Key result
In patients with atrial fibrillation, systemic inflammatory markers (hsCRP, NLR, RDW) were not correlated with the oxidative stress marker 8-iso-PGF2α, despite 8-iso-PGF2α levels being significantly higher in AF patients than in controls.
Cross-Sectional (n=220)
No
Absolute Event Rate: 72.62% vs 47.55%
p-value: p=<0.001
Systemic inflammatory markers do not correlate with oxidative stress markers in atrial fibrillation, suggesting they play different temporal roles in atrial structural and electrical remodeling.
No correlation between inflammatory and oxidative stress markers in AF cautions against assuming mechanistic overlap; leaves open distinct therapeutic targets.
BACKGROUND AND OBJECTIVES: Oxidative stress (OS) plays an important role in the pathophysiology of atrial fibrillation (AF) by amplifying the inflammatory cascade, wherein augmented inflammation facilitates the atrial electrical remodeling process. Few studies have investigated the possible link between systemic inflammation and OS in AF. SUBJECTS AND METHODS: A total of 220 consecutive patients with AF (117 patients) or healthy controls (103 patients) were enrolled. Among the 117 AF patients, 65 paroxysmal AF (PaAF) and 52 persistent AF (PeAF) patients were included. The level of 8-iso-prostaglandin F2α (8-iso-PGF2α) was measured as a marker of OS burden. We evaluated the correlations between 3 systemic inflammatory markers, high-sensitivity C-reactive protein (hsCRP), neutrophil to lymphocyte ratio (NLR), and red cell distribution width (RDW), and 8-iso-PGF2α. RESULTS: The 8-iso-PGF2α concentration in both PaAF and PeAF patients was higher than that of controls (p<0.001 and p=0.024, respectively). The NLR and RDW of PeAF patients were higher than those of both control and PaAF patients (p=0.041 and p=0.031 for NLR, p=0.057 and p=0.031 for RDW, respectively). There were no correlations between specific inflammatory markers and the 8-iso-PGF2α in AF. The 8-iso-PGF2α level decreased gradually with an increase in AF duration (p=0.008), contrary to the graded increase in hsCRP. Multiple regression analysis indicated that AF duration persisted as a significant determinant of 8-iso-PGF2α (β=-0.249, p=0.044). CONCLUSION: Systemic inflammatory marker levels were not proportional to the levels of 8-iso-PGF2α, an OS marker, in AF.
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Nam et al. (2017) conducted a cross-sectional in Atrial Fibrillation (n=220). Atrial fibrillation vs. Healthy controls was evaluated on 8-iso-PGF2α concentration (pg/mL) (p=<0.001). In patients with atrial fibrillation, systemic inflammatory markers (hsCRP, NLR, RDW) were not correlated with the oxidative stress marker 8-iso-PGF2α, despite 8-iso-PGF2α levels being significantly higher in AF patients than in controls.
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