PMC9843673_01
(A and B) Cardiac magnetic resonance imaging demonstrates right ventricle enlargement and late gadolinium enhancement at extensive right ventricle free wall, right ventricle septal-endocardial, and left ventricular lateral-subepicardial areas. (C) The strategy to screw a 3830 lead to the left ventricular septum and plug it into the right ventricle pacing/sensing port (IS-1) while plugging the defibrillation lead into the defibrillation port (DF-1). (D) Bipolar R-wave amplitude at the final site during lead implantation, post-operation test, and follow-up. Rotation x1-4, the first to the fourth rounds of lead rotation. Oprt end, at the operation end; Post-oprt 24 h, 24 h post-operation; FU, follow-up.
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Cardiac magnetic resonance imaging (CMRI) further confirmed RV enlargement, reduced RV ejection fraction (25.88%), increased RV end-diastolic volume index (235.48 mL/m2), and extensive late gadolinium enhancement (LGE) in RV as a sign of fibrofatty replacement (Figure 1A and B; see Supplementary material online, Video S1). Since the LVS myocardium was more preserved, a strategy was proposed to screw a 3830 lead (SelectSecure , Medtronic) to the deep or left septum and plug it into the RV pacing/sensing port (IS-1) to enhance the R-wave sensing, while still plugging the defibrillation lead into the defibrillation port (DF-1) (Figure 1C). At the final targeted site, the bipolar R-wave amplitude sharply elevated from 2.6 to 7.1 mV after the first two rounds of rotation, then decreased to 4.3 mV after successive two rotations but slightly recovered to 5.8 mV at the end (Figure 1D). Device programming 24 h post-operation demonstrated a favourable performance of both 3830 (R-wave = 9.9 mV; impedance = 551 Omega; threshold = 0.5 V/0.4 ms) (Figure 1D) and 6935 (defibrillation impedance = 53 Omega) leads (Table 2). After a 4-month follow-up, the parameters of both 3830 (R-wave = 11.1 mV) (Figure 1D) and 6935 (defibrillation impedance = 64 Omega) leads were stable, detecting 246 short VT episodes (<188 b.p.m.) accompanied by mild palpitation and dyspnoea without inappropriate delivery and device-related complications or adverse events (Table 2).
Paced QRS (100 mm/s, unipolar) during 3830 lead implantation and the left bundle branch potential. The stimulus-to-left ventricular activation time was gradually shortened as the lead moved forward. The V1-V6 inter-peak interval was 44 ms (stimulus-to-right ventricular activation time :stimulus-to-left ventricular activation time). The potential-to-ventricular activation interval was 28 ms, corresponding to that reported in left bundle branch area pacing.
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LBB potential was recorded (Figure 2). Left ventricular septal pacing was eventually defined without documenting the direct evidence of LBB capture.
(A) Post-implantation intrinsic and paced electrocardiography (25 mm/s); epsilon wave could be seen in V1 lead during sinus rhythm, with the bipolar R-wave amplitude of 9.9 mV; similar paced QRS and stimulus-to-left ventricular activation time at low and high pacing outputs. (B) The final lead positions in an anteroposterior fluoroscopic view. (C) The final lead positions in right anterior oblique (RAO) 30  fluoroscopic view with the novel nine-partition method, showing that the 3830 lead was deployed in the most common implanted site of left bundle branch area pacing (junction of the 2nd and 5th partitions). (D) The final lead positions in left anterior oblique (LAO) 30  fluoroscopic view. (E) The intra-septal depth of the 3830 lead measured by echocardiography. EGM, electrogram; VS, ventricular sensing during sinus rhythm; LVSP, left ventricular septal pacing; Stim-LVAT, stimulus-to-left ventricular activation time.
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ECG leads, generally low QRS amplitude, and an Epsilon wave in V1 lead (Figure 3A). Echocardiography revealed a dilated RV (41 mm) and a reduced fractional area change ( 26%). Final lead positions are shown in Figure 3B-D. Paced QRS is shown in Figure 3A. Echocardiography demonstrated that the intra-septal depth of the 3830 lead tip was 6.83 mm, around 1.0 mm from the LVS endocardium (Figure 3E).