Zhonghua xin xue guan bing za zhi · 2011
[Clinical implication and association between local and systemic levels of interleukin-1β and interleukin-10 in patients with coronary artery disease].
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Yan Hong-bing, Li Wen-zheng, Zhao Han-jun, Song Li, Zheng Bin, Zhou Peng, Liu Chen
Аннотация
OBJECTIVE: To compare the systemic and local near atherosclerosis lesion levels of pro-inflammatory 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-1β and anti-inflammatory marker IL-10 could not reliably reflect the local inflammatory status near the atherosclerosis plaque locations.
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-1β and anti-inflammatory marker IL-10 could not reliably reflect the local inflammatory status near the atherosclerosis plaque locations.