کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3446351 1595463 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Elevated Serum Angiopoietin-like Protein 2 in Patients with Acute Coronary Syndrome
ترجمه فارسی عنوان
افزایش سطح پروتئین 2 آنژیوپوئیتین سرم در بیماران مبتلا به سندرم حاد کرونری
کلمات کلیدی
آنژیوپوئیتین مانند پروتئین 2، التهاب سندرم حاد کرونری، آترواسکلروز، پلاک آسیب پذیر
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی پزشکی و دندانپزشکی (عمومی)
چکیده انگلیسی

Background and AimsAngiopoietin-like protein 2 (Angptl2) is regarded as a proinflammatory factor in the pathogenesis of atherosclerosis and is expressed at high levels in patients with coronary artery disease. However, direct evidence of Angptl2 in acute coronary syndrome (ACS) is lacking. Our study was designed to investigate a possible relationship between serum Angptl2 and ACS.MethodsWe evaluated 251 consecutive patients undergoing coronary angiography, consisting of 132 patients with ACS (unstable angina pectoris n = 60, acute myocardial infarction n = 72), 50 patients with stable angina pectoris, and 69 control patients. Serum Angptl2 concentration was measured in peripheral venous blood by an enzyme-linked immunosorbent assay.ResultsSerum Angptl2 levels were significant higher in patients with ACS than in those with stable angina (p <0.05) or controls (p <0.001). The difference between angplt2 levels in unstable angina and acute myocardial infarction subgroups was statistically insignificant (p = 0.831). In multivariable logistic regression models, using quartiles of Angptl2, Angptl2 was closely associated with ACS following adjustment of age, gender, established risk factors and high sensitivity C-reactive protein levels (odds ratio for quartile 4 vs. quartile 1: 10.182, 95% confidence interval 2.440–42.485, p = 0.001).ConclusionsSerum Angptl2 is a new candidate biomarker for risk stratification of ACS.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Archives of Medical Research - Volume 46, Issue 4, May 2015, Pages 257–264
نویسندگان
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