ABSTRACT: Objectives. Postoperative neurological complications (PONC), associated with substantial morbidity and mortality, represent a prevalent clinical challenge following surgical repair of acute type A aortic dissection (AAD). This study aimed to identify novel biomarkers for early diagnosis of PONC to facilitate timely clinical intervention. Methods. We established deep hypothermic circulatory arrest (DHCA) rat models, extracted total RNA from the hippocampus of rats (DHCA group and control group), performed miRNA sequencing, screened for differentially expressed genes (DEGs) between the two groups, and analyzed their associated biological processes (BP) and pathways. A cohort of 95 patients diagnosed with AAD was enrolled in this study. Comprehensive clinical assessments and a standardized neuropsychological test battery were systematically conducted. Serum miR-29 levels were quantified via reverse transcription quantitative real-time polymerase chain reaction. Results. Transcriptomic profiling of rat hippocampus under deep hypothermic circulatory arrest / cardiopulmonary bypass (DHCA/CPB) identified 37 differentially expressed miRNAs (|log2FC|≥1.3, P<0.05), with miR-29a-5p and miR-29b-3p showing the most significant dysregulation. Functional enrichment implicated MAPK signaling and junctional pathways in blood-brain barrier modulation. In a clinical cohort of 95 aortic dissection patients, the PONC group exhibited prolonged CPB time (164.00 (137.00, 193.00) vs. 140.00 (120.25, 161.00), P=0.012), elevated inflammatory biomarkers (pre-op interleukin-6: 106.60 vs. 47.00, P<0.001), and altered miR-29 expression profiles. Multivariate analysis confirmed preoperative miR-29b-3p (OR=2.53, 95%CI 1.17-5.47) and postoperative miR-29a-5p (OR=0.21, 95%CI 0.05-0.96) as independent PONC predictors. The nomogram demonstrated robust discrimination (AUC=0.867, 95%CI 0.771-0.963) and clinical utility (net benefit=0.23), with 30-day survival analysis revealing miR-29b-3p-associated mortality risk (HR=4.372, 95%CI 0.928-20.596, P=0.041). Conclusions. Dual-phase miR-29 dysregulation predicts PONC post-AAD repair, validated by a nomogram and miR-29b-3p-associated mortality risk, guiding early intervention strategies.
