A 59-year-old man with a history of chronic obstructive pulmonary disease presented to the emergency room with severe sinus bradycardia and hypotension. Due to his history of recurrent dizziness and presyncope, prior work up with Holter cardiac event monitor showed predominant sinus bradycardia with no evidence of chronic incompetence and no clear correlation of his symptoms to the bradycardia episodes. His most recent echocardiogram showed normal left ventricular systolic function and wall motion. Myocardial perfusion study done for recurrent chest pain showed normal myocardial perfusion and normal ejection fraction on Gated SPECT. Tilt table test was markedly abnormal consistent with severe dysautonomia. His baseline blood pressure was 113/70 mmHg, and his HR was 49 beats per minute. Only two minutes into the test, his blood pressure dropped to 60/29 mmHg while his heart rate remained at 47 bpm. The patient was offered pacemaker therapy after his abnormal tilt table test but he refused.\nA few weeks later, the patient presented to the emergency room with syncope. Initial ECG showed severe sinus bradycardia, heart rate in the low 40 s with normal PR interval, and left anterior fascicular block. He was hypotensive and diaphoretic. He denied any chest pain, pressure, or tightness. There were no significant signs of cerebral hypoperfusion. The patient was not on any bradycardia-inducing medications, and initial blood work showed no reversible cause of his severe sinus bradycardia.\nThe patient was started on intravenous fluid hydration, and a bedside echocardiogram was obtained. Echocardiogram showed normal biventricular systolic function and no significant valvular abnormalities. Atropine was given but resulted in minimal, transient improvement in his heart rate to the low 50 s. The systolic blood pressure remained below 80 mmHg. Dopamine followed by norepinephrine drips were administered, and the patient was sent to the electrophysiology laboratory for dual-chamber permanent pacemaker therapy.\nDuring implantation of a permanent pacemaker, the right atrial lead was appropriately placed via the left subclavian vein into the right atrial appendage. However, the ventricular lead was placed via the subclavian artery into the left ventricular cavity. He was admitted to the hospital overnight and a chest X-ray was obtained the next day, showing no evidence of pneumothorax (Figure ). Surprisingly, his ECG showed atrial pacing with long AV delay and intermittent ventricular pacing with the paced ventricular beats showing right bundle branch block morphology contrary to the expected left bundle branch block morphology seen when the lead is inside the right ventricular cavity (Figure ). A limited bedside Echo was obtained that showed the ventricular lead clearly crossing the aortic valve to the left ventricular cavity and fixed into the inferolateral wall of the left ventricle (Figure ). Early recognition of this serious pacemaker implantation complication led to pacemaker revision the same day with extraction of the arterial lead and reinsertion of the ventricular lead via the left subclavian vein into the right ventricular cavity (Figure ). The pacemaker revision went uncomplicated.
A 63 year old male with history of ischemic cardiomyopathy and single chamber ICD with a dual coil active fixation lead implanted twelve months prior to presentation, underwent routine echocardiography identifying the lead localized in the aortic root and crossing the aortic valve. The proximal coil was adjacent to the right coronary cusp. The patient had recurrent gastrointestinal bleeding prohibiting long term anticoagulation therapy. Considering the thromboembolic risk of arterial lead placement and concern for adhesion near the ostium of the right coronary artery, we opted to proceed with transarterial lead extraction. Under general anesthesia and in the hybrid operating room, the subpectoral pocket was exposed. Thoracic aortic arch and carotid angiography was performed, and distal embolic filter wires were deployed in the right and left internal carotid arteries following anticoagulation with unfractionated heparin. Intravascular ultrasound of the left subclavian artery was performed to localize the lead entry point at the left subclavian artery and determine appropriate reference vessel sizing for stent graft placement. As the lead was withdrawn, a covered stent was deployed at the entry site as described previously. There were no neurological or vascular complications following the procedure. Reimplantation of a cardiac resynchronization device was performed electively via the left subclavian vein without any complications.