Nishio Kazuaki, Fukui Tomoyasu, Tsunoda Fumiyoshi, Kawamura Kitaro, Itoh Seiji, Konno Noburu, Ozawa Kou, Katagiri Takashi
The Third Department of Internal Medicine, School of Medicine Showa University, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.
Int J Cardiol. 2005 Aug 18;103(2):128-34. doi: 10.1016/j.ijcard.2004.08.039. Epub 2004 Dec 19.
The rationale of this study was to determine whether insulin resistance is an independent risk factor for restenosis after coronary stenting.
Previous studies suggested that hyperinsulinemia may be an important risk factor for ischemic heart disease. Restenosis after coronary stenting is neointimal tissue proliferation and de-novo stenosis is atherosclerosis from the point of view of histology. However, it has not been determined whether insulin resistance is independently related to restenosis after coronary stenting.
Clinical variables of unselected population of 110 patients were analyzed in multivariate logistic regression analyses for both restenosis and de-novo stenosis. Clinical, lesion-related, and procedural variables were analyzed by chi-square analysis, and relative risk.
Multivariate logistic regression analysis showed that homeostasis model assessment insulin resistance (HOMA-IR) and HbA1c were associated with restenosis after coronary stenting (HOMA-IR; P=0.0447, HbA1c; P=0.0462), and HbA1c and low-density lipoprotein cholesterol (LDL-C) were associated with de-novo stenosis (HbA1c; P=0.0201, LDL-C; P=0.0204). Restenosis was influenced by insulin resistance [Relative Risk (RR) 2.06; 95 percent confidence interval (95%CI) 1.20 to 3.56], diabetes mellitus (DM: RR 1.92; 95%CI 1.25 to 2.95), and final minimal lumen diameter (RR 2.83; 95%CI 1.32 to 6.06).
HOMA-IR and DM are the predictors of restenosis after coronary stenting, and HbA1c and LDL-C are the predictors of de-novo stenosis. These results may be reflected in histological differences between neointimal tissue proliferation as restenosis and atherosclerosis as de-novo stenosis.
本研究的目的是确定胰岛素抵抗是否为冠状动脉支架置入术后再狭窄的独立危险因素。
先前的研究表明,高胰岛素血症可能是缺血性心脏病的重要危险因素。从组织学角度来看,冠状动脉支架置入术后的再狭窄是新生内膜组织增生,而新生狭窄是动脉粥样硬化。然而,尚未确定胰岛素抵抗是否与冠状动脉支架置入术后的再狭窄独立相关。
对110例未选择人群的临床变量进行多因素逻辑回归分析,以评估再狭窄和新生狭窄情况。通过卡方分析和相对风险分析临床、病变相关及手术变量。
多因素逻辑回归分析显示,稳态模型评估胰岛素抵抗(HOMA-IR)和糖化血红蛋白(HbA1c)与冠状动脉支架置入术后的再狭窄相关(HOMA-IR;P=0.0447,HbA1c;P=0.0462),HbA1c和低密度脂蛋白胆固醇(LDL-C)与新生狭窄相关(HbA1c;P=0.0201,LDL-C;P=0.0204)。再狭窄受胰岛素抵抗[相对风险(RR)2.06;95%置信区间(95%CI)1.20至3.56]、糖尿病(DM:RR 1.92;95%CI 1.25至2.95)和最终最小管腔直径(RR 2.83;95%CI 1.32至6.06)影响。
HOMA-IR和DM是冠状动脉支架置入术后再狭窄的预测因素,HbA1c和LDL-C是新生狭窄的预测因素。这些结果可能反映了作为再狭窄的新生内膜组织增生和作为新生狭窄的动脉粥样硬化之间的组织学差异。