Adverse reactions during endovascular treatment of aortic aneurysms may be triggered by interleukin 6 release from the thrombotic content.

Abstract

It has been shown that endovascular aortic aneurysm repair might induce a significant inflammatory response, mainly involving tumor necrosis factor (TNF-alpha) release. This study determined in vitro whether these inflammatory responses could depend on white blood cell (WBC) activation caused by the aneurysmal mural thrombus. Mural thrombus specimens obtained from 10 different aortic aneurysms were weighed, homogenized, and assayed for interleukin 1beta (IL-1beta), interleukin 6 (IL-6), TNF-alpha, and soluble TNF receptor (sTNFRI). Only high amounts of IL-6 (mean, 2973 pg/mL) were found. In contrast, after the addition of healthy donor WBCs to the thrombus mass supernatants, elevated levels of TNF-alpha (mean, 523 pg/mL) were seen. Theoretically, WBCs were stimulated by IL-6, resulting in TNF-alpha release. In additional experiments, it was proven that stimulated WBCs, induced by thrombus mass supernatants, synthesize TNF-alpha (mean, 796 pg/mL), and monoclonal antibodies against IL-6, prevented such TNF-alpha production (mean, 62 pg/mL). The biologic responses during endovascular repair may be explained by a release of IL-6 from the aneurysmal thrombus, causing WBC stimulation and production of TNF-alpha. More complex processes cannot be excluded, but the present findings suggest that restrictions of manipulations within the aneurysm may be advisable.