# Inflammation and Thrombophilia Markers in Supra-Aortic Takayasu Arteritis-Associated Stroke: A Digital Subtraction Angiography-Based Case Control Study

**Authors:** Ebru Marzioglu Ozdemir, Gokhan Ozdemir

PMC · DOI: 10.3390/jcm15062308 · Journal of Clinical Medicine · 2026-03-18

## TL;DR

This study investigates how inflammation and blood vessel issues contribute to strokes in young adults with Takayasu arteritis, finding that inflammation plays a bigger role than inherited blood clotting disorders.

## Contribution

The study identifies systemic inflammation and vascular impairment as key contributors over inherited thrombophilia in stroke risk for Takayasu arteritis patients.

## Key findings

- Stroke-positive patients had higher inflammatory activity and more severe supra-aortic artery lesions.
- Hereditary thrombophilia variants and homocysteine levels did not differ significantly between stroke and non-stroke groups.
- Lipoprotein(a) levels were statistically different but remained within normal clinical ranges.

## Abstract

Background/Objectives: Takayasu arteritis is an important non-atherosclerotic cause of ischemic stroke in young adults. However, the relative contribution of systemic inflammation, inherited thrombophilia, and supra-aortic hemodynamic impairment to cerebrovascular events in these patients remains insufficiently defined. This study aimed to evaluate the relative impact of systemic inflammatory activity, hereditary and acquired thrombophilia markers, and supra-aortic vascular involvement on cerebrovascular ischemic events in patients with digital subtraction angiography (DSA) confirmed supra-aortic Takayasu arteritis. Methods: A retrospective cross-sectional analysis was conducted in consecutively evaluated patients with non-atherosclerotic inflammatory stenosis or occlusion of the carotid, subclavian, or vertebral arteries confirmed by digital subtraction angiography. Age- and sex-matched hospital-based individuals without autoimmune, thrombotic, or cerebrovascular diseases served as controls. Laboratory assessments including erythrocyte sedimentation rate, lipoprotein(a), homocysteine, antinuclear antibody, rheumatoid factor, antiphospholipid antibodies, and a hereditary thrombophilia panel were obtained 4–6 weeks after clinical presentation during a stable clinical phase. Results: Among 46 patients with Takayasu arteritis, 21 patients presented with ischemic stroke. The stroke-positive subgroup demonstrated higher inflammatory activity and a slightly greater prevalence of supra-aortic occlusive lesions, particularly involving the common carotid, internal carotid, and subclavian arteries. Although lipoprotein(a) levels showed statistical differences between groups, mean values remained within reference ranges and were not clinically elevated. The distribution of hereditary thrombophilia variants and the prevalence of elevated homocysteine levels did not differ significantly between groups. Clinical outcomes were favorable overall, with no mortality and functional independence achieved in the majority of stroke-positive patients. Conclusions: These findings suggest that systemic inflammation and supra-aortic hemodynamic impairment may play a more prominent role than inherited thrombophilia in the development of cerebrovascular ischemic events in patients with Takayasu arteritis. Selective rather than routine thrombophilia testing may therefore be appropriate in selected clinical contexts, while careful control of inflammatory activity and continuous vascular monitoring remain essential components of management.

## Linked entities

- **Diseases:** Takayasu arteritis (MONDO:0017991), ischemic stroke (MONDO:1060198)

## Full-text entities

- **Genes:** LPA (lipoprotein(a)) [NCBI Gene 4018] {aka AK38, APOA, LP}
- **Diseases:** Inflammation (MESH:D007249), atherosclerotic (MESH:D050197), Takayasu Arteritis (MESH:D013625), Thrombophilia (MESH:D019851), occlusion of the carotid, subclavian, or vertebral arteries (MESH:D013349), inflammatory stenosis (MESH:D003251), rheumatoid factor (MESH:D001171), ischemic stroke (MESH:D002544), autoimmune, thrombotic, or cerebrovascular diseases (MESH:D002561), supra-aortic occlusive lesions (MESH:D001157), Stroke (MESH:D020521), hereditary thrombophilia (MESH:C540694)
- **Chemicals:** homocysteine (MESH:D006710)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC13026892/full.md

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Source: https://tomesphere.com/paper/PMC13026892