Left bundle branch area pacing vs biventricular pacing for cardiac resynchronization: A systematic review and meta-analysis.

Background: Left bundle branch area pacing (LBBAP) may offer greater physiological benefits than traditional biventricular pacing (BiVP). However, there are limited data comparing the efficacy of LBBAP vs BiVP in patients with systolic heart failure (HF). Objective: The purpose of this meta-analysis was to compare the feasibility and electromechanical and clinical outcomes of both LBBAP and BiVP. Methods: We conducted a systematic review of studies retrieved from various databases including PubMed, Embase, Google Scholar, Scopus, and Cochrane Central Register of Control Trials (CENTRAL) published up to May 22, 2023. The risk ratio (RR) and standardized mean difference (SMD) with corresponding 95% confidence intervals (CIs) were calculated for dichotomous and continuous outcomes, respectively. Results: We included 12 studies with a total of 3004 patients (LBBAP = 1242, BiVP = 1762). Pooled results showed that LBBAP resulted in a significant increase in left ventricular ejection fraction (SMD 0.40, 95% CI 0.25, 0.54, P < .00001), echocardiographic response (RR 1.19, 95% CI 1.10 to 1.29, P < .0001), improvement in New York Heart Association functional class (SMD -0.44, 95% CI -0.65 to -0.23, P < .0001), QRS duration reduction (SMD -0.90, 95% CI -1.14 to -0.66, P < .00001), left ventricular end-diastolic diameter reduction (SMD -0.31, 95% CI -0.57 to -0.05, P = .02), fewer HF hospitalizations (RR 0.72, 95% CI 0.62, 0.85, P < .0001), and improved survival (RR 0.73, 95% CI 0.58, 0.92, P = .007). In addition, LBBAP was associated with shorter fluoroscopy time (SMD -0.94, 95% CI -1.42 to -0.47, P < .0001) and lower pacing threshold at implantation (SMD -1.03, 95% CI -1.32 to -0.74, P < .00001) and at 6 months (SMD -1.44, 95% CI -2.11 to -0.77, P < .0001) as compared with BiVP. Conclusion: Compared with BiVP, LBBAP was associated with better electromechanical and clinical outcomes, including left ventricular ejection fraction, QRS duration, echocardiographic response, New York Heart Association functional class, HF hospitalization, and all-cause mortality in patients with systolic HF.

Temporary biventricular pacing decreases the vasoactive-inotropic score after cardiac surgery: a substudy of a randomized clinical trial.

OBJECTIVE: Vasoactive medications improve hemodynamics after cardiac surgery but are associated with high metabolic and arrhythmic burdens. The vasoactive-inotropic score was developed to quantify vasoactive and inotropic support after cardiac surgery in pediatric patients but may be useful in adults as well. Accordingly, we examined the time course of this score in a substudy of the Biventricular Pacing After Cardiac Surgery trial. We hypothesized that the score would be lower in patients randomized to biventricular pacing. METHODS: Fifty patients selected for increased risk of left ventricular dysfunction after cardiac surgery and randomized to temporary biventricular pacing or standard of care (no pacing) after cardiopulmonary bypass were studied in a clinical trial between April 2007 and June 2011. Vasoactive agents were assessed after cardiopulmonary bypass, after sternal closure, and 0 to 7 hours after admission to the intensive care unit. RESULTS: Over the initial 3 collection points after cardiopulmonary bypass (mean duration, 131 minutes), the mean vasoactive-inotropic score decreased in the biventricular pacing group from 12.0 ± 1.5 to 10.5 ± 2.0 and increased in the standard of care group from 12.5 ± 1.9 to 15.5 ± 2.9. By using a linear mixed-effects model, the slopes of the time courses were significantly different (P = .02) and remained so for the first hour in the intensive care unit. However, the difference was no longer significant beyond this point (P = .26). CONCLUSIONS: The vasoactive-inotropic score decreases in patients undergoing temporary biventricular pacing in the early postoperative period. Future studies are required to assess the impact of this effect on arrhythmogenesis, morbidity, mortality, and hospital costs.

