Why the study?
The mechanism underlying pacemaker-mediated tachycardia following the loss of capture in one lead of a dual LV-lead tri-ventricular CRT-D was evaluated.
Key points are not available for this paper at this time.
Population
One 73-year-old gentleman with dilated cardiomyopathy, LBBB, and LVEF of 20%
Design
Case report
Follow-up
12 years after implant
A 73-year-old gentleman with dilated cardiomyopathy, left bundle branch block and a left ventricular (LV) ejection fraction of 20% was implanted with two LV leads in a tri-ventricular cardiac resynchronisation therapy defibrillator (CRT-D) trial. As a part of the trial he was programmed with fusion-based CRT therapy with dual LV lead only pacing. The patient presented to local heart failure service 12 years after implant, after a positive response to CRT therapy, with increase in fatigue, shortness of breath and bilateral pitting oedema. The patient sent a remote monitoring transmission that suggested loss of capture on one of the LV leads. This coupled with atrial ectopics was producing a high burden of pacemaker-mediated tachycardia (PMT) that was not seen when both LV leads had been capturing. What is the mechanism for this? Dual LV-lead tri-ventricular leads have been shown to have variable improvements in CRT response but with an increased complexity of implant procedure. This is the first case report of PMT-induced heart failure exacerbation in a tri-ventricular device following loss of LV capture of one lead.
No takes yet. Share an insight, caveat, or question.
Monkhouse et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: