Atrial Pacing Improves Mitochondrial Function in Peripheral Blood Mononuclear Cells in Patients with Cardiac Implantable Electronic Devices

Mitochondrial dysfunction contributes significantly to the development of atrial fibrillation (AF). Conflicting data regarding the atrial pacing and the risk of AF existed and the impact of atrial pacing on mitochondrial function remains unknown. Therefore, we sought to examine the association between atrial pacing percentage and mitochondrial function in patients with cardiovascular implantable electronic devices (CIED) with atrial pacing capability. This is a cross-sectional study involving 183 patients with CIED with atrial pacing capability. The oxidative stress and mitochondrial function were determined in peripheral blood mononuclear cells (PBMCs). Among 183 patients, 55.7% had permanent pacemakers, 7.7% had defibrillators and 36.6% had cardiac resynchronization therapy. Mean age was 67.5±14.7 years with 51% being male. Mean left ventricular ejection fraction (LVEF) was 53.9 ± 16.8%. We demonstrated that the presence of atrial pacing above 50% correlated with higher levels of mitochondrial spared respiratory capacity (P=0.043) and coupling efficiency (P=0.045). After adjusting with multiple linear regression for age, sex, LVEF, history of AF, sick sinus syndrome, co-morbidities, eGFR, CRT, and percentage of ventricular pacing, our findings revealed a statistically significant association between a higher percentage of atrial pacing and increased spared respiratory capacity (β 0.217, P=0.046), lower non-mitochondrial respiration (β -0.230, P=0.023) and proton leak (β -0.247, P=0.022). We demonstrated that atrial pacing enhances mitochondrial performance in PBMCs and left ventricular contractile performance in patients with CIED. This observation may serve as additional support for the preventive effect of atrial pacing in the prevention of atrial arrhythmia.