Why the study?
To investigate changes in aortic stiffness before and after endovascular aortic repair for thoracic and abdominal aortic disease, along with associated changes in left ventricular function.
Does endovascular aortic repair increase aortic stiffness and induce left ventricular structural remodeling in patients with thoracic and abdominal aortic disease?
Does endovascular aortic repair increase aortic stiffness and induce left ventricular structural remodeling in patients with thoracic and abdominal aortic disease?
Endovascular aortic repair is associated with increased aortic stiffness and subsequent left ventricular structural remodeling (increased LVMI) despite preserved LVEF.
Answers are grounded in this paper and cite their sources.
ER increases aortic stiffness and LVMI post-repair without LVEF change; extends observational data but leaves causal effects and practice change open.
The aim of this systematic review and meta-analysis was to investigate the changes in aortic stiffness before (pre) and after endovascular aortic repair (ER) for thoracic and abdominal aortic disease, along with the associated changes in left ventricular function. PubMed, Web of Science, EMBASE, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov were searched. Two independent reviewers screened and selected eligible studies, and RevMan 5.4 was used for the statistical analysis. A total of 28 studies (including 2227 participants) were included. Abdominal aortic aneurysms (AAA) patients had higher pulse wave velocity (PWV) than volunteer participants (Mean difference [MD]:2.08; 95% confidence interval (CI): 0.54–3.62, I2 = 94%, p = 0.008). The PWV increased after ER (MD 1.22; 95%CI: 0.54–1.91, I2 = 86%, p < 0.001) and subgroup analysis of thoracic endovascular aortic repair (TEVAR, MD: 1.51; 95%CI: 0.83–2.19, I2 = 9%, p < 0.001) and endovascular aneurysm repair (EVAR, MD:1.29; 95%CI: 0.39–2.20, I2 = 90%, p = 0.005) showed similar results. Pooled analysis also showed that the left ventricular mass index (LVMI) increased after ER (MD:5.35; 95%CI: 1.16–9.54, I2 = 24%, p = 0.01), while no significant change was observed in left ventricular ejection fraction (MD:0.08; 95%CI: -0.63–0.79, I2 = 0%, p = 0.82). Patients with AAA have significantly higher PWV than age-matched controls. Endovascular repair may be associated with left ventricular structural remodeling, as reflected by changes in LVMI, while no significant effect on LVEF was observed. These adverse remodeling processes may merit consideration during follow-up. Further high-quality studies are needed to confirm these findings and to clarify strategies for reducing aortic stiffness. This systematic meta-analysis quantified endovascular aortic repair dual impact on cardiovascular dynamics. AAA patients showed significantly elevated aortic stiffness versus controls; both TEVAR and EVAR were associated with further increases in aortic stiffness. Persistently unchanged LVEF despite post-EVAR/TEVAR ventricular remodeling exposed the critical limitation of relying solely on EF for cardiac function assessment.
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A 2026 study studied this question.
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