Abstract

Implantable cardioverter defibrillator (ICD) lead malfunction has been reported after left ventricular assist device (LVAD) implantation, however the incidence and mechanism are not known. The mechanism of RV lead malfunction following LVAD implantation may be related to changes in LV and RV geometry, rather than decrease in LV mass. In this prospective single center study, we collected ICD lead data before, during and after LVAD implantation, including 12 time points during implantation. Data were collected prospectively on 29 patients, including 24 patients undergoing LVAD implantation (ICD implanted 35±34.9 months earlier) and 5 control patients who had LVAD implanted initially followed by ICD implantation. Of the 24 LVAD patients, 17 were male, 15 had coronary artery disease, 15 had LVAD implanted as destination therapy, and mean age was 57.6±13 years. Fifty-four leads were tested before, during, 1 week and 3 months after LVAD implantation, including 18 right atrial, 24 right ventricular (RV), and 12 left ventricular (LV) leads. In 16 patients, ICD leads were tested at 12 intraoperative steps. RV sensing was >50% decreased from baseline in 6 patients (25%) immediately post-op, with RV sensing improving at 1 week in 3 patients (50%). In 2 patients (8%) who also had decreased sensing, RV pacing threshold was >50% elevated from baseline immediately post-op (n=1) and at 1 week (n=1). One RV pacing threshold returned to baseline at 3 months. Of the 4 patients with significant decreases in RV sensing in whom lead function was tested at serial time points during VAD implantation, an RV sensing decrease was not detected until immediately following weaning off cardiopulmonary bypass. One RV lead was turned off and one was replaced due to non-capture. Time from lead implant to LVAD was 77.6±57.9 months in the patients with decreased RV lead sensing (n=6) vs. 33.3±43 months in patients with no decreased RV sensing (n=18). Post-operatively, 14 (58%) patients had ventricular arrhythmias, new onset in 8 (33%); and 15 (63%) had atrial arrhythmias, new onset in 7 (29%). On ECG, sensed QRS width decreased after LVAD (126.5±36.7 vs. 100±35.5ms). Of the 5 control patients, none had >50% decreased RV sensing and 1 had >50% elevation in pacing threshold from the day of implant to 1 year post-implant. Of 29 patients, 6 died (4.9±6.8 months) and 1 underwent cardiac transplant (3 months). ICD lead malfunction can occur following LVAD implantation, but may improve over time. Intraoperative RV sensing problems were not detected until weaning of cardiopulmonary bypass, suggesting the mechanism of RV lead malfunction may be related to changes in LV and RV geometry from LVAD implantation. Ventricular arrhythmias are common in the LVAD population, even in patients who did not have them pre-operatively.

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