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 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.