Abstract

Aim. Although osteopontin (OPN) and osteoprotegerin (OPG) have been associated with abdominal aortic aneurysms (AAAs), no association of these two biomarkers with AAA surgical or endovascular treatment has been reported. Material and Methods. Seventy-four AAA patients were prospectively selected for open or endovascular repair. All aneurysms were classified (Types A–E) according to aneurysmal extent in CT imaging (EUROSTAR criteria). All patients had preoperative serum OPN and OPG values measurements and 1 week after the procedure. Preoperative and postoperative values were compared with a control group of twenty patients (inguinal hernia repair). Results. Preoperative OPN values in patients with any type of aneurysm were higher than in the control group, while OPG values showed no difference. Postoperative OPN values in AAA patients were higher than in the control group. OPN values increased after open surgery and after EVAR. OPG values increased after open surgery but not after EVAR. There was no difference in OPN/OPG values between EVAR and open surgery postoperatively. Conclusions. OPN values are associated with aneurysm presence but not with aneurysm extent. OPG values are not associated either with aneurysm presence or with aneurysm extent. OPN values increase after AAA repair, independently of the type of repair.

Highlights

  • Abdominal aortic aneurysms (AAAs) represent a chronic degenerative disease the exact pathophysiological mechanism of AAA development seems to be obscure [1]

  • From February 2008 to June 2012, out of 130 patients who were prospectively planned for elective abdominal aortic aneurysm repair, 74 AAA patients were screened for the study

  • Out of the 74 patients with AAA included in the study, 78% had arterial hypertension and 81% dyslipidemia, while other risk factors, such as diabetes mellitus, chronic obstructive pulmonary disease, and smoking, showed a lower prevalence (Table 1)

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Summary

Introduction

Abdominal aortic aneurysms (AAAs) represent a chronic degenerative disease the exact pathophysiological mechanism of AAA development seems to be obscure [1]. OPN plasma levels have been associated with the presence and the extentof cardiovascular disease independently of traditional risk factors [8,9,10]. Smooth muscle cells and endothelial cells produce OPG, but its precise role in vascular pathophysiology remains undefined. OPG has been positively associated with the presence and severity of coronary artery disease and the increased risk for cardiovascular diseases in general population [8, 12]

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