| Objective: The purpose of this study is to investigate the atherosclerotic plaquecharacteristics and distribution, seven cycling markers are simultaneously measuredby Cytometric bead array measured through cytometer, to analyze the relationshipbetween vulnerable plaque and seven cycling markers in patients with acute coronarysyndrome (ACS) using intravascular ultrasound (IVUS).Methods: Fifty-five nonbifurcation native coronary lesions (in 76 patients) wereimaged in vivo using 20-MHz 1VUS transducers before implanting stent. Targetlesions were identified on the basis of clinic, electrocardiography, and angiographicdata. Qualitative assessment and quantitative measurements of the lesions wereperformed by IVUS in lesions site. The paramters including external elasticmembrane cross-sectional area,lumen cross-sectional area,plaque burden and plaquecross-sectional were measured in lesions site and references site. The 10 mm-longlesion segment (5 mm proximal and 5 mm distal to the lesion site) was detected forqualitative assessment. As well as, these lesions were divided into groups of softplaque, fibrous plaque, calcified plaque and mixed plaque according to differentdegree of ultrasound signal. Remodeling index (RI)was calculated (RI=the area oflesion external elastic membrane/the area of mean reference external elasticmembrane). These lesions also were divided into 2 groups: positive remodeling group(RI＞1.0) and intermediate/negative remodeling group(RI=1.0). 76 targetlesions were divided into rupture group and no rupture group according to plaquerupture. Their serum IL-6, IL-8, sCD40L, MCP-1, sP-selectin, t-PA and sVCAM-1levels were simultaneously measured by Cytometric bead array measured throughcytometer. Meanwhile, we collected clinical data (such as age, gender, body massindex, hypertension history, hyperlipemia history, diabetes mellitus history andsmoking), and laboratory biochemical data[such as fasting blood glucose, totalcholesterol, triglyceride, high density lipoprotein cholesterol, low density lipoproteincholesterol, Apo-A1, Apo-B and Lp(a)].Results:①RI was significantly higher in rupture group compared to no rupturegroup (1.07±0.19 vs 0.97±0.08, P＜0.05). In rupture group positive remodeling wasmore frequent than that in no rupture group(66.7％vs 36.8％, P＜0.05). Both theplaque areas and the plaque burden were statisticly larger in rupture group than inno rupture group(11.1±2.7 mm~2 vs 9.0±2.6 mm~2, 77.2±12.0％vs 66.0±13.9％, P＜0.01, respectively). The lumen area was smaller in rupture group comparedto no rupture group(3.3±1.6 mm~2 vs 4.9±2.2 mm~2, P＜0.01).②The level ofHDL-C in positive remodeling group was higher than that of negative remodelinggroup (1.33±0.12mg/dl vs 1.20±0.08mg/dl, P=0.024), and TG was higher in positiveremodeling groups (2.47±0.33mg/dl vs 1.30±0.22mg/dl, P=0.046). RI was notsignificantly associated with HDL cholesterol (r=-0.019, P=0.93). But there weremoderate statistical correlation between RI and triglyceride (r=0.41, P=0.02).③The plasma tPA was showed significantly lower in rupture group compared to norupture group (1359.2±714.6 pg/ml vs 2052.8±1700.4 pg/ml, P＜0.05),the othersfactors not show significantly higher, tPA significant correlated with morphology ofpalques, and there were no correlation between each others vascular factors and thesize of plaques.④The results of seven cycling markers measured through cytometershowed that there were no significant correlated between tPA with other biomarkers,but most other biomarkers appeared in deferent stage of atherosis had correlation.Conclusions:①The vulnerable lesion including small lumen, large plaqueburden, large plaque area, positive remodeling, soft plaque, plaque rupture and thrombus were identified by IVUS in the patients with ACS. The direct reasons forACS may be due to small lumen or thrombus formation after plaque rupture, plaquerupture dose not completed reason.②The abnormal change of TG effected oncoronary artery remodeling. Higher TG is associated with positive remodeling.③tPAmay be an independent maker which reflects morphology of coronary atheroscleroticplaque in ACS patients; and that imply auto-protecting mechanism for antithrombosis.
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