Abdominal Organ Dysfunction after Open Surgical Aortic Arch Replacement Using Different Cerebral Protection Strategies

Objectives: A positive impact of antegrade cerebral perfusion (ACP) on neurological function and survival in patients undergoing open surgical aortic arch replacement under deep hypothermic circulatory arrest (DHCA) has been emphasized but the suggested secondary remote protective effects of ACP on the abdominal organ function through collateral perfusion remains controversial.

Methods: Markers of visceral function were retrospectively analyzed in adults with acquired aortic arch disease who underwent DHCA (n = 37) or ACP (70) for open surgical aortic arch replacement at one institution.

Results: Preoperative characteristics (ascending aortic dissection: 78.4 vs. 71.4%, p = 0.436; abdominal extension: 29.1 vs. 31.4%, p = 0.857; hemodynamic instability: 8.1% vs. 10.0%, p = 0.749), intraoperative data and complications were similar. Preoperative lactate, postoperative inotropic support and maximal postoperative GPT, CK and lactate levels were significantly higher in nonsurvivors versus survivors (p < 0.05) in both ACP and DHCA groups. Maximal postoperative CK and lactate correlated with the preoperative lactate values (p < 0.05 and p < 0.01), whereas GPT and lactate correlated with postoperative inotropic index (p < 0.05, p < 0.0001) in both groups. Although maximal postoperative GPT and CK differed in the univariate analysis (p < 0.05), they failed to demonstrate an independent predictor capacity for death. Multivariate analysis revealed an association between mortality and preoperative hemodynamic instability (HR = 3.69, p = 0.023), maximal postoperative lactate (HR = 1.02, p = 0.0001) and maximal postoperative inotropic score (HR = 1.00, p = 0.006).

Conclusions: ACP did not influence postoperative abdominal biomarkers; thus, a direct protective effect through improved arterial collateral circulation remains implausible. Hemodynamic instability and cardio-circulatory failure rather than visceral dysfunction may increase mortality after open surgical aortic arch replacement.