Lev Eli I, Alviar Carlos L, Arikan Mehmet E, Dave Bijal P, Granada Juan F, DeLao Timothy, Tellez Armando, Maresh Kelly, Kleiman Neal S
The Methodist Hospital Research Institute and the Methodist DeBakey Heart Center, The Methodist Hospital, Houston, TX 77030, USA.
Am Heart J. 2007 Jan;153(1):41.e1-6. doi: 10.1016/j.ahj.2006.10.020.
Recent case control studies suggest that patients with subacute stent thrombosis (SAT) have increased platelet reactivity. However, SAT often presents as acute myocardial infarction (AMI), which is also associated with augmented platelet activation. We therefore compared platelet reactivity in patients with SAT and patients with AMI unrelated to stenting.
We identified 20 patients with SAT, 20 patients with ST-elevation AMI who underwent primary percutaneous coronary intervention (PCI), and 20 patients who underwent stenting without SAT occurrence (stable control group). Platelet function was measured > or = 3 days after PCI in the SAT (repeat procedure) and AMI groups and > or = 3 months after stenting in the stable group. All patients received aspirin and clopidogrel. Platelet reactivity was evaluated by aggregation in response to 5 and 20 micromol/L of adenosine diphosphate and 1.5 mmol/L arachidonic acid, and by flow cytometric determination of P-selectin and glycoprotein IIb/IIIa activation.
Clinical characteristics were similar among the groups. Platelet testing was performed 4.9 +/- 1.7, 3.1 +/- 0.3, and 108 +/- 22 days after PCI in the SAT, AMI, and stable groups, respectively. The SAT group had higher platelet aggregation and activation markers than the stable group. However, platelet aggregation and activation was very similar in the SAT and AMI groups.
Patients with SAT have increased platelet reactivity, compared with patients who do not develop SAT following stenting. However, the augmented platelet reactivity does not appear to differ from patients with AMI unrelated to stenting. This study highlights the need for large prospective studies to determine whether platelet hyperreactivity increases the risk of SAT.
近期的病例对照研究表明,亚急性支架血栓形成(SAT)患者的血小板反应性增加。然而,SAT常表现为急性心肌梗死(AMI),这也与血小板激活增强有关。因此,我们比较了SAT患者与非支架置入相关AMI患者的血小板反应性。
我们纳入了20例SAT患者、20例接受直接经皮冠状动脉介入治疗(PCI)的ST段抬高型AMI患者以及20例接受支架置入且未发生SAT的患者(稳定对照组)。在SAT组(重复操作)和AMI组中,于PCI术后≥3天测量血小板功能;在稳定组中,于支架置入术后≥3个月测量血小板功能。所有患者均接受阿司匹林和氯吡格雷治疗。通过检测血小板对5和20 μmol/L二磷酸腺苷以及1.5 mmol/L花生四烯酸的聚集反应,以及通过流式细胞术测定P选择素和糖蛋白IIb/IIIa的激活情况来评估血小板反应性。
各组间临床特征相似。SAT组、AMI组和稳定组分别在PCI术后4.9±1.7天、3.1±0.3天和108±22天进行血小板检测。SAT组的血小板聚集和激活标志物高于稳定组。然而,SAT组和AMI组的血小板聚集和激活情况非常相似。
与支架置入后未发生SAT的患者相比,SAT患者的血小板反应性增加。然而,血小板反应性增强似乎与非支架置入相关AMI患者并无差异。本研究强调需要进行大型前瞻性研究,以确定血小板高反应性是否会增加SAT的风险。