他汀类药物治疗可调节人的心外膜脂肪组织的厚度和炎症特征。
Statin therapy modulates thickness and inflammatory profile of human epicardial adipose tissue.
机构信息
Department of Translational Medical Science, University of Naples Federico II, Italy.
Department of Translational Medical Science, University of Naples Federico II, Italy.
出版信息
Int J Cardiol. 2019 Jan 1;274:326-330. doi: 10.1016/j.ijcard.2018.06.106. Epub 2018 Jun 28.
BACKGROUND
Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation.
METHODS
Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies.
RESULTS
Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001).
CONCLUSIONS
The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.
背景
心外膜脂肪组织（EAT）厚度和促炎状态已被证明与多种心脏病有关，包括主动脉瓣狭窄（AS）。因此，心脏内脏脂肪可能代表一种新的潜在药物靶点。在本研究中，我们评估了他汀类药物治疗对 EAT 积累和炎症的影响。
方法
对 193 例接受心脏手术的 AS 患者（服用他汀类药物 87 例，未服用他汀类药物 106 例）进行超声心动图 EAT 厚度评估。为了探讨他汀类药物治疗与 EAT 炎症之间的关系，我们从 EAT 分泌组中获取 EAT 活检以进行细胞因子免疫测定。还进行了一项体外研究，评估阿托伐他汀对 EAT 和皮下脂肪组织（SCAT）分泌组的调节作用。
结果
他汀类药物治疗与 EAT 厚度降低显著相关（p<0.0001），与 EAT 分泌的促炎介质水平降低显著相关（p<0.0001）。值得注意的是，EAT 厚度与其促炎状态之间存在显著相关性。在体外，阿托伐他汀对 EAT 具有直接的抗炎作用，其作用明显高于他汀孵育对 SCAT 的反应（p<0.0001）。
结论
本研究表明，AS 患者他汀类药物治疗与 EAT 积累减少之间存在强有力的关联。本研究数据还表明，EAT 厚度与其炎症状态之间存在直接关系，他汀类药物治疗均可调节两者。体外结果支持他汀类药物对 EAT 分泌谱的直接作用假设。总体而言，我们的数据表明 EAT 可能是他汀类药物治疗的一个新的潜在治疗靶点。
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