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Published on: May 3, 2018
The association of arterial stiffness index with cerebrovascular and cardiometabolic disease: A Mendelian
Weishi Liu1,2,3, Luyang Zhang1,2, Yuan Gao1,2
1Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Insights
Arterial stiffness index (ASI) may increase the risk of ischemic stroke (IS). This Mendelian randomization study found a link between genetically predicted ASI and higher IS risk, particularly large artery atherosclerosis stroke.
Area of Science:
- Cardiovascular epidemiology
- Genetics
- Neurology
Background:
- Arterial stiffness index (ASI) is a potential risk factor for cerebrovascular and cardiometabolic diseases.
- Causal links between ASI and these diseases remain inconclusive.
Purpose of the Study:
- To evaluate the causal effects of ASI on cerebrovascular and cardiometabolic diseases using Mendelian randomization (MR).
Main Methods:
- Two-sample MR analysis utilizing genetic variants associated with ASI.
- Inverse variance weighted method for effect estimation.
- Sensitivity analyses to assess heterogeneity and pleiotropy.
Main Results:
- Genetically predicted ASI showed a significant association with an increased risk of all-cause ischemic stroke (IS) (OR = 1.894, p = 0.005).
- A suggestive association was observed between genetically predicted ASI and large artery atherosclerosis stroke (LAS) (OR = 3.726, p = 0.020).
- No significant links were found between ASI and other cerebrovascular or cardiometabolic diseases, or specific IS etiologies like cardioembolism or small vessel occlusion.
Conclusions:
- Genetically predicted ASI is associated with an elevated risk of ischemic stroke.
- Further research is needed to elucidate the underlying pathways and mechanisms connecting ASI and IS.
Background:
Arterial stiffness index (ASI) is a potential risk factor for cerebrovascular and cardiometabolic diseases, but the causal links between them are inconclusive. The aim is to evaluate the causal effects of ASI on cerebrovascular and cardiometabolic diseases by Mendelian randomization (MR).
Methods:
Two-sample MR analysis was performed to infer causal links. Genetic variants significantly associated with ASI were extracted. The inverse variance weighted method was used for estimating the effects. Sensitivity analysis was performed to test heterogeneity or pleiotropy.
Results:
MR analysis indicated an effect of genetically predicted ASI on the risk of ischemic stroke (IS) of all causes (OR = 1.894, 95% CI 1.210-2.965, p = 0.005). No links were identified between genetically predicted ASI and other cerebrovascular or cardiometabolic diseases (all p > 0.05). Subgroup analysis of IS etiologies found a suggestive association between genetically predicted ASI and large artery atherosclerosis stroke (LAS) (OR = 3.726, 95% CI 1.230-11.286, p = 0.020). There were no effects of ASI on IS due to cardioembolism or small vessel occlusion.
Conclusion:
The current MR analysis suggested that genetically predicted ASI was associated with higher risk of IS of all causes. The results and the underlying pathways or mechanisms between ASI and IS needs further investigation.
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