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 71-year-old female patient who was diagnosed as “rheumatic valvular heart disease, mitral stenosis and insufficiency” underwent mitral valve replacement in our thoracic surgery department two years ago. After the operation, amiodarone (0.2 mg bid) was administrated to the patient for a long time because of paroxysmal atrial fibrillation. Four days before admission, she suffered from dizziness without syncope or amaurosis, and then came to our emergency room. Electrocardiogram (ECG) indicated atrial fibrillation with slow ventricular rates (37–38/min). Cardiac ultrasound demonstrated postoperative state of mitral valve replacement, enlargement of left atria and mild reflux of pulmonary valve. A temporary pacemaker was implanted before admission. The patient was diagnosed as “rheumatic valvular heart disease, postoperative state of mitral valve replacement, atrial fibrillation with slow heart rate, the state of temporary pacemaker implantation, chronic heart failure (NYHA IIclass), and diabetes”.\nAmiodarone was discontinued after admission. One week later, we regulated the rhythm of patient’s temporary pacemaker to 30/min. ECG monitor suggested the occurrence of significant sinus bradycardia with atrio-ventricular junctional escape beat, and occasionally with pacing rhythm. Considering the degradation of patient’s sinuatrial node and atrioventricular node, a permanent dual-chamber pacemaker was prepared to be implanted. During the course of operation, patient suffered from chest distress, dyspnea, lung rales, and rapid atrial flutter in ECG, which suggested the aggravation of heart failure. After the treatment of oxygen, morphine (5 mg iv), and furosemide (20 mg iv), the patient was getting better. After operation, excess bleeding was found on the puncture site. Considering the severity of patient’s disease and poor operation endurance, a single-chamber pacemaker (PhilosIISR, BIOTRONIK Company) was chosen to take place of dual-chamber pacemaker after contacting with patient’s relatives. Parameters settings of the single-chamber pacemaker were demonstrated as follows: the threshold of ventricular pacing was 0.8 V (0.5mS); the amplitude of R wave was 30.1mv; and the electrode impedance was 856Ω.\nBoth pacemaker function and Holter indicated favorable behavior of the pacemaker after the operation, and stitches were taken out one week later. Nine days later, the reexamination of cardiac ultrasound demonstrated as follows: postoperative state of mitral valve replacement, normal artificial biological mitral valve, enlargement of left atria, mild reflux of aortic valve, mitral valve flow spectrum showing a single peak, and pacemaker in ascending aorta and left ventricle (Fig. ). Chest computed tomography (CT) scan indicated that the pacemaker electrode was put into aorta and left ventricular (Fig. ), which suggested that the pacemaker had been put into subclavian artery by mistake and the pacing electrode was implanted in the left heart.\nTraditional right ventricular apical pacing belongs to unphysiological pacing, while the most studied physiological pacing regions include right ventricular outflow tract (RVOT) and septum, which can improve patients’ heart function [, ]. However, various complications may appear during the course of RVOT and right ventricular septum pacing and increase the risk of operation, such as high threshold of pacing, difficult fixation and location of pacing leads, long-duration operation, easy dislocation, and even the cardiac perforation etc. [–]. Cardiac resynchronization therapy (CRT) has been widely applied in clinics to conduct left ventricular epicardial pacing via coronary sinus currently. However, it is difficult to conduct left ventricular endocardial pacing via the puncture site of atrial septum because of the occurrence of side-effects, such as high risk of thromboembolism, impact on the function of mitral valve, and myocardial damage caused by taking out the pacemaker. Therefore, we reported a case that pacemaker was implanted into left ventricle by mistake which made unnecessary troubles to our doctors.\nIn this case, patient’s diagnosis was definite. On October 6, 2014, a cardiac permanent pacemaker was implanted because the patient was suffering from atrial fibrillation and atrial flutter with sinus bradycardia (30-40/min). The reexamination of cardiac ultrasound demonstrated that the pacing leads were put into left heart, which suggested that pacing electrode was implanted into left ventricle via subclavian artery by mistake. The reasons included: 1) during the course of operation, patient’s heart function aggravated suddenly. Excess bleeding was observed after we performed a puncture on her subclavian artery by mistake. However, we regarded the excess bleeding and the increase of blood pressure as the results of the rise of central venous pressure caused by the aggravation of heart failure. Moreover, acute heart failure could result in hypoxia, which made troubles in recognizing whether the blood was from artery or vein; 2) after the pacing leads were implanted, the fluoroscopy should have been conducted in post-anterior view, 45-degree left anterior oblique view and 30-degree right anterior oblique view, respectively []. However, after the occurrence of chest distress, drugs were administrated to treat acute heart failure immediately, which also induce the operator to shorten the duration of operation. In addition, angiography has not been performed to confirm the location of pacing leads, and multiple body position fluoroscopy wasn’t conducted as well after the implantation of pacing electrode, while post-anterior view scanning during the course of operation couldn’t confirm the location of pacing electrode accurately (Fig. ); 3) it was easy to locate the passive electrode in traditional right ventricular apical pacing. In addition, the temporary pacing is implanted in the right ventricular apex generally, which is relatively helpful to locate the passive electrode in the right ventricular apex also. However, in our operation, the active electrode was used and prepared to implant into ventricular septum, which was difficult to locate. And it was hard to be located with the reference of the temporary pacemaker, which was normally positioned in the right ventricular apex. Therefore, we unfortunately mistook left ventricle for right ventricular low septum, and then the pacing electrode was implanted into left ventricle; 4) the electrocardiogram (ECG) after the pacemaker implantation is helpful in locating pacemaker. For example, the left bundle-branch block showed in ECG is common seen in right ventricular paced patients (Fig. ), while the right bundle-branch block in left ventricular paced patients. In this case, the patient suffered a sudden heart failure. The ECG suggested rapid atrial flutter without any pacemaker signal (Fig. ). Therefore, it was unable to evaluate the position of the lead through ECG.