Inflammation impairs eNOS activation by HDL in patients with acute coronary syndrome
Inflammation impairs eNOS activation by HDL in patients with acute coronary syndrome
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DOI：
10.1093/cvr/cvt169
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发表时间：
2013-10-01
影响因子：
10.8
通讯作者：
Calabresi, Laura
中科院分区：
文献类型：
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作者：
Gomaraschi, Monica;Ossoli, Alice;Calabresi, Laura
为评价急性期炎症反应（APR）不同的ST段抬高型心肌梗死（STEMI）患者高密度脂蛋白（HDL）结构和内皮型一氧化氮合酶（eNOS）活性，将45例STEMI患者按CRP峰值减去入院时CRP峰值（APR peak）的差值进行分层。HDL结构和HDL刺激NO产生的能力在入院时和APR峰值时进行了评估。具有低APR的STEMI患者具有完全保留的HDL结构和HDL激活eNOS和促进NO产生的能力，这在STEMI期间没有改变。相反，STEMI患者的HDL发生显著的APR，其刺激eNOS和促进NO产生的能力受损，并且在STEMI期间经历了显著的颗粒重塑。有缺陷的能力，以刺激NO生产的HDL从STEMI患者与高APR的解释，至少部分，减少PON-1和S1 P含量。HDL通过不同途径促进细胞胆固醇流出的能力在ACS患者中独立于炎症反应而得以保留，目前的结果扩展了先前报道ACS患者HDL的eNOS激活能力受损的研究，表明只有一部分经历STEMI的患者，特别是那些发生重要炎症反应的患者，循环HDL在刺激内皮eNOS和NO产生方面有缺陷。
The aim of the present study was to evaluate the high-density lipoprotein (HDL) structure and endothelial NO synthase (eNOS) activation capacity in ST-elevation myocardial infarction (STEMI) patients with different acute-phase inflammatory response (APR).Forty-five STEMI patients were stratified in quartiles according to the delta CRP level, calculated by subtracting the CRP value at admission from the CRP peak value (APR peak). The HDL structure and HDL capacity to stimulate NO production were evaluated at admission and at APR peak. STEMI patients with a low APR had a completely preserved HDL structure and HDL ability to activate eNOS and promote NO production, which did not change during STEMI. On the contrary, HDL from STEMI patients developing a significant APR had compromised ability to stimulate eNOS and promote NO production, and underwent a significant particle remodelling during STEMI. The defective capacity to stimulate NO production of HDL isolated from STEMI patients with high APR was explained, at least in part, by the reduced PON-1 and S1P content. The HDL ability to promote cell cholesterol efflux through different pathways was preserved in ACS patients independently of the inflammatory response.The present results extend previous studies reporting an impaired eNOS-activating capacity of HDL from ACS patients, showing that only a subset of patients undergoing STEMI, and in particular those developing an important inflammatory response, have circulating HDL defective in stimulating endothelial eNOS and NO production.