摘要目的 观察冠心病患者促炎因子白细胞介素(IL)-1β和抑炎因子IL-10的全身水平与病变局部水平的关系.方法 入选慢性稳定性心绞痛(SA)、不稳定性心绞痛/非ST段抬高型心肌梗死(UA/NSTEMI)、ST段抬高型心肌梗死(STEMI)和拟诊冠心病但冠状动脉造影正常者(对照组)各30例.在所有患者(n=120)的主动脉根部(代表全身水平)、冠状动脉疾病患者(n=90)的冠状动脉病变以远和14例STEMI患者的冠状静脉窦取血,采用ELISA法检测IL-1β和II-10水平,并比较IL-1 β和IL-10全身水平和病变局部水平.结果 对照组、SA、UA/NSTEMI和STEMI组全身IL-1 β水平分别为lg-1(0.97±0.42)、lg-1(0.98±0.43)、lg-11.21±0.42)和lg-1(1.30±0.43)ng/L,UA/NSTEMI和STEMI组均明显高于对照组(P＜0.05,P＜0.01);IL-10水平分别为lg-1(0.77±0.29)、lg-1(0.73±0.45)、lg-1(0.75±0.35)和lg-1(1.14±0.36)ng/L,STEMI组IL-10水平高于对照组(P＜0.01).SA组粥样硬化病变以远IL-1β和IL-10水平分别为lg-1(0.98±0.41)和lg-1(0.67±0.47)ng/L,与全身水平比较差异无统计学意义;UA/NSTEMI组粥样硬化病变以远IL-1 β和IL-10水平分别为lg-1(1.22±0.48)和lg-1(0.89±0.46)ng/L,IL-10血浆浓度高于全身水平(P=0.024),IL-1β水平差异无统计学意义;STEMI组罪犯病变以远IL-1β和IL-10水平分别为lg-1(1.45±0.45)和lg-1(1.35±0.31)ng/L,均高于全身水平(P均＜0.01).左冠状动脉急性闭塞的STEMI患者的全身、冠状动脉内病变以远和冠状静脉窦的IL-1β水平分别为lg-1(1.47±0.37)、lg-1(1.65±0.34)和lg-1(1.53±0.35)ng/L,IL-10水平分别为lg-1(1.06±0.48)、lg-1(1.34±0.39)和lg-1(1.34±0.23)ng/L.冠状静脉窦IL-1β水平显著低于罪犯病变以远水平(P＜0.05),而IL-10水平差异无统计学意义.结论 促炎因子IL-1β和抑炎因子IL-10的全身水平可能不能完全真实反映动脉粥样硬化病变局部的炎症活动程度.

abstractsObjective To compare the systemic and local near atherosclerosis lesion levels of proinflammatory factor interleukin-1β (IL-1β) and anti-inflammatory factor IL-10 in patients with coronary artery disease (CAD). Methods Plasma samples were collected from 30 individuals without angiographical coronary artery stenosis (control group), 90 patients with CAD (stable angina pectoris, SA, n = 30,unstable angina pectoris/non-ST-segment elevation myocardial infarction, UA/NSTEMI, n = 30 and ST-segment elevation myocardial infarction, STEMI, n = 30). During diagnostic coronary angiography or interventional procedures, systemic samples were obtained from aorta root in all patients (n = 120), local samples from distal of the coronary lesion in patients with CAD (n = 90), and samples from coronary sinus of 14 patients with STEMI. IL-1β and IL-10 were determined by ELISA method. Results The result showed systemic levels of IL-1β were lg-1 (0. 97 ±0. 42), lg-1 (0. 98 ±0. 43), lg-1 ( 1.21 ±0. 42), lg-1 ( 1.30 ±0. 43)ng/L in the control, SA,UA/NSTEMI and STEMI groups, were significantly higher in UA/NSTEMI and STEMI groups compared with the control group (P ＜ 0. 05, P ＜0. 01 ); systemic IL-10 levels were lg-1 (0. 77 ± 0. 29), lg - 1 (0. 73 ± 0. 45 ), lg- 1 (0. 75 ± 0. 35 ), lg- 1 ( 1.14 ± 0. 36) ng/L in the four groups and was significantly higher in STEMI group than the control group ( P ＜ 0. 01 ). The local concentration of IL-1β and IL-10 were similar as the systemic levels in SA group [lg-1 (0.98 ±0.41 ), lg-1 (0.67 ±0.47)ng/L], local IL-1β [lg-1 ( 1.22 ±0. 48) ng/L] was similar while local IL-10 [lg-1 (0. 89 ±0. 46) ng/L]was significantly higher than the systemic levels in UA/NSTEMI group. The local levels of IL-1β and IL-10 [lg-1 ( 1.45 ±0. 45), lg-1 ( 1.35 ±0. 31 ) ng/L] were both significantly higher than the systemic levels in STEMI group ( all P ＜ 0. 01 ). The IL-1β levels of systemic, local and coronary sinus in STEMI patients with acute totally occluded left coronary artery [lg-1 ( 1.47 ± 0. 37 ), lg- 1 ( 1.65 ± 0. 34), lg- 1 ( 1.53 ± 0. 35 )ng/L] and the IL-10 levels [lg-1 ( 1.06 ± 0. 48 ), lg- 1 ( 1.34 ± 0. 39 ), lg-1 ( 1.34 ± 0. 23 ) ng/L] were similar. The level of IL-1β in coronary sinus was significantly lower than in culprit lesion (P＜0. 05) while IL-10 levels were similar at these two sites ( P ＞ 0. 05 ). Conclusion The systemic level of pro-inflammatory marker IL-I β and anti-inflammatory marker IL-10 could not rehably reflect the local inflammatory status near the atherosclerosis plaque locations.