Abstract
Introduction: Studies found that the inflammation plays a key role in the pathogenesis of paroxysmal atrial fibrillation (PAF). It is well-known that apolipoprotein-A1 (Apo-A1) demonstrates antiinflammatory and anti-oxidant properties in a healthy physiological system. In the present study, we aimed to determine whether there is any difference of Apo-A1 levels in patients with PAF and healthy subjects. Methods: In this prospective cohort study, we enrolled a total of 35 PAF patients and 34 comparable healthy participants. Apo-A1 levels were measured from each subject using an immunophelometric method. All enrolled subjects were followed-up for one year during the study period. Results: Serum high-sensitivity C-reactive protein (hs-CRP) levels were statistically higher in PAF patients compared to healthy subjects (1.54±1.99 vs. 1.06±2.01, P = 0.016, respectively). Of note, patients with PAF had lower Apo-A1 levels (1.84±0.74 vs. 2.55±0.44, P = 0.001, respectively). There was no statistical difference between the groups in terms of apolipoprotein-B levels (1.08±0.36 vs. 0.99±0.38, P = 0.339, respectively). We did not find any correlation between Apo-A1 levels and PAF attacks in the study. Conclusion: The main finding of this study was that Apo-A1 levels were significantly lower in PAF patients compared to healthy participants. Based on our results, we considered that Apo-A1 may have a key role in the pathogenesis of PAF.
Highlights
Studies found that the inflammation plays a key role in the pathogenesis of paroxysmal atrial fibrillation (PAF)
As the inflammatory status and oxidative stress are involved in the pathophysiology Atrial fibrillation (AF), we considered that Apo-A1 levels might be lower among PAF patients
The left atrium (LA) dimension was higher and E wave velocity was lower in PAF patients (P= 0.02 and P = 0.07, respectively)
Summary
Studies found that the inflammation plays a key role in the pathogenesis of paroxysmal atrial fibrillation (PAF). Results: Serum high-sensitivity C-reactive protein (hs-CRP) levels were statistically higher in PAF patients compared to healthy subjects (1.54 ± 1.99 vs 1.06 ± 2.01, P = 0.016, respectively). Recent studies have found that the inflammation might have a key role in the initiation and perpetuation of PAF.[2,3] The elevation of some inflammatory markers, such as high-sensitivity C-reactive protein (hs-CRP) and interleukin-6, have been found in patients with PAF compared to healthy participants.[4,5] higher hs-CRP levels have been found to be associated with longer AF duration in a previous study.[6] In addition to the inflammation, oxidative stress is shown to be involved in the pathogenesis of PAF.[7]
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