Coskun Selçuk, Atalar Enver, Ozturk Ercan, Yavuz Bunyamin, Ozer Necla, Goker Hakan, Ovünç Kenan, Aksöyek Serdar, Kes Sirri, Sivri Bulent, Kirazli Serafettin, Ozmen Ferhan
Department of Emergency Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
J Natl Med Assoc. 2006 Nov;98(11):1746-50.
The regions of ruptured atherosclerotic plaques have numerous macrophages. Osteopontin that modulates macrophage function has been shown in atherosclerotic plaques. We aimed to study the plasma levels of osteopontin in patients with unstable angina or non-ST-seg ment elevation myocardial infarction (NSTEMI) and the rela tionship between osteopontin and the extent of the coronary artery disease (CAD).
We studied 65 patients with unstable angina or NSTEMI, 25 patients with stable angina and 18 patients as the control group. The extent of coronary artery stenosis was determined by the number of vessels with >50% stenosis. Plasma osteopontin concentrations were measured from the blood samples that were drawn immediately after admission to the emergency department in unstable angina/NSTEMI patients and before the coronary angiograph in the stable angina and control groups.
The plasma osteopontin concentration was (495 118 ng/ml) significantly higher in the patients with unstable angina/NSTEMI compared to the stable angina group (319 106 ng/ml) and control group (125+/-54 ng/ml) (p=0.0001 The plasma osteopontin levels were lower in the patients with stable angina pectoris who had one-vessel disease compared to those with two-vessel disease (p=0.01). How ever, in the unstable angina/NSTEMI group, the plasma osteopontin levels were statistically not different among the patients with one-vessel, and two-vessel and three-vessel disease (p=NS). There was no correlation between the plasma osteopontin levels and the extent of coronary stenosis.
The plasma osteopontin levels are elevatedin patients with unstable angina/NSTEMI, but there appears to be no correlation with the extent of CAD. These results ma suggest that osteopontin may have a role in the pathobiology of ACS.
破裂的动脉粥样硬化斑块区域有大量巨噬细胞。调节巨噬细胞功能的骨桥蛋白已在动脉粥样硬化斑块中被发现。我们旨在研究不稳定型心绞痛或非ST段抬高型心肌梗死（NSTEMI）患者的血浆骨桥蛋白水平，以及骨桥蛋白与冠状动脉疾病（CAD）严重程度之间的关系。
我们研究了65例不稳定型心绞痛或NSTEMI患者、25例稳定型心绞痛患者以及18例作为对照组的患者。冠状动脉狭窄程度通过狭窄>50%的血管数量来确定。在不稳定型心绞痛/NSTEMI患者入院急诊后立即采集血样，在稳定型心绞痛患者和对照组进行冠状动脉造影前采集血样，测定血浆骨桥蛋白浓度。
不稳定型心绞痛/NSTEMI患者的血浆骨桥蛋白浓度（495±118 ng/ml）显著高于稳定型心绞痛组（319±106 ng/ml）和对照组（125±54 ng/ml）（p = 0.0001）。单支血管病变的稳定型心绞痛患者的血浆骨桥蛋白水平低于双支血管病变患者（p = 0.01）。然而，在不稳定型心绞痛/NSTEMI组中，单支血管、双支血管和三支血管病变患者的血浆骨桥蛋白水平在统计学上无差异（p =无显著性差异）。血浆骨桥蛋白水平与冠状动脉狭窄程度之间无相关性。
不稳定型心绞痛/NSTEMI患者的血浆骨桥蛋白水平升高，但似乎与CAD严重程度无关。这些结果可能提示骨桥蛋白在急性冠状动脉综合征的病理生物学中起作用。
