A 76-year-old man with history of ischemic cardiomyopathy and paroxysmal atrial fibrillation who underwent a Dual-Chamber Medtronic Implantable Cardioverter-Defibrillator (ICD) placement 6 years earlier in an outside facility presented to the emergency room with worsening shortness of breath. Initial workup in the emergency room revealed acute on chronic combined congestive heart failure. An AP chest X-ray film was interpreted by the radiologist as cardiomegaly with pulmonary vascular congestion and satisfactory ICD lead position (Figure ). No lateral view was obtained at the time.\nBedside Echo showed severely reduced left ventricular systolic function with dilated right ventricle and moderate-to-severe pulmonary hypertension. Surprisingly, the ICD lead was clearly going from the left atrium through the mitral valve to the left ventricular cavity (Figures , , and ). A lateral chest X-ray view revealed that the ICD shock lead tip is directed posteriorly, indicating its presence in the left ventricular cavity (Figure ). A transesophageal echocardiogram showed the ICD lead went from the superior vena cava to the right atrium, crossing through a small sinus venous atrial septal defect to the left atrium, and into the left ventricular cavity via the mitral valve. Luckily, the patient was on chronic anticoagulant because of chronic atrial fibrillation, so no thromboembolic complications were reported. Interestingly enough, the patient had two prior trans-thoracic echocardiograms that were interpreted by the same cardiologist without mention of abnormal ICD lead placement. Furthermore, prior ICD interrogation reports from his primary cardiologist showed chronically elevated shock lead impedance but pacing threshold and sensing were good. No therapy was needed since device implantation.\nBecause extraction of a chronically implanted ICD lead carries a high risk of major cardiovascular complications (2%-4%) including vascular injury, cardiac perforation resulting in cardiac tamponade, and occasionally thromboembolic complications or even death, and because the patient was chronically anticoagulated, the decision is made to continue conservative management.
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.