# Impact of Endovascular Aortic Repair on Aortic Stiffness: Preliminary Results from a Prospective In Vivo Study Following EVAR

**Authors:** Paolo Bellotti, Emma-Lena Maris, Jasper F. de Kort, Daniele Bissacco, Silvia Romagnoli, Maurizio Domanin, Chiara Grignaffini, Paolo Salvi, Gianfranco Parati, Valentina Mazzi, Karol Calo, Bianca Griffo, Diego Gallo, Umberto Morbiducci, Constantijn E. V. B. Hazenberg, Joost A. van Herwaarden, Santi Trimarchi

PMC · DOI: 10.3390/jcm15041532 · 2026-02-15

## TL;DR

This study shows that endovascular aortic repair increases aortic stiffness and reduces heart muscle perfusion, with longer stent-grafts causing bigger changes.

## Contribution

The study is the first to prospectively measure aortic stiffness and subendocardial perfusion changes after EVAR using cf-PWV and SEVR.

## Key findings

- EVAR caused a 10.6% increase in aortic stiffness (cf-PWV) and a 15.1% decrease in SEVR.
- Longer stent-grafts correlated with greater increases in cf-PWV but not SEVR.
- Findings suggest EVAR has significant hemodynamic effects that could impact cardiovascular risk.

## Abstract

Background: Aortic stiffness (AoS) is an established predictor of cardiovascular morbidity and mortality. Endovascular aneurysm repair (EVAR) introduces a rigid stent-graft into the aorta, potentially increasing AoS and impairing subendocardial perfusion. This prospective study aimed to evaluate changes in AoS and myocardial perfusion following EVAR, measured by carotid-to-femoral pulse wave velocity (cf-PWV) and the Subendocardial Viability Ratio (SEVR), and examined the influence of graft length on post-operative cf-PWV and SEVR. Methods: From October 2023 to April 2025, 38 patients undergoing elective EVAR were prospectively enrolled. Cf-PWV and the SEVR were measured <72 h preoperatively and 7 days postoperatively using the PulsePen® device. Descriptive statistics were used to summarize baseline characteristics. Data were assessed for normality with the Shapiro–Wilk test; non-normally distributed variables were analysed using the Wilcoxon signed-rank test and presented as median [interquartile range, IQR], while normally distributed variables were analysed using paired t-tests and presented as mean ± standard deviation (SD). Linear regression was applied to evaluate associations between graft length and postoperative changes in cf-PWV and SEVR. Results: Cf-PWV increased significantly after EVAR, with a median within-patient change of 1.0 m/s [IQR 3.1] (p < 0.001), corresponding to a 10.6% increase. The SEVR decreased significantly by 15.1% (p = 0.006). Graft length correlated positively with cf-PWV change, with a 0.2% increase in cf-PWV per millimetre of graft length (r = 0.41; p = 0.029), but not with SEVR (r = 0.058, p = 0.763). Conclusions: EVAR was associated with increased AoS and reduced subendocardial perfusion, with greater stiffness changes observed in patients receiving longer grafts. These preliminary findings highlight important haemodynamic consequences of EVAR and may inform patient selection, postoperative management, and the development of future stent-graft designs to mitigate long-term cardiovascular risk.

## Full-text entities

- **Diseases:** peripheral ischemia (MESH:D007511), stenosis (MESH:D003251), impaired coronary flow reserve (MESH:D003323), systole (MESH:D000092244), obesity (MESH:D009765), heart failure (MESH:D006333), ventricular remodelling (MESH:D020257), COPD (MESH:D029424), impaired myocardial perfusion (MESH:D009202), cardiac instability (MESH:D006331), stroke (MESH:D020521), aneurysm (MESH:D000783), arterial (MESH:D012078), diabetes (MESH:D003920), valvular heart disease (MESH:D006349), ischemic subendocardial damage (MESH:D017202), ischemic (MESH:D002545), atrial fibrillation (MESH:D001281), vascular disease (MESH:D014652), aortic aneurysms (MESH:D001014), CKD (MESH:D051436), abdominal aortic aneurysms (MESH:D017544), AoS (MESH:C566100), venous disease (MESH:D004194), injury to (MESH:D014947), microvascular damage (MESH:D017566), myocardial fibrosis and dysfunction (MESH:D005355), death (MESH:D003643), hypertension (MESH:D006973), LV hypertrophy (MESH:D017379), arterial stiffness (MESH:C566112), blood flow (MESH:D054318), coronary microvascular dysfunction (MESH:D003327), atherosclerosis (MESH:D050197)
- **Chemicals:** alcohol (MESH:D000438), glucose (MESH:D005947), creatinine (MESH:D003404), omega-3 fatty acids (MESH:D015525), polyester (MESH:D011091), antiplatelet and anticoagulant agents (-), PTFE (MESH:D011138), Oxygen (MESH:D010100), sodium (MESH:D012964), caffeine (MESH:D002110)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941607/full.md

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Source: https://tomesphere.com/paper/PMC12941607