Downregulation of peroxisome proliferator-activated receptor-γ expression in hypertensive atrial fibrillation

Abstract

Background: Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) has been proved to have anti-inflammatory effects and is implicated as a molecular pathway involved in many cardiovascular diseases, such as hypertension. The correlation between PPARγ inflammation and AF is still unknown. Methods: Using a case-control study design, 57 patients with hypertensive AF (persistent AF: 32, paroxysmal AF: 25) were included into the study groups. A total of 32 age-matched patients with hypertension, but without AF were selected as the control group. The expressions of PPARγ, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)mRNA inmonocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods. Results: The PPARγ mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 ± 0.0702 vs 0.564 ± 0.0436, P<0.01). TNF-α mRNA, IL-6 mRNA, and IL-1 were increased in patients with hypertensive AF compared to the non-AF group and it was even higher in persistent AF than in paroxysmal AF (0.721 ± 0.0541 vs 0.530 ± 0.0496, 0.567 ± 0.044 vs 0.457 ± 0.0505, 325.61 ± 88.10 vs 190.65 ± 59.38, respectively, P<0.01). TNF-α, IL-6, and IL-1 were in negative correlation with PPARγ, the correlation coefficient was -0.854,-0.769, and -0.702, respectively (P<0.01). Conclusions: In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARγ may be involved in the pathogenesis of AF by regulation of inflammation. © 2009 Wiley Periodicals, Inc.