Serum profiles of C-C chemokines in acute myocardial infarction: Possible implication in postinfarction left ventricular remodeling
Serum profiles of C-C chemokines in acute myocardial infarction: Possible implication in postinfarction left ventricular remodeling
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DOI：
10.1089/107999002753536194
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发表时间：
2002-02-01
影响因子：
2.3
通讯作者：
Kremastinos, DT
中科院分区：
文献类型：
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作者：
Parissis, JT;Adamopoulos, S;Kremastinos, DT
C-C趋化因子是白细胞从循环系统募集和激活进入炎症组织的重要因素，并且可能在缺血引起的心肌损伤和急性心肌梗死（AMI）后的左心室重塑中发挥作用。我们研究了 AMI 患者血清中三种主要 C-C 趋化因子、巨噬细胞趋化蛋白-1 (MCP-1)、巨噬细胞炎症蛋白-1α (MIP-1α) 和调节正常 T 细胞表达和分泌的激活 (RANTES) 的动力学，并将结果与疾病的严重程度相关联。在住院第一周和入院后 1 个月内，通过 ELISA 连续测定 35 名 AMI 患者的 C-C 趋化因子血清水平。将无并发症的 AMI（Killip I 级）患者（n = 18）分为 A 组，AMI 并发心力衰竭表现（Killip II 级和 III 级）患者（n = 17）分为 B 组，并以 15 名年龄和性别匹配的志愿者作为健康对照。在 7 天住院期间，两个 AMI 组均观察到血清 C-C 趋化因子持续增加。 B 组这些炎症因子的峰值显着高于 A 组（MCP-1，295 +/- 11 vs. 203 +/- 9 pg/ml，p < 0.01；MIP-1α，30 +/- 1 vs. 24 +/- 2 pg/ml，p < 0.05；RANTES，32 +/- 2 vs. 16 +/- 1 ng/ml，p < 0.01）和健康对照（MCP-1，125 +/- 7 pg/ml，p < 0.001；MIP-1alpha，14 +/- 1 pg/ml，p < 0.001；RANTES，12 +/- 1 ng/ml，p < 0.001）。在 B 组中，MCP-1 峰值和 C 反应蛋白水平峰值 (r = 0.55，p < 0.02) 以及楔压 (r = 0.40，p < 0. 05) 之间存在显着相关性。在同一组中，MIP-1α水平的峰值也与血清肌酸激酶心肌带（MB）（r = 0.51，p < 0.04）和左心室射血分数（LVEF）（r = -0.45，p < 0.05）的峰值显着相关。 1个月后，患有严重左心室功能障碍（LVEF小于或等于35%）的AMI患者（n = 14）表现出比其他AMI患者（n = 21）（LVEF > 35%）显着更高的C-C趋化因子水平（所有p < 0.05）。在该患者群体中，MIP-1α 水平与左心室舒张末期内径之间存在显着相关性（r = 0.47，p < 0.03）。总之，我们检测到 AMI 病程中主要 C-C 趋化因子显着升高，在 AMI 并发心力衰竭表现和严重左心室功能不全的患者中水平最高。这些趋化炎症因子的升高可能积极促进该疾病的病理生理学和随后的左心室重塑。
C-C chemokines are essential factors in the recruitment and activation of leukocytes from the circulation into inflamed tissue and may play a role in ischemia-induced myocardial injury and left ventricular remodeling after acute myocardial infarction (AMI). We investigated the kinetics of three major C-C chemokines, macrophage chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and regulated on activation normally T cell expressed and secreted (RANTES), in the sera of AMI patients and correlated the findings with the severity of the disease. Serum levels of C-C chemokines were determined in 35 AMI patients by ELISA assays serially during the first week of hospitalization and 1 month after hospital admission. Patients (n = 18) with uncomplicated AMI (Killip class I) were classified as group A, patients (n = 17) with AMI complicated by heart failure manifestations (Killip classes II and III) were classified as group B, and 15 age-matched and sex-matched volunteers were used as healthy controls. A sustained increase in serum C-C chemokines was observed in both AMI groups during the 7-day hospitalization period. Peaks of these inflammatory factors were significantly higher in group B than in group A (MCP-1, 295 +/- 11 vs. 203 +/- 9 pg/ml, p < 0.01; MIP-1α, 30 +/- 1 vs. 24 +/- 2 pg/ml, p < 0.05; RANTES, 32 +/- 2 vs. 16 +/- 1 ng/ml, p < 0.01) and healthy controls (MCP-1, 125 +/- 7 pg/ml, p < 0.001; MIP-1alpha, 14 +/- 1 pg/ml, p < 0.001; RANTES, 12 +/- 1 ng/ml, p < 0.001). In group B, significant correlations were found between the peak of MCP-1 and the peak of C-reactive protein levels (r = 0.55, p < 0.02) as well as wedge pressure (r = 0.40, p < 0. 05). In the same group, the peak of MIP-1alpha levels was also significantly correlated with the peak of serum creatine kinase-myocardial band (MB) (r = 0.51, p < 0.04) and left ventricular ejection fraction (LVEF) (r = -0.45, p < 0.05). After 1 month, AMI patients (n = 14) with severe left ventricular dysfunction (LVEF less than or equal to 35%) exhibited significantly higher levels of C-C chemokines (all p < 0.05) than the other AMI patients (n = 21) (LVEF > 35%). A significant correlation was found between MIP-1alpha levels and left ventricular end-diastolic diameter (r = 0.47, p < 0.03) in this patient population. In conclusion, we have detected a significant elevation of major C-C chemokines during the course of AMI, with the highest levels in patients with AMI complicated by heart failure manifestations and severe left ventricular dysfunction. The elevation of these chemotactic inflammatory factors may actively contribute to the pathophysiology of the disease and the subsequent left ventricular remodeling.