Clinical Efficacy and Safety of Left Bundle Branch Area Pacing Using Quantitative Guidance of Multimodal Data in the Treatment of Heart Failure

Heart failure is a common chronic cardiovascular disease that seriously impairs patients' quality of life and long-term prognosis. When heart failure is complicated by complete left bundle branch block, the electrical signals that regulate orderly heart contraction cannot be transmitted normally along the left conduction pathway, causing the left and right ventricles to contract out of sync. This will gradually weaken the heart's pumping capacity, leading to symptoms such as exertional shortness of breath, persistent fatigue and body edema, and significantly increasing the risk of repeated hospital admissions and premature death. Traditional biventricular pacing is the standard treatment recommended by international clinical guidelines for this condition. By implanting pacing leads in both ventricles to deliver synchronized electrical stimulation, it restores cardiac synchrony, improves cardiac function and reduces mortality in most eligible patients. However, the placement of left ventricular leads is entirely dependent on the anatomy of the coronary venous system. Due to wide individual differences in venous structure, many patients encounter intraoperative difficulties such as failed coronary sinus intubation, absence of suitable target veins, phrenic nerve stimulation, high pacing thresholds and postoperative lead displacement. More importantly, approximately 30% to 40% of patients still show no significant improvement in cardiac function or symptoms even after optimized device programming, a condition known as non-response to cardiac resynchronization therapy. Left bundle branch area pacing is an innovative physiological pacing technique originally developed in China. It advances a pacing lead through the ventricular septum to directly activate the heart's intrinsic conduction bundle, allowing electrical impulses to spread along the natural conduction pathway and restore ventricular synchrony. Previous single-center observational studies have shown that this