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 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.