冠心病患者冠状动脉支架植入术后糖代谢异常对非靶病变进展的影响

Effect of abnormal glucose metabolism on the progression of non-target lesions after coronary stenting in patients with coronary heart disease

目的探讨冠心病患者冠状动脉支架植入术后糖代谢异常对非靶病变进展的影响。方法分析中国冠状动脉粥样硬化斑块进展多变量回顾分析研究(RIPPER)中2010年1月至2016年7月接受冠状动脉造影(CAG)并在12~24个月复查CAG的冠心病患者病变进展多变量数据,共1108例患者第1次CAG记录到至少1处冠状动脉非靶病变,采用定量冠状动脉造影(QCA)方法分析2次造影病变程度。冠状动脉支架植入术后非靶病变进展定义:病变冠状动脉先前有≥50%狭窄,其直径减少≥10%;或先前有<50%狭窄,其直径减少≥30%。根据是否出现非靶病变进展分两组,比较两组间人口学特征、临床和实验室检验、QCA分析结果,评估非靶病变进展危险因素。结果1108例中264例(23.8%)有靶病变进展(进展组),844例无进展(无进展组)。进展组患者男性比例明显高于无进展组[80.3%(212/264)对74.3%(627/844),P=0.047],随访期C-反应蛋白(CRP)、基线期餐后2 h血糖均明显高于无进展组[1.18 mg/L对0.80 mg/L,P=0.026;8.33 mmol/L对7.90 mmol/L,P=0.016],非靶病变数明显多于无进展组(P<0.001)。两组间其他糖代谢指标差异均无统计学意义(P>0.05)。多因素logistics回归分析显示,基线期餐后2 h血糖(OR=1.082,95%CI=1.029~1.138,P=0.002)、非靶病变数(OR=1.741,95%CI=1.447~2.094,P<0.001)为冠心病患者非靶病变进展的独立危险因素,提示基线期餐后2 h血糖每升高1 mmol/L,非靶病变斑块进展风险提高8.2%,非靶病变数每增加1枚,非靶病变斑块进展风险提高74.1%。结论基线期餐后2 h血糖升高、非靶病变数是冠心病患者支架植入术后非靶病变进展的独立危险因素。

Objective To investigate the effect of abnormal glucose metabolism on the progression of non-target lesions after coronary stenting in patients with coronary heart disease(CHD).Methods The multivariate data of the lesion progression in the CHD patients,who received coronary angiography(CAG)during the period from January 2010 to July 2016 and received CAG again within 12-24 months after initial CAG,were collected from the retrospective analysis data of Chinese Coronary Plaque Progression Multivariate(RIPPER)study.A total of 1108 patients were enrolled in this study,whom at least one non-target coronary lesion was recorded in the initial CAG.By using quantitative coronary angiography(QCA)method,the degrees of non-target coronary lesions observed on the two CAGs were analyzed.The pathological progression of nontarget lesions after coronary stenting was defined as follows:the previous stenosis of diseased coronary artery was≥50%and the reduction in its diameter was≥10%;or the previous stenosis of diseased coronary artery was<50%and the reduction in its diameter was≥30%.Depending on whether there was pathological progression of non-target lesion,the patients were divided into progression group and non-progression group.The demographic characteristics,clinical features and laboratory testing findings and QCA analysis results were compared between the two groups.The risk factors for progression of non-target lesions were evaluated.Results Among 1108 patients,264 patients(23.8%)had non-target lesion progression(progression group)and 844 patients(76.2%)showed no non-target lesion progression(non-progression group).The proportion of male in the progression group was 80.3%(212/264),which was significantly higher than 74.3%(627/844)in non-progressive group(P=0.047).During the follow-up period,C-reactive protein(CRP),2-hour postprandial glucose at the baselinein the progression group were 1.18 mg/L and 8.33 mmol/L respectively,which were 0.80 mg/L and 7.90 mmol/L respectively in the non-progressive group,the differences between the two groups were statistically significant(P=0.026 and P=0.016 respectively).The number of non-target lesionsin the progression group was strikingly higher than that in the non-progressive group(P<0.001).No statistically significant differences in other glucose metabolism indicators existed between the two groups(P>0.05).Multivariate logistics regression analysis indicated that 2-hour postprandial glucose(OR=1.082,95%CI=1.029-1.138,P=0.002)and number of non-target lesions(OR=1.741,95%CI=1.447-2.094,P<0.001)were the independent risk factors for the progression of non-target lesions in CHD patients,suggesting that every one mmol/L increase of blood glucose in basic 2-hour postprandial glucose level would increase the risk of non-target plaque progression by 8.2%;and that every increase of one in the number of non-target lesions would increase the risk of non-target plaque progression by 74.1%.Conclusion The elevated 2-hour postprandial glucose level and the number of non-target lesions are independent risk factors for the progression of non-target lesions in CHD patients after coronary stenting.