A 75-year-old caucasian male patient with a diagnosis of dilative cardiomyopathy (echocardiographic biplane ejection fraction (EF) 23%) had sinus rhythm with left LBBB ECG (Figure a-b) (QRS with 136 ms) and a profound dyssynergic contraction profile. There was a history of Diabetes Typ II, hypertension and mild renal insufficiency (serum creatinine 1.63 mg/dl). Significant coronary artery disease had been excluded by angiography. Currently, he suffered from New York Heart Association (NYHA) III heart failure status and was admitted for implantation of a CRT – implantable cardioverter defibrillator (ICD). The operative procedure was unremarkable, although some difficulties advancing the right electrode into the right ventricle were reported. Chest X-ray after implantation (Figure a-b) excluded pneumothorax and electrodes appeared well placed. The patient was discharged one day after the procedure when the pacing ECG showed a narrowed QRS complex (Figure c-d) with optimal values of all three electrodes (Table ).\nOne month later on follow-up, the patient reported a marked improvement of his exercise capacity (NYHA II). Electrode values remained stable. An unscheduled echocardiogramm (Philips iE33) revealed a marked reduction of left ventricular dimensions with an improved monoplane ejection fraction (51%). However, through the mitral valve leaflets a thick electrode proceeded into the apex of the left ventricle. An additional transesophageal echocardiographic examination demonstrated the coronary sinus (CS) electrode in place (Figure a) but a malposition of the RV electrode passing the patent foramen ovale (PFO) via an Eustachian valve into the left ventricle (3 b-d).\nAfter studying the literature and informing the patient about possible consequences a revision procedure was performed. The RV electrode was easily removed from the left ventricle but could not be safely placed in the right heart without a sheat. A new electrode was advanced and fixed at the base of the right ventricle. Postprocedure chest x-ray (Figure c-d), ECG (Figure e-f), and measurements (Table ) all documented good results. This time a postprocedure echocardiogramm showed an intact mitral valve, persistent good left performance, and the RV electrode within the right heart.\nThis was a clinical study and no experimental work. No ethical committee had to be involved. Everything happened in the compliance with the Helsinki Declaration.
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.