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Cardiovascular risk in inflammatory bowel disease: focus on lipids and visceral adipose tissue
Eva Karaskova1, David Friedecky2, David Kleparnik1
1Department of Pediatrics, University Hospital Olomouc, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czechia.
Insights
Patients with inflammatory bowel diseases (IBD) have a higher risk of atherosclerotic cardiovascular disease (ASCVD) due to chronic inflammation and gut microbiome changes. Managing IBD activity and cardiovascular risk factors is crucial for better long-term outcomes.
Area of Science:
- Gastroenterology and Cardiology
- Immunology and Metabolism
Background:
- Inflammatory bowel diseases (IBD), encompassing Crohn's disease and ulcerative colitis, are increasingly recognized as systemic conditions with substantial cardiovascular implications.
- Epidemiological data indicate an elevated risk of atherosclerotic cardiovascular disease (ASCVD) in IBD patients, exceeding that attributable to traditional risk factors, particularly in younger individuals and during active inflammation.
Purpose of the Study:
- To review the pathogenic mechanisms linking IBD and ASCVD.
- To highlight the role of chronic inflammation, gut dysbiosis, and lipid abnormalities in this association.
- To discuss current and future strategies for cardiovascular risk assessment and prevention in IBD patients.
Main Methods:
- Literature review of studies investigating the interplay between IBD and ASCVD.
- Analysis of pathogenic mechanisms including systemic inflammation, endothelial dysfunction, hypercoagulability, and gut microbiome alterations.
- Examination of the "lipid paradox" and emerging lipidomic biomarkers in IBD.
Main Results:
- Chronic systemic inflammation is a key driver of accelerated atherogenesis in IBD.
- Gut barrier dysfunction, microbial translocation, and dysbiosis contribute to cardiovascular risk.
- IBD is associated with a "lipid paradox" where reduced lipid levels correlate with increased ASCVD risk due to inflammation-induced lipoprotein dysfunction.
Conclusions:
- Effective management of IBD, including controlling disease activity and minimizing corticosteroid use, is vital for cardiovascular risk reduction.
- Traditional cardiovascular risk calculators may underestimate risk in IBD; integrated approaches using inflammatory burden and imaging are needed.
- Individualized cardiovascular prevention strategies, optimized anti-inflammatory therapies, and addressing modifiable risk factors are essential for improving long-term outcomes in IBD patients.
Abstract:
Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are chronic immune-mediated diseases that are increasingly recognized as systemic diseases with significant cardiovascular consequences. Growing epidemiological evidence suggests that patients with IBD face an increased risk of atherosclerotic cardiovascular disease (ASCVD) that cannot be fully explained by traditional cardiovascular risk factors. This excess risk is most pronounced in younger patients and during periods of active intestinal inflammation. This review summarizes current knowledge on common pathogenic mechanisms linking IBD and ASCVD. Chronic systemic inflammation plays a central role, promoting endothelial dysfunction, hypercoagulability, immune cell activation, and accelerated atherogenesis. Other factors include intestinal barrier disruption with microbial translocation, dysbiosis of the gut microbiome, dysfunctional visceral adipose tissue, and adverse metabolic effects of some IBD therapies. Particular emphasis is placed on lipid abnormalities observed in IBD, including the "lipid paradox", a phenomenon in which reduced circulating lipid levels paradoxically coexist with increased cardiovascular risk due to inflammation-mediated changes in lipid metabolism leading to lipoprotein dysfunction, and emerging lipidomic biomarkers that suggest causal relationships between specific lipid species, inflammatory mediators, and cardiovascular risk. Attention is also given to current strategies for the assessment and prevention of cardiovascular risk in IBD, emphasizing the importance of controlling disease activity, minimizing corticosteroid exposure, and aggressive treatment of modifiable cardiovascular risk factors. Traditional risk calculators may underestimate risk in this population, highlighting the need for tools that integrate inflammatory burden and imaging of subclinical atherosclerosis. Optimization of anti-inflammatory therapy along with individualized cardiovascular prevention strategies may improve long-term outcomes in patients with IBD.
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