中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2011年
2期
142-146
,共5页
颜红兵%李文铮%赵汉军%宋莉%郑斌%周鹏%刘臣
顏紅兵%李文錚%趙漢軍%宋莉%鄭斌%週鵬%劉臣
안홍병%리문쟁%조한군%송리%정빈%주붕%류신
冠状动脉疾病%白细胞介素-1β%白细胞介素-10
冠狀動脈疾病%白細胞介素-1β%白細胞介素-10
관상동맥질병%백세포개소-1β%백세포개소-10
Coronary disease%Interleukin-1beta%Interleukin-10
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.
目的 觀察冠心病患者促炎因子白細胞介素(IL)-1β和抑炎因子IL-10的全身水平與病變跼部水平的關繫.方法 入選慢性穩定性心絞痛(SA)、不穩定性心絞痛/非ST段抬高型心肌梗死(UA/NSTEMI)、ST段抬高型心肌梗死(STEMI)和擬診冠心病但冠狀動脈造影正常者(對照組)各30例.在所有患者(n=120)的主動脈根部(代錶全身水平)、冠狀動脈疾病患者(n=90)的冠狀動脈病變以遠和14例STEMI患者的冠狀靜脈竇取血,採用ELISA法檢測IL-1β和II-10水平,併比較IL-1 β和IL-10全身水平和病變跼部水平.結果 對照組、SA、UA/NSTEMI和STEMI組全身IL-1 β水平分彆為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組均明顯高于對照組(P＜0.05,P＜0.01);IL-10水平分彆為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組IL-10水平高于對照組(P＜0.01).SA組粥樣硬化病變以遠IL-1β和IL-10水平分彆為lg-1(0.98±0.41)和lg-1(0.67±0.47)ng/L,與全身水平比較差異無統計學意義;UA/NSTEMI組粥樣硬化病變以遠IL-1 β和IL-10水平分彆為lg-1(1.22±0.48)和lg-1(0.89±0.46)ng/L,IL-10血漿濃度高于全身水平(P=0.024),IL-1β水平差異無統計學意義;STEMI組罪犯病變以遠IL-1β和IL-10水平分彆為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).左冠狀動脈急性閉塞的STEMI患者的全身、冠狀動脈內病變以遠和冠狀靜脈竇的IL-1β水平分彆為lg-1(1.47±0.37)、lg-1(1.65±0.34)和lg-1(1.53±0.35)ng/L,IL-10水平分彆為lg-1(1.06±0.48)、lg-1(1.34±0.39)和lg-1(1.34±0.23)ng/L.冠狀靜脈竇IL-1β水平顯著低于罪犯病變以遠水平(P＜0.05),而IL-10水平差異無統計學意義.結論 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實反映動脈粥樣硬化病變跼部的炎癥活動程度.
목적 관찰관심병환자촉염인자백세포개소(IL)-1β화억염인자IL-10적전신수평여병변국부수평적관계.방법 입선만성은정성심교통(SA)、불은정성심교통/비ST단태고형심기경사(UA/NSTEMI)、ST단태고형심기경사(STEMI)화의진관심병단관상동맥조영정상자(대조조)각30례.재소유환자(n=120)적주동맥근부(대표전신수평)、관상동맥질병환자(n=90)적관상동맥병변이원화14례STEMI환자적관상정맥두취혈,채용ELISA법검측IL-1β화II-10수평,병비교IL-1 β화IL-10전신수평화병변국부수평.결과 대조조、SA、UA/NSTEMI화STEMI조전신IL-1 β수평분별위lg-1(0.97±0.42)、lg-1(0.98±0.43)、lg-11.21±0.42)화lg-1(1.30±0.43)ng/L,UA/NSTEMI화STEMI조균명현고우대조조(P＜0.05,P＜0.01);IL-10수평분별위lg-1(0.77±0.29)、lg-1(0.73±0.45)、lg-1(0.75±0.35)화lg-1(1.14±0.36)ng/L,STEMI조IL-10수평고우대조조(P＜0.01).SA조죽양경화병변이원IL-1β화IL-10수평분별위lg-1(0.98±0.41)화lg-1(0.67±0.47)ng/L,여전신수평비교차이무통계학의의;UA/NSTEMI조죽양경화병변이원IL-1 β화IL-10수평분별위lg-1(1.22±0.48)화lg-1(0.89±0.46)ng/L,IL-10혈장농도고우전신수평(P=0.024),IL-1β수평차이무통계학의의;STEMI조죄범병변이원IL-1β화IL-10수평분별위lg-1(1.45±0.45)화lg-1(1.35±0.31)ng/L,균고우전신수평(P균＜0.01).좌관상동맥급성폐새적STEMI환자적전신、관상동맥내병변이원화관상정맥두적IL-1β수평분별위lg-1(1.47±0.37)、lg-1(1.65±0.34)화lg-1(1.53±0.35)ng/L,IL-10수평분별위lg-1(1.06±0.48)、lg-1(1.34±0.39)화lg-1(1.34±0.23)ng/L.관상정맥두IL-1β수평현저저우죄범병변이원수평(P＜0.05),이IL-10수평차이무통계학의의.결론 촉염인자IL-1β화억염인자IL-10적전신수평가능불능완전진실반영동맥죽양경화병변국부적염증활동정도.
Objective 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.
