A 64-year-old female, with multiple previous hospitalizations for acute heart failure, was admitted for shortness of breath, peripheral edema, and increasing abdominal size in her local hospital emergency department with subsequent hospitalization. She had a history of idiopathic dilated cardiomyopathy with severe biventricular systolic dysfunction, secondary severe mitral and tricuspid regurgitation, and permanent atrial fibrillation. As part of the sequence of heart failure therapies, the patient also had a previous implant of an ICD for primary prevention 5 years before.\nDuring hospitalization, the patient developed diverse infectious complications which contributed to a slow resolution of acute heart failure, with the need of many days of inotropic and vasopressor support and subsequent suboptimization of heart failure therapy. As the patient was recognized as having criteria for advanced heart failure, she was referred and transferred to our advanced heart failure center.\nFollowing admission to our hospital, an ECG was performed, showing ventricular paced rhythm with RBBB pattern in V1 through V5 leads and extreme right axis displacement of the mean QRS in the frontal plane clearly indicating an electrical activation from the left ventricle [], which raised suspicion of ICD lead malposition. Chest radiography was performed also showing an abnormal lead path, suggestive of implantation of the lead in the left ventricle []. To confirm our suspicion, our patient then performed a transthoracic echocardiogram, which showed biventricular dilatation with moderate systolic dysfunction, severe mitral and tricuspid regurgitation, and signs of right ventricular pressure overload with plethoric inferior vena cava and abnormal septal motion with systolic “flattening” toward the left ventricle. Peak systolic gradient between the right ventricle and the right atrium was normal, probably underestimated because of right ventricular dysfunction and severe enlargement of the right atrium. However, the implanted ICD appeared to pass through the interatrial septum, with its lead tip in contact with the midsegment of the left ventricular anterolateral wall [-]. Our patient also underwent a transesophageal echocardiogram to better clarify valvular regurgitations and the behavior of the ICD lead at the level of the interatrial septum [-].\nInitially, our patient registered an important decrease in body weight and improvement in symptoms; however, after many days of stay, her hospitalization was complicated with refractory ascites and cardiogenic shock, with fast progression in INTERMACS classification. As our patient reached INTERMACS Level 2, we launched a desperate appeal for cardiac transplantation, as neither extracorporeal membrane oxygenation nor left ventricular assist devices were available at our center at the time. After a couple of days, we got contacted as there was an available heart, and our patient was promptly transferred to our cardiac surgery unit where she underwent successful orthotopic heart transplantation. Analysis of the explanted heart confirmed the presence in the left ventricle of the ICD catheter. Immediate postoperative course was favorable with extubation after 24 h, requiring inotropic support with dobutamine for 2 days with no need for mechanical support. The patient was discharged after 72 days after transplantation, and to this day remains symptom-free with no further hospitalizations.
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.