# Case Report: Rapid progression of inflammation-driven coronary artery lesions in a normolipidemic patient with ANCA-associated vasculitis complicated by Stanford type A aortic dissection

**Authors:** Guangzhen Lu, Xiaoting Wang, Xinye Wang, Hong Zhuang, Gang Zhao

PMC · DOI: 10.3389/fimmu.2026.1736895 · Frontiers in Immunology · 2026-03-12

## TL;DR

A patient with ANCA-associated vasculitis developed severe heart artery disease rapidly despite normal cholesterol levels, linked to inflammation rather than typical risk factors.

## Contribution

This case highlights a rare, inflammation-driven coronary artery progression in normolipidemic AAV patients, emphasizing the need for tailored treatment strategies.

## Key findings

- Rapid coronary artery stenosis occurred in a normolipidemic AAV patient with p-ANCA/MPO positivity.
- Inflammation-driven remodeling was observed via IVUS, showing soft plaques with minimal calcification.
- Parallel coronary and aortic progression was noted, suggesting a systemic inflammatory mechanism.

## Abstract

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic autoimmune small- to medium-vessel vasculitis. Reports of rapidly progressive left main/left anterior descending (LM/LAD) disease under normolipidemic conditions with parallel coronary–aortic progression are scarce.

We report a case of perinuclear antineutrophil cytoplasmic antibody (p-ANCA) and myeloperoxidase (MPO)–positive ANCA-associated vasculitis (AAV) in which, despite persistently normal lipid levels, the coronary arteries developed rapidly progressive stenosis and occlusion within one year. Intravascular ultrasound (IVUS) revealed concentric thickening of the coronary arterial wall characterized predominantly by soft plaques with minimal calcification, which was consistent with an inflammation-driven remodeling phenotype. Because the admission electrocardiogram (ECG) revealed an ST-segment elevation myocardial infarction (STEMI)-equivalent pattern (aVR ST elevation with diffuse ST depression), the patient was treated for acute myocardial infarction, and urgent LM-to-LAD drug-eluting stent (DES) implantation was performed. During a four-month follow-up after discharge, no recurrent angina or ischemic events were reported.

In a p-ANCA/MPO-positive AAV patient with sustained normolipidemia, we observed rapidly progressive LM/LAD disease occurring in parallel with aortic involvement, which was consistent with an inflammation-driven coronary phenotype that precipitated acute coronary syndrome. Integrating sequential coronary–aortic imaging with inflammatory biomarker surveillance and individualized immunomodulatory and antithrombotic strategies may enable earlier risk detection and optimize outcomes in patients with AAV.

## Linked entities

- **Proteins:** MPO (myeloperoxidase)
- **Diseases:** ANCA-associated vasculitis (MONDO:0012105), ST-segment elevation myocardial infarction (MONDO:0041656), acute myocardial infarction (MONDO:0004781)

## Full-text entities

- **Genes:** MPO (myeloperoxidase) [NCBI Gene 4353]
- **Diseases:** depression (MESH:D003866), acute coronary syndrome (MESH:D054058), LAD disease (MESH:C535887), coronary artery lesions (MESH:D003324), STEMI (MESH:D000072657), AAV (MESH:D014657), aortic involvement (MESH:C564676), stenosis (MESH:D003251), plaques (MESH:D003773), Stanford type A aortic dissection (MESH:D000784), ANCA-associated vasculitis (MESH:D056648), acute myocardial infarction (MESH:D009203), ischemic (MESH:D002545), angina (MESH:D000787), inflammation (MESH:D007249), calcification (MESH:D002114), autoimmune small- to medium-vessel vasculitis (MESH:C565222)
- **Chemicals:** lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC13017790/full.md

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Source: https://tomesphere.com/paper/PMC13017790