A Randomized Controlled Trial Comparing Different Programming Strategies of Left Bundle Branch Area Pacing on Left
Miao Liu1, Yonghong Yang1, Zijun Zhao1
1Department of Cardiology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
The American Journal of Cardiology
|April 6, 2026
Summary
This study compares two programming strategies for left bundle branch area pacing (LBBAP) in sinus node dysfunction patients. Optimized AV synchrony pacing may be non-inferior to minimal ventricular pacing in preventing left atrial remodeling.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Devices
Background:
- Left bundle branch area pacing (LBBAP) offers physiological ventricular synchrony.
- Sinus node dysfunction (SND) patients often have conduction delays, complicating LBBAP programming.
- Minimal ventricular pacing (MVP) algorithms may prolong AV delay, risking left atrial (LA) remodeling and arrhythmias.
Purpose of the Study:
- To compare a fixed optimized AV delay strategy versus MVP in SND patients with LBBAP.
- To assess non-inferiority of optimized AV delay in preventing LA volume increase at 12 months.
- To evaluate the impact on atrial tachyarrhythmias, including atrial high-rate episodes (AHRE) and atrial fibrillation (AF) burden.
Main Methods:
- Prospective, single-center, randomized, open-label trial with blinded endpoint assessment (PROBE design).
- 216 SND patients with successful LBBAP randomized 1:1 to two groups.
- Group 1: Fixed optimized AV delay (paced 150 ms, sensed 120 ms, MVP disabled). Group 2: MVP strategy (paced 200 ms, sensed 150 ms).
Main Results:
- Primary endpoint: Change in left atrial volume (LAV) from baseline to 12 months (non-inferiority analysis).
- Secondary endpoints: Device-detected AHRE and AF burden.
- Study designed to provide insights into optimal LBBAP programming for atrial health.
Conclusions:
- The trial will determine if active AV synchrony optimization post-LBBAP is non-inferior to MVP for LA remodeling.
- It will also assess if optimized AV synchrony reduces the burden of atrial arrhythmias.
- Findings will guide programming strategies for LBBAP in SND patients.
Related Concept Videos
Dysrhythmias IV: Characteristics of Bradyarrhythmias
835
Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
835
Dysrhythmias VI: Management of Dysrhythmias
633
Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...
633
Cardiomyopathy III: Hypertrophic Cardiomyopathy
748
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
748
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
2.3K
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
2.3K


