Elevated levels of matrix metalloprotein-3 in patients with coronary aneurysm: A case control study.

Istemihan Tengiz, Ertugrul Ercan, Emil Aliyev, Cevad Sekuri, Can Duman, Imre Altuglu
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引用次数: 1

Abstract

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. The aim of this study was to investigate the association between MMPs and presence of coronary aneurysms. METHODS: Thirty patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Fourteen coronary artery disease patients with stable angina were selected as control group (Group 2). MMP-1, MMP-3 and C-reactive protein (CRP) were measured in peripheral venous blood and matched between the groups. RESULTS: Serum MMP-3 level was higher in patients with aneurismal coronary artery disease compared to the control group (20.23 +/- 14.68 vs 11.45 +/- 6.55 ng/ml, p = 0.039). Serum MMP-1 (13.63 +/- 7.73 vs 12.15 +/- 6.27 ng/ml, p = 0.52) and CRP levels (4.78 +/- 1.47 vs 4.05 +/- 1.53 mg/l, p = 0.13) were not significantly different between the groups. CONCLUSION: MMPs can cause arterial wall destruction. MMP-3 may play role in the pathogenesis of coronary aneurysm development through increased proteolysis of extracellular matrix proteins.

Abstract Image

冠状动脉瘤患者基质金属蛋白-3水平升高:一项病例对照研究。
背景:基质金属蛋白酶(MMPs)通过增加细胞外基质蛋白的蛋白水解参与了动脉瘤的发病机制。动脉壁基质降解酶活性升高引起的蛋白水解增加可能是冠状动脉瘤发生的一个易感因素。本研究的目的是探讨MMPs与冠状动脉瘤存在之间的关系。方法:选取30例动脉瘤性冠状动脉病变合并稳定型心绞痛患者作为研究对象(1组),选取14例冠状动脉病变合并稳定型心绞痛患者作为对照组(2组),测定外周血静脉血MMP-1、MMP-3、c反应蛋白(CRP)水平,并进行组间比较。结果:动脉瘤性冠状动脉疾病患者血清MMP-3水平高于对照组(20.23 +/- 14.68 vs 11.45 +/- 6.55 ng/ml, p = 0.039)。血清MMP-1 (13.63 +/- 7.73 vs 12.15 +/- 6.27 ng/ml, p = 0.52)和CRP水平(4.78 +/- 1.47 vs 4.05 +/- 1.53 mg/l, p = 0.13)在两组间无显著差异。结论:MMPs可引起动脉壁破坏。MMP-3可能通过增加细胞外基质蛋白的蛋白水解作用在冠状动脉瘤的发病机制中发挥作用。
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