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 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.