Heart failure potentially affects the cortical structure of the brain
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Published on: December 28, 2014
Yinqin Hu1, Tianyun Shi1, Zhaohui Xu1
1Department of Cardiovascular Disease, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Insights
Heart failure may causally affect brain structure. This study found potential links between heart failure and changes in cerebral cortex thickness and specific lobule surface areas.
Area of Science:
- Neuroscience
- Cardiology
- Genetics
Background:
- Heart failure (HF) is known to impact cerebral cortex structure, but the causal factors remain unclear.
- Investigating the link between HF and brain structural changes is crucial for understanding neurological comorbidities.
Purpose of the Study:
- To determine the causal relationship between heart failure and structural alterations in the cerebral cortex using Mendelian randomization.
- To identify specific brain regions potentially affected by heart failure.
Main Methods:
- Employed Mendelian randomization (MR) with heart failure as the exposure and cerebral cortex structure as the outcome.
- Utilized inverse-variance weighted (IVW), MR-Egger, and weighted median methods for MR analysis.
- Performed sensitivity analyses including MR-PRESSO and leave-one-out to assess pleiotropy and robustness.
Main Results:
- Mendelian randomization analysis suggested a potential causal effect of heart failure on cerebral cortex thickness (P=0.0402).
- Significant causal effects were observed on the surface area of the caudal middle frontal lobule (P=0.009), insula lobule (P=0.01), precuneus lobule (P=0.049), and superior parietal lobule (P=0.044).
Conclusions:
- Heart failure may be causally associated with reduced cerebral cortical thickness.
- Heart failure is linked to altered surface area in key brain regions, including the caudal middle frontal, insula, precuneus, and superior parietal lobules.
Background:
Heart failure (HF) has been reported to affect cerebral cortex structure, but the underlying cause has not been determined. This study used Mendelian randomization (MR) to reveal the causal relationship between HF and structural changes in the cerebral cortex.
Methods:
HF was defined as the exposure variable, and cerebral cortex structure was defined as the outcome variable. Inverse-variance weighted (IVW), MR-Egger regression and weighted median (WME) were performed for MR analysis; MR-PRESSO and Egger's intercept was used to test horizontal pleiotropy; and "leave-one-out" was used for sensitivity analysis.
Results:
Fifty-two single nucleotide polymorphisms (SNPs) were defined as instrumental variables (IVs), and there was no horizontal pleiotropy in the IVs. According to the IVW analysis, the OR and 95% CI of cerebral cortex thickness were 0.9932 (0.9868-1.00) (P=0.0402), and the MR-Egger intercept was -15.6× 10-5 (P = 0.7974) and the Global test pval was 0.078. The P-value of the cerebral cortex surface was 0.2205, and the MR-Egger intercept was -34.69052 (P= 0.6984) and the Global Test pval was 0.045. HF had a causal effect on the surface area of the caudal middle frontal lobule (P=0.009), insula lobule (P=0.01), precuneus lobule (P=0.049) and superior parietal lobule (P=0.044).
Conclusions:
HF was potentially associated with changes in cortical thickness and in the surface area of the caudal middle frontal lobule, insula lobule, precuneus lobule and superior parietal lobule.
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