Abstract 2228: Downregulation of Peroxisome Proliferator-activated Receptor-γ Expression in Hypertensive Atrial Fibrillation
Introduction: Increasing attention has focused on the role of inflammation in patients with atrial fibrillation. The presence of systemic inflammation by elevations of CRP and TNFα has been associated with AF. Peroxisome proliferator-activated receptor γ (PPARγ) has been implicated as a molecular pathway involved in many cardiovascular diseases, but the relationship between PPARγ and AF is still poorly understood.
Hypothesis: The expression of PPARγ mRNA may be decreased in patients with hypertnsive atrial fibrillation and inflammation cytokines may effect the expression of PPARγ mRNA.
Methods: Fifty-seven consecutive patients with hypertnsive atrial fibrillation(persistent AF 32, paroxysmal AF 25) were included into the study group. An additional 32 patients with hypertension without atrial fibrillation were selected as the control group. The expressions of the PPARγ mRNA, IL-6 mRNA and TNF-αmRNA in monocytes in peripheral blood were detected by using reverse transcription-polymerase chain reaction (RT-PCR).IL-1 was measured by radioimmunoassay .
Results: The expression of PPARγ mRNA in patients with persistent AF, paroxysmal AF, and the control group was 0.222± 0.0702,0.564 ± 0.0436,0.650 ± 0.064 respectively (P < 0.01), IL-6 mRNA was 0.567 ± 0.044,0.457 ± 0.0505,0.414 ± 0.0406 respectively (P < 0.01), TNF-αmRNA was 0.721 ± 0.0541,0.530 ± 0.0496,0.483 ± 0.0487 respectively (P < 0.01);and IL-1 was325.61 ± 88.10,190.65 ± 59.38,130.77 ± 42.22 respectively (P < 0.01). The PPARγ mRNA was decreased in AF group as compared with the control group, and in persistent AF was lower than paroxysmal AF (P < 0.01). The expression of TNFα mRNA IL-6mRNA and serum IL-1 was increased in patients with hypertensive atrial fibrillation compared to the control goup, and in persistent AF was even higher than paroxysm AF. TNFα IL-6 and IL-1 was in negative correlation with the expression of PPARγ mRNA and the correlation coefficient was −0.854, −0.769, −0.702 respectively (P < 0.01).
Conclusions: These results suggest that inflammation cytokines were increased in patients with hypertensive AF compared to control group, and also suggest that PPAR may involved in the pathologic mechanism of AF by regulation of inflammation cytokines.