Baylor University Medical Center Proceedings April 2017 - 230

Successful treatment of a cardiac resynchronization therapy
nonresponder by identifying lead malpositioning
Karthik Venkatesh Prasad, MD, Krittapoom Akrawinthawong, MD, MSc, Scott Wayne Ferreira, MD, MSE,
and Ali Akbar Mehdirad, MD

This case describes some of the commonly overlooked device-related issues
in patients who have reportedly failed to respond to cardiac resynchronization
therapy (CRT). The case demonstrates voltage-dependent right ventricular
capture instead of right atrial capture by a subtly malpositioned right atrial
lead. CRT therapy failed to improve symptoms of heart failure and the diagnosis of "CRT nonresponder" was made. With a detailed fact-finding approach,
the mechanism behind this nonresponse was identified, and the outcome of
CRT was significantly improved with rectification of the problems.

ardiac resynchronization therapy (CRT) is a well-established device therapy for heart failure (HF) that is based on
simultaneous pacing of both ventricles in order to mimic
normal cardiac electromechanical contraction. Unfortunately, about one-third of CRT-implanted patients do not respond
to this therapy, and most causes remain a conundrum. Nevertheless,
suboptimal lead placement is commonly overlooked in clinical
practice. Here, we describe a detailed evaluation with successful
rectiﬁcation of the mechanisms in a case of a CRT nonresponder.
CASE DESCRIPTION
An 80-year-old woman with paroxysmal atrial ﬁbrillation, left
bundle branch block (QRS of 154 ms), and severe nonischemic
cardiomyopathy (ejection fraction of 30%) underwent implantation of a CRT with a deﬁbrillator for management of severe HF
symptoms despite optimal medical therapy. Three months later, she
continued to have HF class III-IV symptoms. Device interrogation
showed 74% biventricular pacing and 74% right atrial (RA) pacing
with stable lead impedances since implant. Pacing thresholds of the
right ventricular (RV) and left ventricular (LV) lead were 0.9 V at
0.5 ms and 0.75 V at 0.5 ms, respectively. During a detailed and
step-by-step RA lead capture threshold testing with continuous
12-lead electrocardiogram monitoring, RV capture instead of RA
capture starting at 5 V at 0.8 ms down to 1.75 V at 0.8 ms was
discovered. Interestingly, at or lower than 1.5 V at 0.8 ms, RV
capture by pacing through RA lead was switched to RA capture
only, with an RA capture threshold of 0.75 V at 0.8 ms (Figures 1
and 2). Malposition of the RA lead was suspected.
After chest radiography was found to be inconclusive, a
computed tomography scan demonstrated that the RA lead tip
was near the atrioventricular groove abutting the base of the RV
230

outﬂow tract (Figure 3). As such, the RA lead pacing at pulse
amplitude ≥1.75 V was indeed capturing the RV, and true biventricular pacing using the RV and LV lead was not happening,
as the RV had already been inappropriately captured by RA lead
pacing. In other words, DDD pacing (atrial-paced biventricular
paced rhythm) with RA pacing amplitude at or above 1.75 V was
resulting in right ventricular VVI pacing only, as there was no
RA capture (loss of atrial kick), RV and LV were in the refractory
period, and pacing through the RV and LV leads was not capturing (eﬀectively 0% biventricular pacing). Pacing outputs were
therefore reprogrammed (RA 1 V at 0.8 ms, RV 2 V at 0.5 ms,
and LV 1 V at 0.5 ms). At follow-up, the patient reported a signiﬁcant improvement of HF symptoms (from HF class III-IV
to class II), and device interrogation revealed 99% appropriate
atrial-paced and biventricular-paced rhythm via RV and LV leads.
DISCUSSION
We described this case to highlight the importance of performing detailed troubleshooting of various components of a CRT
system when managing HF patients. Demonstration of eﬀective
and optimal biventricular pacing is critical in patients undergoing
CRT. Current consensus recommends that atrial ﬁbrillation and/
or ventricular arrhythmias should be controlled pharmacologically
or with invasive procedures to allow for over 90% of biventricular
pacing in order to improve HF symptoms. In this case, placement
of the RA lead tip on the atrioventricular groove was the cause of
the loss of RA capture and in fact inappropriate RV capture with
higher pulse amplitude. This could have potentially been avoided at
the time of implant by more careful ﬂuoroscopic imaging in diﬀerent views and more careful attention to the morphology of evoked
response to the pacing in a given chamber. A detailed device interrogation incorporated with simultaneous detailed electrocardiogram
analysis was the only way to troubleshoot and eventually rectify
the problem. A computed tomography scan further conﬁrmed
the diagnosis. The discovery that the higher output pacing via the
RA lead was capturing the RV rather than the RA resulting in no
From Electrophysiology Services and the Center for Comprehensive Cardiovascular
Care (C4), St. Louis University Hospital and School of Medicine, St. Louis, Missouri.
Corresponding author: Krittapoom Akrawinthawong, MD, MSc, Center for
Comprehensive Cardiovascular Care, St. Louis University Hospital, Desloge Tower,
13th Floor, St. Louis, MO 63110 (e-mail: krittapoom.a@gmail.com).
Proc (Bayl Univ Med Cent) 2017;30(2):230-231

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