Soluble, platelet-bound, and total P-selectin as indices of platelet activation in congestive heart failure
Soluble, platelet-bound, and total P-selectin as indices of platelet activation in congestive heart failure
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DOI：
10.1080/07853890802227089
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发表时间：
2009-01-01
影响因子：
4.4
通讯作者：
Lip, Gregory Y. H.
中科院分区：
文献类型：
--
作者：
Chung, Irene;Choudhury, Anirban;Lip, Gregory Y. H.
背景资料。许多与充血性心力衰竭(CHF)相关的并发症都与血栓形成相关。血小板在血栓形成中起着重要作用，但目前尚不清楚循环中的血小板是否积极参与了与心力衰竭相关的血栓相关并发症。目标。目的：比较慢性心力衰竭(CHF)患者与疾病对照组和健康对照组的血小板活化指标--可溶性P-选择素、血小板表面P-选择素和总P-选择素，并评价其在CHF中的预后价值。方法：研究方法。用流式细胞仪检测108例稳定性充血性心力衰竭患者(左心室射血分数均为50%)的可溶性P-选择素(P-sel)、总P-选择素(PP-sel)、血小板表面P-选择素(CD62P%G)和CD63%G(CD63%G)。并与50名健康对照组和70名“疾病对照组”(左心室收缩功能正常的冠心病患者)进行比较。结果。CHF患者和疾病对照组的sP-SEL、CD62P%G和CD63%G均高于健康对照组。SP-SEL、PP-SEL、CD62P%G、CD63%G与射血分数无显著相关性(P均0.05)。当对CHF的缺血性和非缺血性病因进行比较时，这些标记物没有差异。平均随访490天(范围340-)，有7例死亡，15例因心力衰竭恶化住院，1例心脏再同步治疗，4例血管重建，4例心肌梗死，1例中风。在随访时，所有的血小板标志物都不能预测复合终点。结论。尽管使用了抗血小板药物，但稳定性充血性心力衰竭患者仍有异常血小板激活的证据。这些异常并不决定预后，与疾病对照中看到的大致相似，表明CHF中的血小板异常可能只是与相关的合并症有关。
Background. Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF. Objective. To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHF patientscompared to 'disease controls' and 'healthy controls'and to assess their prognostic value in CHF. Methods. We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel 'platelet lysate' assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometryin 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) 50%). Levels were compared with 50 healthy controls and 70 'disease controls' (patients with coronary artery disease with normal left ventricular systolic function). Results. CHF patients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340-535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up. Conclusions. Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in 'disease controls' indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.