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.
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.