Acute aortic dissection-induced acute respiratory distress syndrome: pathogenesis and clinical implications

Acute aortic dissection, a life-threatening cardiovascular emergency, is frequently complicated by acute respiratory distress syndrome. This complication exacerbates perioperative risks, poses challenges for clinical management, and impacts patient postoperative recovery. However, a comprehensive understanding of its pathogenesis remains elusive. This review synthesizes evidence to delineate aortic intimal tearing trigger the key initiating events comprising systemic inflammatory response, renin-angiotensin system dysregulation, high mobility group box 1 release, coagulation/fibrinolysis disorder, platelet hyperactivation/consumption, and intestinal ischemia/reperfusion injury. These upstream pathways converge on the lung, inducing injury through sustained inflammation, damage to pulmonary vascular endothelium and alveolar type II epithelial cells, microvascular constriction, microthrombosis, and alveolar fibrin deposition. Notably, crosstalk among some of these pathways may amplify lung injury. By systematically presenting these mechanisms, this review highlights translational opportunities for early diagnosis, monitoring disease progression, and designing targeted therapies to mitigate lung injury and enhance outcomes in these patients.