bstract
ATTR amyloidosis patient with initial atrial capture failure showed delayed threshold improvement over time. Stable current of injury and impedance guided expectant management, avoiding unnecessary device repositioning while achieving successful outcomes.
Transthyretin cardiac amyloidosis (ATTR) is frequently accompanied by conduction abnormalities, including sinus node dysfunction requiring permanent pacing. Dual‐chamber leadless pacemakers provide an option for patients with frailty, infection risk, or limited venous access [1]. During atrial leadless pacemaker implantation, however, elevated acute pacing thresholds or absent atrial capture create uncertainty regarding device stability and repositioning needs.
An 84‐year‐old woman with ATTR amyloidosis presented with recurrent syncope and exertional dyspnea. Cardiac imaging demonstrated diffuse left ventricular hypertrophy with apical sparing, and pyrophosphate scintigraphy showed increased myocardial uptake. Fat aspiration biopsy confirmed amyloid deposition. Ambulatory monitoring revealed profound bradycardia with recurrent asystolic pauses.
Considering the patient's diminished activities of daily living and the need to minimize postoperative mobility demands, we proceeded with implantation of a dual‐chamber leadless pacemaker (Aveir DR, Abbott). Following implantation of the right ventricular device, which exhibited favorable acute electrical parameters (threshold 0.75 V/0.4 ms; impedance 290 Ω), we proceeded with implantation of the atrial leadless pacemaker. The blood pool impedance measured in the inferior vena cava at that time was 260 Ω. Multiple pre‐mapping attempts were performed within the right atrial appendage; however, even at maximal output (6 V/1.5 ms), atrial capture was intermittent, and stable atrial capture could not be achieved. At a pulse width of 0.4 ms, no atrial capture was observed, even at maximal output. Despite the absence of capture, the current of injury (COI) characterized by ST‐segment elevation on the intracardiac electrogram, was clearly present (1 mV), and impedance remained stable (290 Ω; Figure 1).
FIGURE 1.
Commanded intracardiac electrogram during tether mode. Commanded intracardiac electrogram obtained during tether mode demonstrating a steep current of injury exceeding 1 mV in amplitude with a rapid upstroke. Despite the presence of current of injury and stable impedance (290 Ω), atrial capture could not be achieved at maximal output (6 V/1.5 ms).
We considered retrieving the atrial device and proceeding with right ventricular implantation alone. However, isolated right ventricular pacing in patients with sinus node dysfunction has been associated with an increased risk of heart failure [2]. In this patient, the underlying ATTR cardiomyopathy with diastolic dysfunction created conditions in which chronic right ventricular apical pacing would be expected to cause further hemodynamic deterioration. Therefore, following atrial leadless pacemaker implantation, we elected to observe whether the atrial pacing threshold would improve during the chronic phase. After a 30‐min observation period, the atrial pacing threshold remained unchanged; however, the COI and impedance were stable.
Previous reports in atrial leadless pacemaker implantation have shown that a steep increase COI ≧ 2 mV and impedance reflects adequate contact with viable atrial myocardium and is predictive of subsequent improvement in chronic pacing thresholds [3]. In our case, although the magnitude of COI elevation was limited to approximately 1 mV, the increase was steep, and an increase in local impedance relative to the blood pool impedance was observed at the implantation site.
In conventional transvenous pacemaker systems with active‐fixation leads, a sustained positive deflection of the current of injury measured at 80 milliseconds after its onset (CI80) has been shown to reflect secure helix engagement and to predict subsequent improvement in pacing thresholds over the chronic phase, spanning several weeks to months [4]. In our case, CI80 also demonstrated a sustained positive deflection.
Accordingly, the atrial leadless pacemaker was left in situ, with the expectation of potential improvement in chronic‐phase thresholds (Figure 2). By postoperative Day 3, atrial capture appeared (3.0 V/1.5 ms; 5.5 V/0.4 ms). At 2 weeks, the thresholds improved (2.5 V/1.5 ms; 3.0 V/0.4 ms) and the impedance increased to 330 Ω. At 2 months, the thresholds further improved (0.5 V/1.5 ms; 1.0 V/0.4 ms) with impedance stabilizing at 280 Ω (Figure 3). The device was programmed to AAI mode at 50 beats per minute with VVI backup at 40 beats per minute. The patient predominantly maintained sinus rhythm with pacing support during occasional bradycardic episodes (Figure 4). Throughout the 4‐month follow‐up period, she has remained asymptomatic without recurrence of syncope or dyspnea.