Anzai Toshihisa, Yoshikawa Tsutomu, Kaneko Hidehiro, Maekawa Yuichiro, Iwanaga Shiro, Asakura Yasushi, Ogawa Satoshi
Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Chest. 2004 Feb;125(2):384-9. doi: 10.1378/chest.125.2.384.
Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI.
We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI.
LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (+/- SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 +/- 12.6 vs 9.4 +/- 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of > or =20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (> or =60 years old), peak CK level (> or =3,000 IU/L), and peak WBC count (> or =12,000 cells/ microL).
A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.
大多数急性心肌梗死（AMI）后发生的左心室（LV）血栓在2周内形成，此时炎症细胞已浸润至坏死心肌。心内膜表面的炎症变化可能通过与促炎细胞因子相互作用诱导血小板沉积和纤维蛋白网形成。我们试图确定急性心肌梗死后血清C反应蛋白（CRP）升高所反映的炎症反应在左心室血栓形成中的意义。
我们检查了160例首次发生前壁急性心肌梗死的患者。通过连续测量确定血清肌酸激酶（CK）和CRP的峰值水平。发病后10至14天进行超声心动图检查。我们评估了急性心肌梗死后血清CRP水平升高与左心室血栓形成之间的关联。
13例患者（8%）观察到左心室血栓。两组患者在年龄、性别、冠状动脉危险因素、梗死前心绞痛、血管重建治疗和抗凝治疗的使用、血小板计数以及入院时纤维蛋白原水平方面无差异。尽管左心室血栓患者与无血栓患者的CK峰值水平相似，但左心室血栓患者的平均（±标准差）血清CRP峰值水平明显高于无血栓患者（18.0±12.6对9.4±8.1mg/dL；p = 0.001）。多变量分析显示，在包括年龄较大（≥60岁）、CK峰值水平（≥3000IU/L）和白细胞峰值计数（≥12000个细胞/微升）等变量中，CRP峰值水平≥20mg/dL是血栓形成的独立预测因素（相对风险，4.82；p = 0.037）。
血清CRP水平升高幅度越大，急性心肌梗死后左心室血栓的发生率越高，提示炎症反应在壁血栓形成中起重要作用。
