# Endovascular reperfusion followed by delayed open aortic repair in stable acute type A aortic dissection with malperfusion syndrome: a single-center experience

**Authors:** Mengmeng Ye, Chao Xue, Dongxu Wang, Yi Si, Yong Mao, Bo Xu, Bo Yu, Weiguang Wang, Kai Ren, Jian Xu, Hongliang Zhao, Shiqiang Yu, Jincheng Liu, Weixun Duan

PMC · DOI: 10.3389/fmed.2025.1701176 · Frontiers in Medicine · 2026-02-11

## TL;DR

This study shows that using endovascular stenting followed by delayed surgery can improve outcomes for stable patients with aortic dissection and organ failure.

## Contribution

The study introduces a two-step treatment approach for aortic dissection with malperfusion syndrome that achieves comparable survival to standard surgery.

## Key findings

- Hospital mortality in malperfusion syndrome patients was 37.2%, but dropped to 11.7% with delayed repair after stenting.
- Stenting followed by delayed surgery provided short-term survival similar to immediate surgery in non-malperfusion patients.
- Hypertension and blood markers like D-dimer predicted mortality from organ failure.

## Abstract

We aimed to evaluate the outcomes of endovascular reperfusion followed by delayed open aortic repair in patients with acute type A aortic dissection (ATAAD) and malperfusion syndrome (MPS), as well as risk factors for mortality associated with organ failure.

We retrospectively selected 777 patients with ATAAD admitted to our center. Patients with MPS (n = 121; 15.6%), who were hemodynamically stable and without evidence of aortic rupture/tamponade, underwent interventional reperfusion (IR) through aortic/mesenteric branch stenting, followed by delayed open aortic repair (OR). Patients without MPS (non-MPS) (n = 656; 84.4%) received immediate open aortic repair.

Overall hospital mortality was 37.2% in patients with ATAAD and MPS, significantly higher than in those without MPS (8.2%). However, patients with MPS who successfully underwent delayed repair after stenting had hospital mortality rates comparable to non-MPS patients (11.7% vs. 8.2%; p = 0.306) and similar short-term survival. Hypertension, leukocytosis, fibrin degradation products (FDP), D-dimer, and FDP/D-dimer ratios were independent predictors of mortality associated with irreversible organ failure.

Endovascular stenting followed by delayed open aortic repair in stable patients with ATAAD and MPS had favorable short-term outcomes. Stenting of the aorta and/or aortic branches is a relatively simple, minimally invasive intervention with short-term patency.

## Full-text entities

- **Genes:** OTOR (otoraplin) [NCBI Gene 56914] {aka FDP, MIAL1}, MB (myoglobin) [NCBI Gene 4151] {aka MYOSB, PVALB}
- **Diseases:** Aortic dissection (MESH:D000784), rupture (MESH:D012421), renal failure (MESH:D051437), ATAAD (MESH:D000094683), aortic rupture (MESH:D001019), chronic kidney disease (MESH:D051436), abdominal pain (MESH:D015746), cerebral MPS (MESH:D002547), shock (MESH:D012769), inflammatory (MESH:D007249), coronary MPS (MESH:D054058), MPS (MESH:D013577), coronary trunk lesions (MESH:D003327), neurological deficits (MESH:D009461), ischemia (MESH:D007511), hypotensive shock (MESH:D007022), Renal MPS (MESH:D006030), tear (MESH:D012167), damage (MESH:D020263), end-organ dysfunction (MESH:D009102), bleeding (MESH:D006470), CVA (MESH:D020521), bloody diarrhea (MESH:D003967), acute kidney injury (MESH:D058186), spinal cord ischemia (MESH:D020760), cerebral infarction (MESH:D002544), cardiovascular disease (MESH:D002318), leukocytosis (MESH:D007964), metabolic acidosis (MESH:D000138), compartment syndrome (MESH:D003161), thrombosis (MESH:D013927), Hypertension (MESH:D006973), cardiac catastrophe (MESH:D002388), death (MESH:D003643), coronary malperfusion (MESH:D003323), necrosis (MESH:D009336), tamponade (MESH:D002305), coma (MESH:D003128), motor/sensory dysfunction (MESH:C536988), arterial embolism (MESH:D004617), tenderness (MESH:D063806), extremity MPS (MESH:C563475), aortic regurgitation (MESH:D001022)
- **Chemicals:** lactate (MESH:D019344), aspirin (MESH:D001241), creatine (MESH:D003401), D (MESH:D003903), antiplatelet (-), heparin (MESH:D006493), creatinine (MESH:D003404)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12933946/full.md

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Source: https://tomesphere.com/paper/PMC12933946