Post-implantation syndrome: the impact of different devices for endovascular abdominal aortic aneurysm repair and related etiopathogenetic implications.

BACKGROUND

Postimplantation syndrome (PIS) is a systemic inflammatory response occurring in early phase after abdominal aortic aneurysm (AAA) endovascular repair (EVAR). PIS can also occur after endovascular aneurysm sealing (EVAS) with Nellix system which prevent new onset of mural thrombus inside. Aim was to compare the incidence of PIS after EVAS and EVAR to evaluate the possible role of the new-onset thrombus inside the aneurysmal sac. Secondary aims were to assess the effect of AFX (Endologix) endoskeleton compared with other commercially available exoskeleton PTFE stent grafts on inflammatory response and its relationship with the clinical outcomes.

METHODS

From 2013 to 2017, data on 60 elective EVAS with Nellix system (Endologix, Irvine, CA, USA) and 110 EVAR with ePTFE devices (56 AFX devices and 54 other stent grafts) for AAA patients were retrospectively collected. PIS was defined as composite of body temperature ≥38 °C coinciding with leukocyte count >12,000/mL and hs-CPR >10 mg/L. New-onset thrombus volume after EVAR was calculated by: endograft volume - preoperative luminal volume=volume of new-onset thrombus, whereas post-EVAS thrombus volume was calculated from difference between AAA volume and volume of Nellix endobags, including balloon expandable stents. Nonparametric χ

RESULTS

EVAS with Nellix system was associated with lower incidence of PIS compared to EVAR using both AFX device and other endografts (8.3%, 30%, 35%, respectively, P=0.001). No significant new-onset of mural thrombus occurred following EVAS while an avarage new-onset thrombus of 21% and 14% was found in EVAR group A and group B, respectively. No statistically significant difference of PIS incidence was observed after endoskeleton AFX device deployment compared with other EVAR exoskeleton endografts. During follow-up, major complications were proportionally but not significantly (P=0.43) less frequent after EVAS (10.3%) than after EVAR and after EVAR using AFX device (8.9%) than after EVAR with other PTFE stent grafts (16.4%).

CONCLUSIONS

The etiology and pathophysiology of PIS is not yet well understood. It is speculated that the type of the stent graft or the mural thrombus within the AAA may play a role in determing this inflammatory response. In this study, PIS was significantly less frequent after EVAS than EVAR. The lower inflammatory reaction observed after EVAS might be related to the endobags of Nellix system which completely seal the aneurysm sac reducing the new onset of mural thrombus. This could confirm the role of new-onset mural thrombus in the genesis of PIS. The systemic inflammatory response does not significantly differ after endoskeleton AFX device deployment compared with other EVAR exoskeleton stent grafts. PIS does not seem to have any significant prognostic implications in terms of major adverse events.