Background: Endovascular repair (ER) of aortic aneurysm, though being consi
dered minimally invasive, may be associated with a nonspecific inflammatory
reaction known as "post-implantation syndrome". The aim of the study was t
o compare the immunologic responses to ER and conventional repair (CR).
Methods: A prospective, non-randomized study included 8 patients each with
ER and CR. Blood samples were taken pre-, intra- and postoperatively. The f
ollowing parameters were analyzed quantitatively using ELISA: tumor necrosi
s factor (TNF)-alpha, interleukin (IL)-6, IL-10, IL-1 receptor antagonist (
IL-1 RA), cortisol, procalcitonin (PCT), soluble IL-2 receptor (sIL-2R) and
polymorphonuclear leucocyte elastase (PMN-E). To test the in vitro secreto
ry capacity of monocytes, TNF-alpha and IL-1 beta were measured in whole bl
ood cultures after stimulation with LPS. Secretory capacity of PMN leucocyt
es was measured after stimulation with PMA. Statistical analysis was perfor
med using the Mann-Whitney test for comparison of ER and CR groups and Wilc
oxon's test for comparison of values within each group.
Results: There were significant elevations of PCT, IL-6, and TNF-alpha afte
r ER and CR with significantly higher values of IL-6 (intraop.) and TNF-alp
ha (7 d postop.) in CR as compared to ER. SIL-2R was significantly elevated
(intraop.-4 h postop., 7 d postop.) in CR versus ER despite an intraoperat
ive decrease in both ER and CR. Though anti-inflammatory cytokines IL-10 an
d IL-1RA showed significant intra- and postoperative increases in ER and in
CR, both IL-1RA. and IL-10 as well as cortisol demonstrated lower plasma c
oncentrations in ER as compared to CR. Accordingly, in CR but not in ER, th
ere was a marked suppression of in vitro secretion capacity of monocytes wi
th significantly lower concentrations of TNF-alpha (1 h post clamp., 4 h an
d 3 d postop.) and IL-1 beta (1 h post clamp., 4 h postop.). Plasma (4 h-3
d postop.) and PMA-stimulated (intra-, postop.) PMN-E were significantly hi
gher with EA.
Conclusion: Moderate inflammation and lacking immunodepression with minimal
ly invasive ER might fail to induce a relevant anti-inflammatory response.
This might explain the presence of clinical symptoms associated with the "p
ost-implantation syndrome" in ER.