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.
We report the case of a 65-year-old man affected by dilated cardiomyopathy associated with severe mitral valve regurgitation, recently treated by 2 MitraClip System devices (Abbott Vascular, Lake Bluff, IL) implantation. Three months after valve repair, the patient underwent to dual-chamber defibrillator implantation because the persistence of seriously dilatation and marked systolic impairment of the LV (ejection fraction = 30%) with mild mitral valve regurgitation. The patient performed a predischarge electronic check of the device that showed its normal function. He came to our observation, 2 months later, for marked deterioration of the dyspnea, despite his strict compliance to medical therapy. At this time, the 2-dimensional (2D) echocardiographic examination showed malposition of the shock lead that appeared placed in the apex of the LV through an iatrogenic atrial septal defect (ASD) persisted after the percutaneous valve repairing procedure, previously performed (Fig. A); the LV appeared markedly dilated and presented a severe systolic dysfunction (ejection fraction = 30%). The echocardiographic color-Doppler view showed a moderate mitral valve regurgitation and a significant mitral valve stenosis attested by an accelerated transvalvular diastolic flow (Fig. B). The transesophageal 3-dimensional-echocardiographic short axis view on mitral annulus showed a normal implantation of the MitraClip devices on the edges of mitral valve leaflets and a noncontinuity solution between MitraClip devices and the defibrillator lead (Fig. ). The 12-lead standard electrocardiogram (ECG) showed normal sinus rhythm to 67 bpm and its record during the pacing threshold test bared a right bundle branch block (RBBB) pattern of the QRS complex (Fig. A). Chest X-ray documented a very lateral position of the defibrillator lead (Fig. A). Oral anticoagulation therapy with adjusted-dose warfarin was directly started and, after obtaining the patient's informed consent, a mechanical lead extraction with subsequently lead repositioning in the right ventricle (RV) was performed 3 weeks later. The patient was discharged in good clinical condition and the 12-lead ECG and the chest X-ray, performed in the predischarge phase, confirmed the right position of the defibrillator lead, respectively, showing a left and superior direction of the QRS complex axis, during ventricular pacing (Fig. B) and a conventional position of the lead in the apex of the RV (Fig. B). The predischarge echocardiographic examination showed left ventricular systolic dysfunction (ejection fraction 34%) with mild mitral valve regurgitation and a not relevant velocity of trans-mitral diastolic flow. The follow-up performed 1 month after discharge was uneventful. Ethical approval for this paper was not required by the Ethics Committee of our institute, as it is a case report. The patient provided informed consent for this report and his medical data have been anonymized.