Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization.
Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization.
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DOI：
10.1016/s0022-5223(94)70286-1
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发表时间：
1994-10
期刊：
影响因子：
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通讯作者：
H. Hennein;Hailu Ebba;Jorge L. Rodriguez;S. Merrick;F. Keith;M. Bronstein;J. Leung;D. Mangano;L. Greenfield;J. Rankin
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文献类型：
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作者：
H. Hennein;Hailu Ebba;Jorge L. Rodriguez;S. Merrick;F. Keith;M. Bronstein;J. Leung;D. Mangano;L. Greenfield;J. Rankin
促炎细胞因子涉及介导与心肌梗塞、严重充血性心力衰竭和脓毒症相关的心肌功能障碍。我们检验了这样的假设：简单的冠状动脉旁路移植术后细胞因子水平升高，并且与术后心肌缺血和功能障碍的发作相关。冠状动脉搭桥术在全身麻醉下进行，全身中度低温和冷血钾心脏停搏液。通过生物测定法测定肿瘤坏死因子-α和白细胞介素6水平，通过夹心酶联免疫吸附测定法测定白细胞介素8水平。通过术中经食管超声心动图和围手术期 12 通道动态心电图监测评估心肌功能和缺血发作。总共有 22 名患者接受了研究，没有死亡或并发症。动脉肿瘤坏死因子-α呈双峰分布上升，分别在术后2小时和18至24小时达到峰值（20.2±6.4pg/ml，[平均值±平均值标准误差]）和5.8±1.6pg/ml；体外循环前：0.90 ± 0.20 pg/ml，两个峰 p < 0.001），然后逐渐下降至体外循环前的水平。动脉白细胞介素 6 在心肺转流终止后立即达到最高水平，并在心肺转流后 12 至 18 小时再次达到峰值（分别为 7520 ± 2439 pg/ml 和 6216 ± 1928 pg/ml；转流前：746 ± 187 pg/ml，两个峰值的 p< 0.0001）。动脉白细胞介素8水平变化较大，但遵循相似的模式，在体外循环后的早期达到峰值，并在术后16至18小时再次达到峰值（分别为4110±1403pg/ml和1760±1145pg/ml；在体外循环之前：两个峰值均为461±158.p<0.05）。通过多变量分析，主动脉钳夹时间可以独立预测术后细胞因子水平。左心室壁运动异常与白细胞介素 6 和白细胞介素 8 水平相关，评分恶化与白细胞介素 6 水平升高相关（白细胞介素 6，p= 0.003；白细胞介素 8，p= 0.05）。术后心肌缺血发作与白细胞介素 6 水平相关，七名患者中有六名 (85%) 在白细胞介素 6 浓度达到峰值后发生心肌缺血 (p< 0.01)。我们的结论是，在简单的冠状动脉血运重建后，促炎细胞因子升高，可能导致术后心肌缺血和节段性室壁运动异常。 (胸心血管外科杂志 1994;108:626-35)
The proinflammatory cytokines have been implicated in mediating myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. We tested the hypothesis that cytokine levels are elevated after uncomplicated coronary artery bypass grafting and associated with episodes of postoperative myocardial ischemia and dysfunction. Coronary artery bypass grafting was performed under general anesthesia with moderate systemic hypothermia and cold-blood potassium cardioplegic solution. Tumor necrosis factor-α and interleukin-6 levels were determined by bioassays, and interleukin-8 levels were measured by a sandwich enzyme-linked immunosorbent assay. Myocardial function and ischemic episodes were assessed by intraoperative transesophageal echocardiography and perioperative 12-channel Holter monitoring. A total of 22 patients were studied, with no deaths or complications. Arterial tumor necrosis factor-α rose in a bimodal distribution, peaking at 2 and 18 to 24 hours after the operation (at 20.2 ± 6.4 pg/ml, [mean ± standard error of the mean]) and 5.8 ± 1.6 pg/ml, respectively; before cardiopulmonary bypass: 0.90 ± 0.20 pg/ml, p < 0.001 for both peaks) then progressively declined to levels before bypass. Arterial interleukin-6 was maximally elevated immediately on termination of cardiopulmonary bypass and peaked again 12 to 18 hours after cardiopulmonary bypass (at 7520 ± 2439 pg/ml and 6216 ± 1928 pg/ml, respectively; before bypass: 746 ± 187 pg/ml,p< 0.0001 for both peaks). Arterial interleukin-8 levels were more variable but followed a similar pattern, peaking in the early period after cardiopulmonary bypass and again at 16 to 18 hours after the operation (at 4110 ± 1403 pg/ml and 1760 ± 1145 pg/ml, respectively; before bypass: 461 ± 158.p< 0.05 for both peaks). By multivariate analysis, the aortic crossclamp time was independently predictive of postoperative cytokine levels. Left ventricular wall motion abnormalities were associated with both interleukin-6 and interleukin-8 levels, worsening scores being associated with increasing levels (for interleukin-6,p= 0.003; for interleukin-8,p= 0.05). Postoperative myocardial ischemic episodes were associated with interleukin-6 levels, six of seven (85%) patients with episodes of myocardial ischemia after a peak in interleukin-6 concentrations (p< 0.01). We conclude that proinflammatory cytokines are elevated after uncomplicated coronary revascularization and may contribute to postoperative myocardial ischemia and segmental wall motion abnormalities. (J THORACCARDIOVASCSURG1994;108:626-35)