Intermittent capture of the right ventricular outflow tract by atrial pacing in a patient with a dual-chamber pacemaker

Pastori, Julio D.; Garro, Hugo A.; Baranchuk, Adrián; Chiale, Pablo A.

doi:10.1016/j.jelectrocard.2012.06.018

Cited by 3 publications

(3 citation statements)

References 3 publications

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“…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 outfl ow tract from a malpositioned RA lead in the anteromedial RA (2). Th e RA appendage lies adjacent to the RV outfl ow tract, making it challenging at times to evaluate the location of the tip of the pacing lead on fl uoroscopy or chest radiography.…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment of a Cardiac Resynchronization Therapy Nonresponder by Identifying Lead Malpositioning

Prasad

Akrawinthawong

Ferreira

et al. 2017

Baylor University Medical Center Proceedings

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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. C 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 rectifi cation of the mechanisms in a case of a CRT nonresponder. CASE DESCRIPTIONAn 80-year-old woman with paroxysmal atrial fi brillation, left bundle branch block (QRS of 154 ms), and severe nonischemic cardiomyopathy (ejection fraction of 30%) underwent implantation of a CRT with a defi brillator for management of severe HF symptoms despite optimal medical therapy. Th ree 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 outfl ow 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 (eff ectively 0% biventricular pacing). Pacing outputs were therefore reprogr...

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Section: Discussionmentioning

confidence: 99%

Successful Treatment of a Cardiac Resynchronization Therapy Nonresponder by Identifying Lead Malpositioning

Prasad

Akrawinthawong

Ferreira

et al. 2017

Baylor University Medical Center Proceedings

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“…There are several possible causes for atrial stimulus coincident ventricular pacing complexes. These include direct and preferential activation of the right ventricular outflow tract by an atrial lead positioned at the anterior and medial right atrium [2]; an atrial lead positioned at the tricuspid annulus causing simultaneous capture of both chambers during atrial pacing (cross-stimulation) with high atrial output [3]; insulation break with resultant lead cross-talk; and, a dislodged atrial lead physically prolapsing into RVO intermittently [4], as was seen in our case also. Very rarely it can also be due to pseudo-pseudo fusion with atrial stimulus coincident with a ventricular ectopic beat.…”

Section: Discussionmentioning

confidence: 99%

Intermittent Right Ventricular Outflow Tract Capture due to Chronic Right Atrial Lead Dislodgement

Choudhury

Chaturvedi

Mukhopadhyay

et al. 2014

Indian Pacing and Electrophysiology Journal

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A 58 year old male, known case of type 2 diabetes and hypertension, had undergone implantation of a dual chamber pacemaker(DDDR) in 2007 for complaints of recurrent syncope and trifascicular block with a normal ejection fraction andnormal coronaries. His post implantation parameters were normal at that time.He now presented to our pacemaker clinic where his ECG done showed two types o fpaced complexes. The first few complexes were consistent with atrial sensed right ventricular apical pacing with left superior axis. Later complexes showed loss of atrial sensing with pacing from right ventricular outflow tract(inferior axis) with subtle oscillation in it's axis. On application of magnet, two pacemaker spikes were visible withinterspike interval of 120 ms and paced complexes with inferior axis starting from the first spike suggesting that the atrial lead was responsible for RVOT depolarization. On interrogation of the pacemaker, atrial EGM showed sensed activity from atrium followed by large sensed ventricular complex. Fluoroscopy confirmed that the atrial lead was dislodged and was intermittently prolapsing into the RVOT. Since the patient was asymptomatic, he refused any intervention and subsequentlyhis atrial lead was switched off by telemetry. The above case signifies that asymptomatic lead dislodgement is no talways manifested as loss of capture and even subtle variation of the axis o fthe paced complexes can provide us with a clue that can be confirmed by telemetry of the pacemaker and fluoroscopy.

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“…[1][2][3] An alternative explanation is refractoriness of the conduction system caused by intermittent capturing of the right ventricular outflow tract by a local effect of the atrial pacing stimulus. 4 However, increasing the atrial pacing rate and amplitude did not mimic these changes. Of note, when this report was being prepared, the patient's original device had been replaced, and further testing opportunities were lost.…”

Section: See Next Page For the Answer As Well As A Link To The Focusmentioning

confidence: 99%

Varying Morphology of QRS Complexes: A Possible Explanation

Laeeq¹,

Pollet²,

Faza³

et al. 2017

Texas Heart Institute Journal

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A 62-year-old man with nonischemic cardiomyopathy (left ventricular [LV] ejection fraction, 0.30-0.34) presented for evaluation of weakness. In 2011, he had undergone placement of a D224TRK Consulta ® CRT-D (Medtronic, Inc.; Minneapolis, Minn) biventricular implantable cardioverter-defibrillator. The pacemaker, programmed in DDD mode, had a lower rate limit of 60 beats/min (cycle length, 1,000 ms) and an upper limit of 130 beats/min (cycle length, 430 ms), a paced atrioventricular (AV)-delay period of 130 ms, and a sensed AV-delay period of 100 ms. The LV lead threshold was 1.25 V at 0.6 ms and was programmed to deliver 1.75 V at 0.6 ms. The right atrial and right ventricular leads were in standard positions. The electrocardiogram appeared as follows (Fig. 1). What explains the different QRS morphology seen in complexes 3 and 7?A) Intermittent programmed interventricular pacing delay B) Decreased ventricular threshold for pacing because of intermittent lead malfunction C) Unintended atrial lead mobility causing atrial capture at multiple sites and leading to variance in the AV interval D) Atrial pacing causing a frequency-dependent alteration in the Purkinje fiber conduction velocity

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Intermittent capture of the right ventricular outflow tract by atrial pacing in a patient with a dual-chamber pacemaker

Cited by 3 publications

References 3 publications

Successful Treatment of a Cardiac Resynchronization Therapy Nonresponder by Identifying Lead Malpositioning

Successful Treatment of a Cardiac Resynchronization Therapy Nonresponder by Identifying Lead Malpositioning

Intermittent Right Ventricular Outflow Tract Capture due to Chronic Right Atrial Lead Dislodgement

Varying Morphology of QRS Complexes: A Possible Explanation

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