ReviewFrontiers in cardiovascular medicine2025
Acute aortic dissection-induced acute respiratory distress syndrome: pathogenesis and clinical implications.
Review in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Early Prone Positioning After Acute Type A Aortic Dissection Surgery for Moderate-to-Severe Acute Respiratory Distress Syndrome Is Safe and Shortens Duration of Mechanical Ventilation.Critical care explorations · 2026Article
- Admission creatinine level predicts postoperative acute hepatic dysfunction in patients aged ≤30 years with acute type A aortic dissection: a multi-center retrospective study.Frontiers in cardiovascular medicine · 2026Article
- Integrated biomarker model based on cTnI, BNP, and D-dimer for early risk stratification in acute aortic dissection.Frontiers in cardiovascular medicine · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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