Feasibility and Safety of Atrioventricular Node Pacing in a Patient With Heart Failure and Atrioventricular Block

Abstract

Background

Conduction system pacing (CSP) serves as a physiological alternative for managing heart failure and atrioventricular block.

Case Summary

A 77-year-old woman was admitted with worsening shortness of breath. Her diagnoses included chronic heart failure classified as NYHA functional class IV, permanent atrial fibrillation, third-degree atrioventricular block after pacemaker implantation, and rheumatic heart valve disease. Atrioventricular node pacing (AVNP) was successfully achieved, with a stable threshold of 0.75 V at 0.4 ms. Over a 2-year period, the patient's left ventricular ejection fraction improved from 26% to 44%, left ventricular end-diastolic diameter decreased from 63 to 56 mm, and NYHA functional classification improved from IV to II.

Discussion

AVNP may present a viable alternative for patients experiencing failure of His bundle pacing and left bundle branch pacing. This case demonstrates to our knowledge the first report of AVNP with sustained electrophysiological stability and clinical efficacy during a 2-year follow-up, thereby addressing existing gaps in the applicability of CSP for patients with anatomically complex conditions.

Take-Home Message

AVNP may provide an alternative for patients with failure of traditional CSP.

Graphical Abstract

Take-Home Message

• •AVNP may provide an alternative for patients with failure of traditional CSP.

History of presentation

A 77-year-old woman underwent mitral and aortic valve replacement as well as tricuspid valvuloplasty for rheumatic heart valve disease, and a surgical maze procedure for persistent atrial fibrillation in 2009. Subsequently, she received right ventricular apical pacing owing to permanent atrial fibrillation and third-degree atrioventricular block (AVB) in 2015 at a local hospital.

In 2021, she presented to our center for an elevated pacing threshold of 2.5 V at 0.4 ms and cardiac dysfunction, evidenced by a left ventricular ejection fraction (LVEF) of 36%. During the upgrade procedure, severe tricuspid regurgitation and endocardial rigidity were addressed, enabling the electrode (model 3830, Medtronic) to reach the deep septal region of the paroxysmal left bundle branch area. A W-shaped pattern was observed at the bottom of lead V1, gradually ascending. However, the electrode could not be fully secured to the left side because of severe fibrosis or scarring, resulting in ineffective capture of the left bundle branch. Ultimately, deep septal pacing (DSP) was accepted, with a left ventricular activation time of 80 ms and a QRS duration of 138 ms.

In 2023, the patient was readmitted for sustained ventricular tachycardia and heart failure (HF) (Figure 1).

Figure 1.

Timeline Showing the Clinical Course in Different Pacing Modalities

AVNP = atrioventricular node pacing; DSP = deep septal pacing; LVEDD = left ventricular end-diastolic diameter; LVEF = left ventricular ejection fraction; RVP = right ventricular pacing.

Differential diagnosis

The patient's blood pressure was recorded at 120/90 mm Hg, with a heart rate of 60 beats/min, accompanied by jugular venous distension. Lung auscultation revealed bilateral basilar crackles, and mechanical valve clicks were audible over the mitral and aortic regions, with bilateral pitting edema observed below the knees. Laboratory evaluations indicated normal hepatic and renal function, as well as a complete blood count and thyroid function. However, B-type natriuretic peptide was elevated at 1943 ng/L. Coronary computed tomography angiography demonstrated mild stenosis (20%-30%) in 3 major coronary arteries. Thoracic computed tomography revealed cardiomegaly, with a cardiothoracic ratio of 0.60. An electrocardiogram exhibited a pacing rhythm. Transthoracic echocardiography showed a left ventricular end-diastolic diameter of 63 mm and an LVEF of 26%. The mechanical prosthetic valve exhibited normal functionality. As acute exacerbation of HF is primarily attributed to cardiac electrical dyssynchrony rather than ischemic etiology or structural valve deterioration, this electrical-mechanical dyssynchrony likely precipitated impaired ventricular filling and reduced cardiac output, consistent with pacemaker-induced cardiomyopathy.

Management

An upgrade to cardiac resynchronization therapy with defibrillator (CRT-D) became necessary given sustained ventricular tachycardia and advanced HF despite optimized pharmacological therapy. Throughout the therapeutic process, bipolar cardiac resynchronization therapy was consistently considered. Initially, it was declined owing to financial constraints during the first upgrade, but it was offered as an alternative if conduction system pacing (CSP) failure occurred during the second upgrade. Despite our thorough communication of the guideline recommendations, the patient remained skeptical about whether bipolar ventricular pacing would achieve better electrical synchronization compared with DSP. Instead, she expressed a more favorable outlook regarding the potential for CSP to provide optimal electrical synchronization and cardiac performance.

However, both left bundle branch pacing (LBBP) and His bundle pacing (HBP) were unsuccessful given the rigid septal myocardium. During the LBBP attempt, the tip of the electrode was close to, yet ultimately failed to reach, the left intraventricular membrane despite support from the coronary sinus sheath. This was evidenced by the W-shaped sluggishness observed at the bottom of lead V1, which gradually rose to the tail of the QS complex without the formation of an R wave, alongside the absence of other typical indicators of left bundle branch capture. Clear His bundle potential was identifiable, but the pacing threshold was as high as 4.0 V at 0.5 ms (Figure 2). At a right anterior oblique angle of 30°, the tricuspid annulus was displayed more clearly. The electrode was slowly withdrawn from the marked point of the His bundle and moved downward and slightly to the right toward the atrial side.¹ Pacing mapping technology should be employed; in certain cases, the far-field His bundle potential can be recorded, serving as a marker to locate the distal atrioventricular (AV) node.

