Inflammatory mediators after endovascular aortic aneurysm repair
Introduction
Abdominal aortic aneurysm (AAA) mainly affects males and is a common and potentially life threatening condition due to the risk for aneurysm rupture [1]. The pathophysiologic mechanisms involved in the development and growth of AAA are multifactorial; previous studies have shown associations with inflammatory activity, changes in coagulation, endothelial dysfunction as well as with the classical risk factors of atherosclerosis [2], [3], [4], [5].
Patients with large AAAs can undergo either open (OR) or endovascular (EVAR) aneurysm repair to prevent rupture. The long-term effects of EVAR on systemic inflammatory mediators remain poorly understood. The retention of a biologically active mural thrombus and aneurysm sac following EVAR may be a source of inflammatory mediators, which may influence postoperative protection against aneurysm sac expansion and rupture and overall cardiovascular morbidity [6]. It may also lead to clinical failure, and increase the risk of reintervention [6]. Postoperative levels of inflammatory mediators may also be useful markers of cardiovascular disease activity.
The inflammatory activity in AAA is reflected in increased values of several different inflammatory mediators [2]. One of these is glycosylphosphatidylinositol phospholipase D (GPI-PLD), which is an enzyme that cleaves the GPI anchor of the urokinase plasminogen activator receptor (uPAR), forming a free suPAR. SuPAR is involved in tissue remodelling [7], [8] and is a marker of low-grade inflammation associated with risk of developing cardiovascular disease [9]. Endothelin (ET)-1 is a potent vasoconstrictor regulating release of vasoactive substances and stimulating muscle cell mitogenesis [10], [11]. It has a putative role in the pathogenesis of atherosclerosis and might also be associated with aneurysm growth [12]. Tumour necrosis factor (TNF)-α [13], [14] and interleukin (IL)-6 [15], [16], [17], [18] are pro-inflammatory cytokines in the acute phase inflammatory response, and involved in both atherogenesis and AAA development [19]. CD40L is a key mediator in B-cell activation and is also increased in cells involved in the atherosclerotic process [20], [21]. IgM anti-PC, on the other hand, are natural antibodies against oxidised low-density lipoprotein (oxLDL), an important mediator in the development of atherosclerosis and atherogenesis [22]. Low levels of IgM anti-PC are associated with an increased risk of atherosclerotic cardiovascular disease [23], [24], [25], but the marker has not yet been evaluated in patients with AAA.
The main aims of this study where to evaluate potential relationships between levels of suPAR, ET-1, TNF-α, IL-6, CD40L, IgM anti-PC and aneurysm sac size change after elective EVAR for AAA. A small group of patients undergoing open surgery for AAA was studied for comparison.
Section snippets
Patients
We studied AAA patients included in a scientific follow-up program at the Vascular Centre, Malmö University Hospital [26]. Among 57/206 study patients undergoing elective AAA repair between 2003 and 2010, 26 consented to a postoperative follow-up blood sample and were included in the present study in which pre- and postoperative laboratory analyses and repeated computed tomography (CT) scans were evaluated. Among EVAR patients (n = 21), 14 underwent standard EVAR and seven underwent fenestrated
Patient characteristics
Twenty-six patients (23 [89%] men) with a median age of 74 (IQR 69–78) years were included in this study. Twenty-three (88%) were smokers and 20 (77%) suffered from hypertension. At a preoperative CT scan, 12 (46%) patients had medium sized AAA, whereas nine patients had large aneurysms. Five patients had small AAAs and were operated because of either rapid growth or symptomatic AAA (Table 1).
Preoperative correlations between laboratory markers and AAA diameter
A significant inverse correlation (r = −0.41, p = 0.04) was found between preoperative level of suPAR and
Discussion
In the present study, levels of different inflammatory mediators, such as suPAR, ET-1 and IL-6 all increased after EVAR for AAA, whereas levels of the protective mediator IgM anti-PC decreased [23], [24], [25]. EVAR may elicit a postoperative systemic inflammatory response, referred to as post-implantation syndrome (PIS) featuring pyrexia, negative blood culture results, leucocytosis, increased C-reactive protein and/or coagulation disturbances [28]. The reported incidence of PIS after EVAR
Conflict of interest
No conflicts of interest exist for any of the authors.
Funding acknowledgement
This research received no specific Grant from any funding agency in the public, commercial, or not-for-profit sectors.
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