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.
We report the case of a 65-year-old man affected by dilated cardiomyopathy associated with severe mitral valve regurgitation, recently treated by 2 MitraClip System devices (Abbott Vascular, Lake Bluff, IL) implantation. Three months after valve repair, the patient underwent to dual-chamber defibrillator implantation because the persistence of seriously dilatation and marked systolic impairment of the LV (ejection fraction = 30%) with mild mitral valve regurgitation. The patient performed a predischarge electronic check of the device that showed its normal function. He came to our observation, 2 months later, for marked deterioration of the dyspnea, despite his strict compliance to medical therapy. At this time, the 2-dimensional (2D) echocardiographic examination showed malposition of the shock lead that appeared placed in the apex of the LV through an iatrogenic atrial septal defect (ASD) persisted after the percutaneous valve repairing procedure, previously performed (Fig. A); the LV appeared markedly dilated and presented a severe systolic dysfunction (ejection fraction = 30%). The echocardiographic color-Doppler view showed a moderate mitral valve regurgitation and a significant mitral valve stenosis attested by an accelerated transvalvular diastolic flow (Fig. B). The transesophageal 3-dimensional-echocardiographic short axis view on mitral annulus showed a normal implantation of the MitraClip devices on the edges of mitral valve leaflets and a noncontinuity solution between MitraClip devices and the defibrillator lead (Fig. ). The 12-lead standard electrocardiogram (ECG) showed normal sinus rhythm to 67 bpm and its record during the pacing threshold test bared a right bundle branch block (RBBB) pattern of the QRS complex (Fig. A). Chest X-ray documented a very lateral position of the defibrillator lead (Fig. A). Oral anticoagulation therapy with adjusted-dose warfarin was directly started and, after obtaining the patient's informed consent, a mechanical lead extraction with subsequently lead repositioning in the right ventricle (RV) was performed 3 weeks later. The patient was discharged in good clinical condition and the 12-lead ECG and the chest X-ray, performed in the predischarge phase, confirmed the right position of the defibrillator lead, respectively, showing a left and superior direction of the QRS complex axis, during ventricular pacing (Fig. B) and a conventional position of the lead in the apex of the RV (Fig. B). The predischarge echocardiographic examination showed left ventricular systolic dysfunction (ejection fraction 34%) with mild mitral valve regurgitation and a not relevant velocity of trans-mitral diastolic flow. The follow-up performed 1 month after discharge was uneventful. Ethical approval for this paper was not required by the Ethics Committee of our institute, as it is a case report. The patient provided informed consent for this report and his medical data have been anonymized.