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Genetically predicted ankylosing spondylitis increases the risk of heart failure: a Mendelian randomization study
Chennan Liu1,2, Laicheng Wang3, Mei Lin1,2
1Department of Cardiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Insights
Ankylosing spondylitis may causally increase heart failure risk. This link might be partly explained by increased arterial stiffness, suggesting a cardiovascular disease connection.
Area of Science:
- Rheumatology
- Cardiology
- Genetics
Background:
- Observational studies suggest a link between ankylosing spondylitis and cardiovascular disease (CVD).
- The causal nature of this association requires further investigation.
- Mendelian randomization is a suitable method to explore causality.
Purpose of the Study:
- To investigate the causal relationship between ankylosing spondylitis and the risk of six prevalent cardiovascular diseases.
- To assess the influence of potential confounding factors on this relationship.
Main Methods:
- A two-sample Mendelian randomization analysis was performed.
- Six cardiovascular diseases were examined: hypertension, heart failure, atrial fibrillation, coronary heart disease, myocardial infarction, and peripheral artery disease.
- Multivariate Mendelian randomization was used to adjust for confounding variables.
Main Results:
- Genetically predicted ankylosing spondylitis was associated with an increased risk of heart failure (OR=1.02; 95% CI=1.00-1.04; p=0.030).
- The association remained significant after adjusting for hypertension, diabetes, smoking, BMI, and pulse wave reflection index.
- The causal link diminished after adjusting for pulse wave peak-to-peak time and arterial stiffness index.
Conclusions:
- Genetically predicted ankylosing spondylitis increases the risk of heart failure.
- Arterial stiffness may be a mediating factor in the causal pathway between ankylosing spondylitis and heart failure.
Background:
Observational studies have indicated a potential association between ankylosing spondylitis and elevated cardiovascular disease (CVD) risk. However, it remains uncertain whether this association reflects a causal association. Therefore, we conducted this Mendelian randomization to investigate the causal relationship between ankylosing spondylitis and CVD.
Methods:
We performed a two-sample Mendelian randomization analysis to establish a causal relationship between ankylosing spondylitis and the risk of six prevalent CVDs: hypertension, heart failure, atrial fibrillation, coronary heart disease, myocardial infarction, and peripheral artery disease. Furthermore, multivariate Mendelian randomization was employed to determine the influence of confounding factors.
Results:
Genetically predicted ankylosing spondylitis increased the risk of heart failure according to the Mendelian randomization analysis (OR = 1.02; 95% CI = 1.00-1.04; p = 0.030). Multivariate analysis results indicated that the causal relationship between ankylosing spondylitis and heart failure risk remained significant after adjusting for hypertension, diabetes, smoking, body mass index, and pulse wave reflection index. The associations diminished and lost significance after adjusting for pulse wave peak-to-peak time and pulse wave arterial stiffness index.
Conclusion:
Genetically predicted ankylosing spondylitis increased the risk of heart failure, and the causality may partly be mediated by increased arterial stiffness.
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