Short-term reduction in intrinsic heart rate during biventricular pacing after cardiac surgery: a substudy of a randomized clinical trial.

BACKGROUND: The Biventricular Pacing After Cardiac Surgery trial investigates hemodynamics of temporary pacing in selected patients at risk of left ventricular dysfunction. This trial demonstrates improved hemodynamics during optimized biventricular pacing compared with atrial pacing at the same heart rate 1 and 2 hours after bypass and reduced vasoactive-inotropic score over the first 4 hours after bypass. However, this advantage of biventricular versus atrial pacing disappears 12 to 24 hours later. We hypothesized that changes in intrinsic heart rate can explain variable effects of atrial pacing in this setting. METHODS: Heart rate, mean arterial pressure, cardiac output, and medications depressing heart rate were analyzed in patients randomized to continuous biventricular pacing (n = 16) or standard of care (n = 18). RESULTS: During 30-second testing periods without pacing, intrinsic heart rate was lower in the paced group 12 to 24 hours after bypass (76.5 ± 17.5 vs 91.7 ± 13.0 beats per minute; P = .040) but not 1 or 2 hours after bypass. Cardiac output (4.4 ± 1.2 vs 3.6 ± 1.9 L/min; P = .054) and stroke volume (53 ± 2 vs 42 ± 2 mL; P = .051) increased overnight in the paced group. Vasoactive medication doses were not different between groups, whereas dexmedetomidine administration was prolonged over postoperative hours 12 to 24 in the paced group (793 ± 528 vs 478 ± 295 minutes; P = .013). CONCLUSIONS: These observations suggest that hemodynamic benefits of biventricular pacing 12 to 24 hours after cardiopulmonary bypass lead to withdrawal of sympathetic drive and decreased intrinsic heart rate. Depression of intrinsic rate increases the apparent benefit of atrial pacing in the chronically paced group but not in the control group. Additional study is needed to define clinical benefits of these effects.

Comparative electromechanical and hemodynamic effects of left ventricular and biventricular pacing in dyssynchronous heart failure: electrical resynchronization versus left-right ventricular interaction.

OBJECTIVES: The purpose of this study was to enhance understanding of the working mechanism of cardiac resynchronization therapy by comparing animal experimental, clinical, and computational data on the hemodynamic and electromechanical consequences of left ventricular pacing (LVP) and biventricular pacing (BiVP). BACKGROUND: It is unclear why LVP and BiVP have comparative positive effects on hemodynamic function of patients with dyssynchronous heart failure. METHODS: Hemodynamic response to LVP and BiVP (% change in maximal rate of left ventricular pressure rise [LVdP/dtmax]) was measured in 6 dogs and 24 patients with heart failure and left bundle branch block followed by computer simulations of local myofiber mechanics during LVP and BiVP in the failing heart with left bundle branch block. Pacing-induced changes of electrical activation were measured in dogs using contact mapping and in patients using a noninvasive multielectrode electrocardiographic mapping technique. RESULTS: LVP and BiVP similarly increased LVdP/dtmax in dogs and in patients, but only BiVP significantly decreased electrical dyssynchrony. In the simulations, LVP and BiVP increased total ventricular myofiber work to the same extent. While the LVP-induced increase was entirely due to enhanced right ventricular (RV) myofiber work, the BiVP-induced increase was due to enhanced myofiber work of both the left ventricle (LV) and RV. Overall, LVdP/dtmax correlated better with total ventricular myofiber work than with LV or RV myofiber work alone. CONCLUSIONS: Animal experimental, clinical, and computational data support the similarity of hemodynamic response to LVP and BiVP, despite differences in electrical dyssynchrony. The simulations provide the novel insight that, through ventricular interaction, the RV myocardium importantly contributes to the improvement in LV pump function induced by cardiac resynchronization therapy.