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Updated: Aug 16, 2026

A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Subclinical carotid atherosclerosis in inflammatory bowel disease: a population-based cross-sectional study
Alexander Akhgar1, Bernhard Wernly2, Alexandra Feldman2
1Paracelsus Medical University, Salzburg, Austria a.akhgar@salk.at.
Objective:
Patients with inflammatory bowel disease (IBD) have an increased risk of cardiovascular and cerebrovascular events, but the underlying mechanisms remain unclear. We aimed to assess subclinical carotid atherosclerosis in IBD in a large population-based cohort.
Methods:
We performed a cross-sectional analysis of the Paracelsus 10 000 cohort in Salzburg, Austria. Adults aged 40-77 years underwent standardised clinical evaluation, laboratory testing and bilateral carotid ultrasonography. The primary endpoint was carotid plaque burden; secondary endpoints included plaque presence, intima-media thickness, carotid stenosis, coronary artery calcium and polygenic risk scores. Multivariable ordered logistic regression models were adjusted for age, sex and comprehensive cardiovascular risk measures including Systematic Coronary Risk Evaluation 2 and Life's Essential 8.
Results:
Among 9723 participants, 70 had IBD and 9653 served as controls. Patients with IBD had higher levels of high-sensitivity C reactive protein (median 0.15 vs 0.12 mg/dL; p=0.039) and lower ferritin levels (86 vs 117 ng/mL; p=0.018). Carotid plaque prevalence (40% vs 38%; p=0.79) and plaque burden distribution (p=0.82) were similar between groups. Intima-media thickness, carotid stenosis, coronary artery calcium score categories and polygenic risk scores were also comparable. In multivariable analysis, IBD was not associated with higher plaque burden (adjusted OR 1.49; 95% CI 0.88 to 2.55; p=0.139).
Conclusions:
In this population-based cohort, IBD was not associated with increased subclinical carotid atherosclerosis. These findings suggest that cardiovascular risk in IBD may not be fully explained by atherosclerotic burden alone and may involve inflammation-related and prothrombotic mechanisms beyond atherosclerosis.
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