Aortic dissection is not predicted by diameter alone: hypertension, genetics, aortic geometry, pregnancy, medications, sleep apnea, inflammation, and environmental triggers all reshape individual risk. The full paper is worth reading because it maps where classic thresholds fail — and where modern risk stratification may prevent missed catastrophic events.
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Abstract: This review aims to synthesize the diverse clinical, genetic, environmental, and anatomical risk factors associated with the development, propagation, and prognosis of aortic dissection based on recent cohort and case-control evidence. The review utilises 191 references. Across the mapped evidence, uncontrolled hypertension emerged as the most prominent and consistently replicated modifiable signal for aortic dissection, accounting for more than 50% of the population-attributable risk and supported by hazard ratios such as 2.64 for incident dissection in population cohorts. Smoking, older age, male sex, family history (relative risk 6.82), and syndromic predisposition including Marfan syndrome (present in 44% of necropsy dissection cases), bicuspid aortic valve (9–18-fold excess risk), and ACTA2 mutations (76% lifetime aortic-event risk) further dominated the topic-level synthesis. The map also highlighted that a substantial share of dissections occur below the conventional 5.5 cm surgical threshold (with one series reporting 80.4% dissecting below 55 mm), supporting a role for geometric, length-based, volumetric, and polygenic risk metrics alongside diameter for refined stratification. Recurrent secondary signals included malperfusion, persistent false lumen patency, elevated D-dimer and inflammatory composites, renal dysfunction, pregnancy, fluoroquinolone and vascular endothelial growth factor inhibitor exposures, sleep-disordered breathing, and environmental triggers such as low ambient temperature and air pollution, all of which indicate clinically actionable pharmacovigilance, perioperative, and public-health touchpoints. A practical implication is that risk assessment and surveillance pathways should integrate blood-pressure variability, anatomical and genomic indices, and exposure history rather than relying on diameter alone, particularly in women and non-syndromic patients. Future research should prioritize prospective validation of geometric and polygenic predictors, mechanistic clarification of the diabetes paradox, and longitudinal evaluation of environmental and pharmacological triggers to resolve the heterogeneity observed across the predominantly retrospective evidence base.
Final search date and database lock: 2026-04-26 16:52:17 CEST
Plan: Pro (expanded craft tokens; source: PubMed)
Source: PubMed
Total Abstracts/Papers: 2466
Downloaded Abstracts/Papers: 2466
Included original and non-original Abstracts/Papers (all): 1467
Included original Abstracts/Papers (Vote counting by direction of effect): 1366
Reference Index (links used in paper): 191
Total participants (topic deduplicated ΣN): 10835367
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