Abdominal Aortic Aneurysm: Systematic Review with ☸️SAIMSARA.

• Generated: 2026-02-12 23:58:55 CET
• Plan: Pro (expanded craft tokens; source: Semantic Scholar)
• Source: Semantic Scholar
• Scope: All fields
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• Total Abstracts/Papers: 98848
• Downloaded Abstracts/Papers: 1000
• Included original Abstracts/Papers: 410
• Total study participants (naïve ΣN): 150739

• Bias: Qualitatively inferred from study design fields. Randomized controlled trials (RCTs) generally offer lower risk of bias for intervention efficacy, while cohort and case-control studies are more susceptible to confounding. Animal models and studies with unspecified design or population may have limited generalizability to human clinical practice.

• Genetic and Cardiometabolic Predisposition: Genetic correlations exist between AAA and 21 cardiometabolic traits, suggesting shared causal variants and pathways, particularly in cholesterol metabolism and inflammation [1]. Specific genetic variants like those on 9p21 [25] and within the DAB2IP gene [48] confer susceptibility, and familial aggregation is recognized [62, 295, 400, 401, 409].
• Pathophysiology and Molecular Mechanisms: AAA development involves complex processes including upregulation of long noncoding RNA H19 [5], activation of matrix metalloproteinase-3 (MMP3) by Netrin-1 [6], and increased levels of proteins associated with proteolysis, oxidative stress, lipid metabolism, and inflammation [8]. MicroRNAs (e.g., miR-29b, miR-21, miR-24, miR-181b) play regulatory roles [22, 24, 27, 36, 329], and inhibition of histone demethylase JMJD3 [337] or maintenance of VSMC homeostasis by unspliced XBP1 [338] can protect against AAA. Intraluminal thrombus contributes to local hypoxia and wall weakening [46, 196, 199, 215, 228, 302].
• Risk Factors and Epidemiology: Key risk factors include older age, male sex, smoking, and hypercholesterolemia [2, 29, 33, 136, 225, 341, 402]. Chronic kidney disease and dilated proximal neck are independent predictors of sac enlargement [2]. Diabetes has shown a negative association with AAA events [136] and lower growth rates [344, 253]. Aortic rupture in murine models can occur in 25% of mice within 7 days of angiotensin II infusion [50].
• Diagnosis and Monitoring: Ultrasonography is a primary screening method [63, 65, 83, 131, 162, 212, 252, 271, 290, 396]. Biomarkers like growth/differentiation factor 15 (GDF15) and cystatin B show diagnostic potential, while myeloperoxidase has prognostic value for growth [8]. Imaging techniques, including CT and MRI, are used for assessment, rupture prediction, and follow-up [31, 45, 175, 237, 310, 316, 374, 392]. Wall stress calculations, influenced by diameter, asymmetry, and intraluminal thrombus, are important for rupture risk assessment [31, 45, 157, 159, 188, 192, 250, 262, 379].
• Medical Management and Stabilization: Doxycycline, a matrix metalloproteinase inhibitor, did not significantly reduce AAA growth over 2 years in small AAAs (difference, 0.0 cm; 95% CI, -0.07 to 0.07 cm) [4], but preclinical studies suggest potential stabilization [219, 251, 254, 353]. Angiotensin receptor blockers like telmisartan suppressed experimental aneurysms [11, 223]. Statins are associated with reduced growth [193, 273, 356, 369]. Other targets include c-Jun N-terminal kinase [60], glycolysis restriction [30], and microRNA modulation [22, 24, 36, 329].
• Surgical and Endovascular Repair: For asymptomatic AAAs, long-term overall survival is similar between endovascular repair (EVAR) and open repair (hazard ratio 0.96, 95% CI 0.82 to 1.13 for all-cause mortality) [3], though EVAR is associated with more secondary procedures [3]. For ruptured AAAs, an endovascular strategy was associated with a survival advantage, gain in quality-adjusted life years (QALYs), similar reintervention rates, and reduced costs at three years compared to open repair [7]. However, 30-day mortality for suspected ruptured AAA was not significantly reduced (35.4% EVAR vs 37.4% open) [14]. Technical success for EVAR is high (e.g., 93.8% for AAA/TAA [324], 97.7% for large bore arteriotomy closure [330]), but persistent type II endoleaks are associated with significantly higher rates of AAA-related mortality, rupture, sac enlargement, and reintervention [2].
• Small AAA Management: Surveillance intervals for small AAAs (3.0-5.4 cm) are recommended based on size, with several years for 3.0-4.0 cm, around 1 year for 4.0-4.9 cm, and 6 months for 5.0-5.4 cm [344]. Rupture rates are almost fourfold higher in women than men, and current smokers have doubled rupture rates [344]. Men with aortic diameters of 25-29 mm have an increased risk of mortality and subsequent hospital admissions compared to those with ≤24 mm [29].
• Associated Conditions: AAA is associated with other vascular conditions such as peripheral vascular disease [63, 66, 123] and carotid stenosis [132]. Patients with aortic aneurysms have an overall prevalence of intracranial aneurysms of 11.8%, with female patients having a higher risk (OR=2.08, 95% CI 1.49–3.03) [325]. Splanchnic artery aneurysms can also be associated with infrarenal AAAs [335].

