, she was referred and transferred to our advanced heart failure center.\nFollowing admission to our hospital, an ECG was performed, showing ventricular paced rhythm with RBBB pattern in V1 through V5 leads and extreme right axis displacement of the mean QRS in the frontal plane clearly indicating an electrical activation from the left ventricle [], which raised suspicion of ICD lead malposition. Chest radiography was performed also showing an abnormal lead path, suggestive of implantation of the lead in the left ventricle []. To confirm our suspicion, our patient then performed a transthoracic echocardiogram, which showed biventricular dilatation with moderate systolic dysfunction, severe mitral and tricuspid regurgitation, and signs of right ventricular pressure overload with plethoric inferior vena cava and abnormal septal motion with systolic “flattening” toward the left ventricle. Peak systolic gradient between the right ventricle and the right atrium was normal, probably underestimated because of right ventricular dysfunction and severe enlargement of the right atrium. However, the implanted ICD appeared to pass through the interatrial septum, with its lead tip in contact with the midsegment of the left ventricular anterolateral wall [-]. Our patient also underwent a transesophageal echocardiogram to better clarify valvular regurgitations and the behavior of the ICD lead at the level of the interatrial septum [-].\nInitially, our patient registered an important decrease in body weight and improvement in symptoms; however, after many days of stay, her hospitalization was complicated with refractory ascites and cardiogenic shock, with fast progression in INTERMACS classification. As our patient reached INTERMACS Level 2, we launched a desperate appeal for cardiac transplantation, as neither extracorporeal membrane oxygenation nor left ventricular assist devices were available at our center at the time. After a couple of days, we got contacted as there was an available heart, and our patient was promptly transferred to our cardiac surgery unit where she underwent successful orthotopic heart transplantation. Analysis of the explanted heart confirmed the presence in the left ventricle of the ICD catheter. Immediate postoperative course was favorable with extubation after 24 h, requiring inotropic support with dobutamine for 2 days with no need for mechanical support. The patient was discharged after 72 days after transplantation, and to this day remains symptom-free with no further hospitalizations.