Successful treatment of a cardiac resynchronization therapy nonresponder by identifying lead malpositioning

Abstract

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.

Cardiac 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.

Figure 1.

Right atrial lead threshold testing showing inappropriate right ventricular capture with maximum right atrial output.

Figure 2.

An electrocardiogram showing mode DDD, 80 beats per minute, biventricular pacing, right ventricle/left ventricle, 2 volts at 0.5 milliseconds, right atrium; 1 volt at 0.9 milliseconds.

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 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.

Figure 3.

Noncontrast cardiac computed tomography scans with (a) coronal view and (b) sagittal view showing the tip of the right atrial (RA) lead abutting the base of the right ventricular (RV) outflow tract.

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 RA capture and loss of atrial kick along with 0% biventricular pacing explained why this patient was a CRT nonresponder.

Previous reports have discussed two similar concepts: “cross-stimulation,” described as capture of the RV by high-output RA pacing due to malposition of the RA lead in the anterior tricuspid annulus (1), and “intermittent capture” of the RV outflow tract from a malpositioned RA lead in the anteromedial RA (2). The RA appendage lies adjacent to the RV outflow tract, making it challenging at times to evaluate the location of the tip of the pacing lead on fluoroscopy or chest radiography. A noncontrast computed tomography scan might be beneficial in these scenarios, highlighting the importance of lead position verification prior to a diagnosis of CRT nonresponder.

Care of HF patients undergoing device therapy should be an integrated approach involving HF and electrophysiology specialists during routine follow-up. Periodic device interrogations, electrocardiogram, and multimodality imaging should be used in these patients prior to premature diagnosis of CRT nonresponse. A more careful review of fluoroscopic images in different views and careful attention to the evoked response to pacing in a given chamber are the key elements in reducing the rate of CRT nonresponse.