Do platelet-derived microparticles play a role in depression, inflammation, and acute coronary syndrome?
Do platelet-derived microparticles play a role in depression, inflammation, and acute coronary syndrome?
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DOI：
10.1016/j.psym.2013.09.004
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发表时间：
2014-05
期刊：
影响因子：
3.4
通讯作者：
Ziegelstein, Roy C.
中科院分区：
文献类型：
--
作者：
Williams, Marlene S.;Rogers, Heather L.;Wang, Nae-Yuh;Ziegelstein, Roy C.
重度抑郁症是急性冠脉综合征（ACS）患者死亡率增加的独立预测因子。已经提出了几种机制来解释抑郁症和缺血性心脏病之间的联系。血小板生理学异常和炎症都被认为是潜在的混杂变量。我们着手研究ACS住院患者的血小板活化、炎症和抑郁水平。我们招募了28例ACS患者，并通过PHQ-9评估抑郁水平。通过测量血小板微粒水平和血小板对二磷酸腺苷和5-羟色胺的聚集来评估血小板活化。通过测量TNF α、IL-6和CRP评估炎症标志物。我们发现有中度抑郁症状的ACS患者TNF α、IL-6和CRP水平较高，血小板微粒水平也较高。PHQ-9 ≥ 10的ACS患者血小板聚集率高于ADP。我们的研究结果表明，患有中度抑郁症的急性冠脉综合征住院治疗的患者血小板聚集增加。这些患者的炎症标志物升高与血小板活化之间也存在正相关性，因此提示ACS患者中有可能改变血小板功能的抑郁症状的促炎成分。这些结果是有趣的，因为当测量血小板活化和炎症时，可能会发现解释抑郁症，炎症和心血管血栓形成增加之间联系的潜在途径。
Major depression is an independent predictor of increased mortality in patients presenting with acute coronary syndromes (ACS). There have been several mechanisms proposed to explain the link between depression and ischemic heart disease. Both abnormal platelet physiology and inflammation have been suggested as potential confounding variables. We set out to examine platelet activation, inflammation, and levels of depression in hospitalized patients presenting with ACS. We enrolled 28 patients with ACS and assessed levels of depression by PHQ-9. Platelet activation was assessed by the measurement of platelet microparticle levels and platelet aggregation to adenosine diphosphate and serotonin. Inflammatory markers were assessed by the measurement of TNF alpha, IL-6, and CRP. We found that ACS patients with moderate depressive symptoms who had higher TNF alpha, IL-6, and CRP levels had higher levels of platelet microparticles. We also found that ACS patients with PHQ-9 ≥ 10 had higher platelet aggregation to ADP. Our results suggest that patients hospitalized for the treatment of an ACS who have moderate depression have increased platelet aggregation. These patients also have a positive association between elevated inflammatory markers and platelet activation, thus suggesting a pro-inflammatory component in ACS patients with depressive symptoms that may alter platelet function. These results are intriguing in that a potential pathway to explain the connection between depression, inflammation, and increased cardiovascular thrombosis might be found when both platelet activation and inflammation are measured.
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