Background: Myeloperoxidase (MPO), secreted by neutrophils under inflammatory conditions, is elevated in atrial fibrillation (AF). MPO may be involved in atrial remodeling that underpins AF progression characterized by a switch from paroxysmal to persistent AF and the formation of low-voltage areas (LVA). MPO levels are modulated by renin-angiotensin system antagonists (RAS-A), commonly used to treat AF comorbidities, and are associated with reduced AF incidence, implicating a potential link.
Objective: We investigated MPO levels in progressing AF in peripheral and left atrial (LA) blood and analyzed a potential effect of RAS-A.
Methods: Samples of AF patients were collected from the femoral vein and the LA during catheter ablation (n = 121) and at follow-up (n = 23). No-AF probands (n = 37) served as controls. MPO was determined using commercial ELISA.
Results: MPO levels were significantly increased in AF patients compared to controls (median, 27.7 ng/ml (IQR 14.3-66.6) versus 12.6 (IQR 9.9-17.7), p < 0.001), without differences between clinical AF progression phenotypes. MPO concentration was tenfold higher in LA than periphery (279.2 ng/ml (IQR 202.2-342.9) versus 27.7 ng/ml (IQR 14.3-65.9), p < 0.001). MPO remained increased at midterm follow-up irrespective of rhythm outcome. RAS-A was associated with significantly lower peripheral (22.2 ng/ml (IQR 12.7-48.2) versus 37.1 ng/ml (IQR 18.2-85.2), p < 0.05) MPO levels in AF patients.
Conclusion: The pro-fibrotic enzyme MPO is generally elevated in AF patients irrespective of AF type, the presence of LVA or midterm rhythm outcome. Our data suggest that MPO may directly originate from the LA. RAS-A decrease peripheral MPO levels in AF patients.
Keywords: Atrial fibrillation; Atrial fibrillation progression; Myeloperoxidase; Renin–angiotensin system antagonists.