Ederhy Stéphane, Di Angelantonio Emanuele, Mallat Ziad, Hugel Bénédicte, Janower Sandra, Meuleman Catherine, Boccara Franck, Freyssinet Jean-Marie, Tedgui Alain, Cohen Ariel
Cardiology Department, Saint-Antoine University and Medical School, Université Pierre et Marie Curie, and INSERM U689, Hôpital Lariboisière, Paris, France.
Am J Cardiol. 2007 Sep 15;100(6):989-94. doi: 10.1016/j.amjcard.2007.04.040. Epub 2007 Jul 2.
Circulating procoagulant microparticles (MPs) arising from cell activation or fragmentation during apoptosis retain procoagulant properties and are increased in severe thrombotic states. We investigated whether circulating procoagulant MP levels would be increased in nonvalvular atrial fibrillation (AF). Using a hospital case-control study design, circulating procoagulant MP levels were measured in 45 patients with permanent and/or persistent AF who were not receiving anticoagulant therapy and 90 age-matched control subjects (45 with cardiovascular risk factors and 45 without). Annexin V-positive MP levels (expressed as nanomoles per liter of phosphatidylserine equivalent) were higher in patients with AF (median 9.3, interquartile range 6.8 to 17.3 nmol/L) than in control subjects with cardiovascular risk factors (median 4.9, interquartile range 3.7 to 8.4 nmol/L) and control subjects without cardiovascular risk factors (median 3.2, interquantile range 2.3 to 4.6 nmol/L; p<0.001). Platelet-derived MPs (captured with antiglycoprotein Ib) and endothelial-derived MPs (captured with anti-CD31) were similar in patients with AF and control subjects with cardiovascular risk factors but were significantly higher than in control subjects without cardiovascular risk factors. On multiple regression analysis, the presence of AF was a strong predictor of annexin V-positive MP level (p<.001). In conclusion, circulating procoagulant MPs are increased in persistent and/or permanent AF and might reflect a hypercoagulable state that could contribute to atrial thrombosis and thromboembolism.
凋亡过程中因细胞活化或破碎产生的循环促凝微粒(MPs)保留了促凝特性,并且在严重血栓形成状态下数量会增加。我们研究了非瓣膜性心房颤动(AF)患者的循环促凝MP水平是否会升高。采用医院病例对照研究设计,对45例未接受抗凝治疗的永久性和/或持续性AF患者以及90例年龄匹配的对照者(45例有心血管危险因素,45例无心血管危险因素)测量循环促凝MP水平。AF患者中膜联蛋白V阳性MP水平(以每升磷脂酰丝氨酸当量的纳摩尔数表示)(中位数9.3,四分位间距6.8至17.3 nmol/L)高于有心血管危险因素的对照者(中位数4.9,四分位间距3.7至8.4 nmol/L)和无心血管危险因素的对照者(中位数3.2,四分位间距2.3至4.6 nmol/L;p<0.001)。AF患者和有心血管危险因素的对照者中血小板衍生的MPs(用抗糖蛋白Ib捕获)和内皮衍生的MPs(用抗CD31捕获)相似,但显著高于无心血管危险因素的对照者。多因素回归分析显示,AF的存在是膜联蛋白V阳性MP水平的强预测因素(p<.001)。总之,持续性和/或永久性AF患者的循环促凝MPs增加,可能反映了一种高凝状态,这可能导致心房血栓形成和血栓栓塞。