Daniel Hunnybun, BSc, MSc.
Jonathan Behar, MBBS PhD MRCP CCDS CEPS FEHRA
Royal Brompton Hospital, Guys and St Thomas’ NHS Foundation Trust
A 75-year-old female was admitted to hospital in March 2021 with a suspected acute heart failure decompensation. She had a dual chamber pacemaker in situ (ProponentTM, Boston Scientific) which was implanted in 2012, following periods of sinus arrest, following a redo typical atrial flutter ablation. In 2013, she had a surgical atrial septal defect (ASD) closure and bi-atrial dilation had been seen on echocardiography. A third ablation was performed in 2015 for symptomatic atrial tachycardia (AT). During this procedure, a focal AT was identified proximal to the position of the right atrial pacing lead and ablated. Since the ablation in 2015, the atrial threshold had been chronically elevated (2.8v@1 ms) with evidence of atrial latency (Figure 1). Otherwise, pacing checks had been normal with no further arrhythmic events. The device was programmed DDDR 60 BPM with 100% atrial pacing and approximately 90% ventricular pacing.
Figure 1: January 2019 Atrial Threshold Test
Clinically she had evidence of fluid overload and clinical heart failure with >10 kg recent weight gain. Despite a high dose IV with furosemide, weight loss plateaued prompting a device check. On interrogation, no arrhythmia episodes had been recorded and RV thresholds were normal. The atrial threshold test can be seen in Figure 2.
Figure 2: March 2021 Atrial Threshold Test
A: Device EGMs with lead II, B: 12-lead ECG.
What is the most likely cause of the heart failure decompensation based upon this pacing follow-up?
A: Further atrial latency
B: Loss of AV synchrony
C: Atrial tachycardia
D: Poor medication compliance
E: Complete heart block
Figure 3: AT with variable AV conduction
Atrial latency can be described as a delay between atrial pacing stimulation and surface ECG p waves. Typically, such delays occur due to significant scarring which slows conduction in the immediate vicinity of the pacing lead.1 It is important, particularly for patients with ventricular pacing indications, to consider atrial latency when programming the pacing mode and optimal AV delays.2 In this case study, ablation and subsequent fibrotic processes proximal to the lead tip are the probable causes of the conduction delay and eventual loss of capture.
The patient was scheduled for an atrial lead reposition to restore AV synchrony. During the procedure the right atrial appendage was the only viable location. Atrial latency was still present with a much-improved pacing threshold (0.75V@0.5 ms). The generator was also replaced during this procedure (AssurityTM, Abbott).
How should this patient’s device be programmed to avoid ventricular pacing?
A: DDD with extended fixed AV delays
B: DDD with AV hysteresis
D: DDD with nominal AV delays
DDD = Dual-chamber antibradycardia pacing, AAI = Atrial demand pacing, VVI = Ventricular demand pacing.
Table 1: Programming Considerations for Atrial Latency Without Ventricular Pacing Indications
|How to Programme
|Atrial based pacing (AAI)
|AAI programming completely avoids the possibility of ventricular pacing.
|Fixed long AV delays
|AV hysteresis algorithms
|AV hysteresis algorithms periodically extend AV delays to search for intrinsic conduction up to a maximum value. The maximum value must be greater than the atrial latency interval + PR interval to avoid ventricular pacing.
Following the atrial lead replacement, AV synchrony was restored, and the lower rate limit set to 70 BPM. Further fluid offloading was subsequently much easier on the wards over the following days. Unfortunately, a few days later (with normal device function), the patient developed spontaneous atrial fibrillation. This was initially successfully treated with amiodarone but after recurrence was treated with catheter ablation. Several complex atrial tachycardias were found and ablated (Figure 4). Extensive atrial fibrosis and atrial chamber dilation (RA 290 mls, LA 180 mls) was demonstrated as can be seen below (Figure 5). Given the extensive chamber dilation and scarring, further atrial arrhythmia was likely and AV node ablation alongside biventricular pacing was a proposed future option should this occur.
Figure 4: Septal Left Atrial Tachycardia (CartoTM 3 V7)
Figure 5: Right Atrial Bipolar Voltage Map (CartoTM 3 V7, bipolar thresholds 0.05-0.5mV)
Carto© 3 V7, bipolar threshold 0.05-0.5 mV.
In summary, this case describes a patient with extensively scarred atria, arrhythmia and prior ablation which contributed to extreme atrial latency. Such patients can present several clinical challenges and as demonstrated here restoration of AV synchrony can help to facilitate diuresis. In addition, the residual atrial latency does present programming challenges and attempts should be made to optimise AV delays while avoiding ventricular pacing where possible.
1. Tanabe J, Fujita S, Watanabe N, et al. A case of prolonged atrial pacing latency. European Heart Journal – Case Reports 2020;4(4):1-2. https://doi.org/10.1093/ehjcr/ytaa215.
2. Grant S and Bennet G. Atrial latency in a dual chambered pacing system causing inappropriate sequence of cardiac chamber activation. Pacing and Clinical Electrophysiology 1992;15:116-8. https://doi.org/10.1111/j.1540-8159.1992.tb02907.x.