Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
Clin Cardiol. 2009 Jun;32(6):337-45. doi: 10.1002/clc.20566.
Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-gamma (PPARgamma) 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 PPARgamma inflammation and AF is still unknown.
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 PPARgamma, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) mRNA in monocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods.
The PPARgamma 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-alpha 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-alpha, IL-6, and IL-1 were in negative correlation with PPARgamma, the correlation coefficient was -0.854, -0.769, and -0.702, respectively (P<0.01).
In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARgamma may be involved in the pathogenesis of AF by regulation of inflammation.
大量证据表明,高血压或心房颤动(AF)均与全身炎症相关。过氧化物酶体增殖物激活受体-γ(PPARγ)具有抗炎作用,并被认为是参与多种心血管疾病(如高血压)的分子途径。PPARγ炎症与 AF 之间的相关性尚不清楚。
采用病例对照研究设计,纳入 57 例高血压合并 AF(持续性 AF:32 例,阵发性 AF:25 例)患者作为研究组。选择 32 例年龄匹配的高血压但无 AF 患者作为对照组。采用逆转录-聚合酶链反应(RT-PCR)检测单核细胞中 PPARγ、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)mRNA 的表达。采用免疫酶标法检测白细胞介素-1(IL-1)。
与高血压非 AF 组相比,高血压 AF 组的 PPARγ mRNA 明显降低,持续性 AF 组比阵发性 AF 组明显降低(0.222±0.0702 比 0.564±0.0436,P<0.01)。与非 AF 组相比,高血压 AF 患者的 TNF-α mRNA、IL-6 mRNA 和 IL-1 均升高,持续性 AF 组高于阵发性 AF 组(0.721±0.0541 比 0.530±0.0496,0.567±0.044 比 0.457±0.0505,325.61±88.10 比 190.65±59.38,均 P<0.01)。TNF-α、IL-6 和 IL-1 与 PPARγ 呈负相关,相关系数分别为-0.854、-0.769 和-0.702(均 P<0.01)。
在高血压患者中,炎症细胞因子的增加与 AF 发生率和心房重构的增加有关;PPARγ 可能通过调节炎症参与 AF 的发病机制。