Preoperative acute lung injury and oxygenation impairment occurred in the patients with acute aortic dissection

Abstract

Acute lung injury (ALI) and oxygenation impairment (OI) frequently occur in the patients with acute aortic dissection (AAD), which may necessitate mechanical ventilation and result in adverse outcomes. This paper aims to increase clinicians' awareness of the severe respiratory complications in the patients with AAD, and provide the overview of the epidemiology, adverse outcomes, pathogenesis, predictive markers and therapeutic modalities of the concurrent conditions. Currently, it is considered that inflammatory response plays a great role in the pathogenesis of ALI and OI in the patients with AAD, but the definite pathogenesis remains unclear. Given the great importance of the prediction of the occurrence of the severe respiratory complication at a very early stage, some inflammatory biomarkers have been investigated to predict the occurrence of ALI and OI in several studies. C-reactive protein was found to have a significant predictive effect for the development of ALI and OI. Early use of beta-blockers and the use of bindarit could prevent the occurrence of OI and ALI. Ulinastatin could also improve oxygenation in the patients with type-A AAD. Prevention and management of ALI and OI in AAD remain a great challenge. The definite pathogenesis should be clearly clarified and further studies should be performed to look for potential effective way to predict and manage the severe respiratory conditions.

Keywords: Acute aortic dissection; Acute lung injury; Inflammatory response; Oxygenation impairment.

Fig. 1

There are three major possible mechanisms of ALI complicated by AAD. (1) AngII could trigger overexpression of MCP-1 in PMVECs by activating NF-κB signaling pathway. MCP-1 plays a great role in the recruitment of macrophages in lung tissues, and MMP-9 derived from macrophages could induce the degradation of extracellular matrix and vascular basilar membrane; (2) AngII could induce the apoptosis of PMVECs through activating the caspase-3, up-regulating the expression of Bax and down-regulating the expression of Bcl-2; (3) AngII could trigger endothelial barrier injury, which may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement. AngII angiotensin II, MCP-1, monocyte chemoattractant protein-1, PMVECs pulmonary microvascular endothelial cells, MMP-9, matrix metalloproteinase 9