Figure 2.

ECGs in Different Pacing Modalities

(Left to Right) ECGs are shown for right ventricular pacing, deep septal pacing, AVNP with rate response model, and AVNP without rate response model. AVNP = atrioventricular node pacing; ECG = electrocardiogram.

During pacing mapping around the proximal His bundle region, it was noted that the AV node could be captured with a favorable pacing threshold of 1.0 V at 0.5 ms, and a Wenckebach phenomenon (WP) was observed (Figure 3). The duration from the stimulus signal to the onset of the QRS complex progressively increased from 229 to 328 ms with 1:1 AV intrinsic conduction at a pacing rate of 100 beats/min (Figure 4). The 2:1 AV conduction was noted at a pacing rate of 110 beats/min, and loss of capture occurred while pacing at 140 beats/min. The pacing mode was programmed to DDD model without rate response, with a low rate of 60 beats/min and a sleep rate of 50 beats/min. The upper track rate was set at 100 beats/min, with an AV delay of 350 ms and a VV delay of 50 ms as double backups. The patient ultimately received a CRT-D, with an AV node lead in the atrial port, the right septal lead in the left ventricular port, and the defibrillator lead in the right ventricular port.

Figure 3.

EGCs During CSP Procedure

(Left to Right) ECGs are shown demonstrating deep septal pacing, AVNP at 100 beats/min (Wenckebach phenomenon), AVNP at 60 beats/min, and His bundle pacing (HV duration: 42 ms). AVNP = atrioventricular node pacing; CSP = conduction system pacing; ECG = electrocardiogram.

Figure 4.

X-Ray in RAO 30° View

The arrow points to the site of atrioventricular node pacing. RAO = right anterior oblique.

Outcome and follow-up

After AVNP, the patient's LVEF improved significantly from 26% to 44%. A stable and favorable pacing threshold of 0.75 V at 0.4 ms was confirmed, with pacing percentage of approximately 100%. Additionally, her NYHA functional classification improved from IV to II, and left ventricular end-diastolic diameter demonstrated a significant reduction from 63 to 56 mm at 2 years after AVNP (Figure 1).

Discussion

CSP has emerged as a physiological alternative to right ventricular pacing and biventricular pacing for specific cases involving HF and AVB.2, 3, 4, 5 However, HBP and LBBP may not be viable for patients with anatomical irregularities, including markedly enlarged cardiac cavities, significantly thickened or scarred interventricular septum, and substantial tricuspid regurgitation.6, 7, 8 The AV node is positioned farther from the central fibrous body than the His bundle and proximal left bundle branch; nevertheless, reports of AVNP remain limited. Three years ago, we documented a WP during the CSP procedure, underscoring the potential feasibility of AVNP.¹ Could AVNP serve as an alternative in cases with HBP and LBBP failure? This report presents, for the first time to our knowledge, the favorable cardiac performance and stable pacing threshold of AVNP after approximately 2 years of follow-up.

CSP has been associated with lower rates of mitral regurgitation, pacing-induced cardiomyopathy, mortality, and hospitalizations due to HF.⁹ In the present case, in additional to dilated cardiomyopathy and severe tricuspid regurgitation, we found that myocardial interstitial fibrosis and endocardial thickening, resulting from rheumatic heart disease and valve replacement, may also contribute to HBP and LBBP failure.¹⁰ The AV node, located on the atrial side and positioned farther from the central fibrous body, may serve as a potential conduction pacing site, with less fibrosis or scarring. The WP is a well-documented electrophysiological characteristic of the AV node. Pacing-related WP was previously observed in a case of HBP lead-induced injury.¹¹ In our earlier investigation, both the WP and His bundle potential were recorded when the lead was positioned at the distal end of the AV node.¹ Additionally, conducting a duration test from the stimulus signal to the onset of the QRS complex at varying pacing rates is essential to prevent pacing loss due to prolonged AV conduction time. We noted that the duration progressively increased from 229 to 328 ms with 1:1 AV intrinsic conduction at the pacing rate of 100 beats/min during the procedure, and 1:1 AV intrinsic conduction remained intact at the 2-year follow-up.

In contrast to previous studies, this report presents to our knowledge the first demonstration of the feasibility and safety of AVNP, alongside a stable and favorable pacing threshold during nearly 2 years of follow-up. In the context of challenging CSP procedures, should we consider AVNP? A major concern associated with HBP or AVNP is the potential for increased capture thresholds. The delayed increase in pacing threshold may be attributed to factors such as inadequate fixation, lead slack, local fibrosis, or disease progression.¹² In the current case, a stable and favorable pacing threshold was confirmed during follow-up, possibly owing to reduced scarring. Notably, symptoms and cardiac performance exhibited significant improvement after AVNP, indicating that true CSP, rather than DSP, will be beneficial for cardiac performance. However, in patients with distal conduction disturbances such as His-ventricular block or left bundle branch block, AVNP may not be sufficient.

Conclusions

This report is to our knowledge the first to present the use of AVNP in a patient with AVB and HF. The outcomes with 2-year follow-up suggest that AVNP may serve as an alternative option for patients with failure of current physiological pacing.

Funding Support and Author Disclosures

Support was received from the Scientific and Technological Innovation Foundation of Dalian City (2020JJ26SN055 & 2024JJ12PT016). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.