• Screening Benefits: Population-based screening for AAA, particularly in men aged 65-74, demonstrates a maintained mortality benefit and favorable cost-effectiveness over 10 years [53, 238].
• Tailored Surveillance: Surveillance intervals for small AAAs should be individualized based on size, with shorter intervals for larger aneurysms (e.g., 6 months for 5.0-5.4 cm) and longer intervals for smaller ones (e.g., several years for 3.0-4.0 cm) [344].
• Ruptured AAA Management: An endovascular strategy for ruptured AAA is associated with a survival advantage, improved quality of life, and reduced costs at 3 years compared to open repair [7], despite similar 30-day mortality rates [14].
• Post-EVAR Monitoring: Persistent type II endoleaks after endovascular aneurysm repair (EVAR) are associated with significantly higher rates of AAA-related mortality, rupture, sac enlargement, and reintervention, necessitating careful follow-up [2].
• Comorbidity Awareness: Clinicians should be aware of the increased risk of intracranial aneurysms in patients with aortic aneurysms, particularly in women, and consider screening for other vascular diseases [325].

• Optimal Medical Therapies — Further randomized controlled trials are needed to definitively establish the efficacy of medical therapies (e.g., doxycycline, telmisartan, statins) in limiting AAA growth and rupture risk across diverse patient cohorts [4, 11, 160, 193].
• Sex-Specific Pathophysiology — Research should further investigate the distinct pathophysiological mechanisms and risk factor profiles for AAA in women, given their lower prevalence but higher rupture rates for small aneurysms [2, 202, 260, 341, 344].
• Biomarker Integration into Practice — Prospective studies are required to validate and integrate novel diagnostic and prognostic biomarkers (e.g., GDF15, cystatin B, myeloperoxidase, microRNAs) into clinical decision-making algorithms for AAA surveillance and intervention [8, 27, 36, 329].
• Long-term EVAR Outcomes for Ruptured AAA — Extended follow-up data from randomized trials comparing EVAR and open repair for ruptured AAA are needed to confirm the durability of initial survival advantages and evaluate long-term reintervention burdens [7, 14].
• Personalized Rupture Risk Prediction — Development and validation of advanced biomechanical models incorporating patient-specific factors (e.g., wall thickness, geometry asymmetry, intraluminal thrombus properties) are crucial for more accurate rupture risk prediction beyond simple diameter [31, 45, 157, 190, 192, 250, 262, 379].

• Heterogeneity of Study Designs — The diverse range of study designs limits the ability to perform quantitative meta-analysis and generalize findings consistently.
• Variable Follow-up Periods — Inconsistent follow-up durations across studies make it challenging to compare long-term outcomes for interventions and natural history.
• Missing Quantitative Data — Many summary entries lack specific numerical data for sample sizes, statistics, or follow-up, hindering comprehensive quantitative synthesis.
• Qualitative Bias Inference — Bias was inferred qualitatively, which may not fully capture the methodological rigor or limitations of individual studies.
• Focus on Male Populations — A significant portion of screening and epidemiological studies primarily focused on men, limiting direct applicability to women.

• Standardized Outcome Reporting — Implement standardized reporting of key clinical and molecular outcomes in AAA research.
• Sex-Specific Clinical Trials — Conduct clinical trials specifically designed to evaluate AAA interventions and therapies in women.
• Multi-Omics Biomarker Panels — Develop and validate multi-omics biomarker panels for early detection and personalized risk stratification.
• Advanced Imaging for Risk — Utilize advanced imaging techniques combined with computational fluid dynamics for precise rupture risk assessment.
• Targeted Drug Delivery — Explore nanotherapy and targeted drug delivery systems for localized therapeutic intervention in AAA.