Mutual effect of homocysteine and uric acid on arterial stiffness and cardiovascular risk in the context of predictive, preventive, and personalized medicine

EPMA Journal - Tập 13 - Trang 581-595 - 2022
Zhiyuan Wu1,2, Haiping Zhang1, Zhiwei Li1, Haibin Li3, Xinlei Miao1, Huiying Pan1, Jinqi Wang1, Xiangtong Liu1, Xiaoping Kang4, Xia Li5, Lixin Tao1, Xiuhua Guo1,2
1Beijing Municipal Key Laboratory of Clinical Epidemiology, Department of Epidemiology and Health Statistics, School of Public Health, Capital Medical University, Beijing, China
2Centre for Precision Health, School of Medical and Health Sciences, Edith Cowan University, Perth, Australia
3Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China
4Beijing Xiaotangshan Hospital, Beijing, China
5Department of Mathematics and Statistics, La Trobe University, Melbourne, Australia

Tóm tắt

Arterial stiffness is a major risk factor and effective predictor of cardiovascular diseases and a common pathway of pathological vascular impairments. Homocysteine (Hcy) and uric acid (UA) own the shared metabolic pathways to affect vascular function. Serum uric acid (UA) has a great impact on arterial stiffness and cardiovascular risk, while the mutual effect with Hcy remains unknown yet. This study aimed to evaluate the mutual effect of serum Hcy and UA on arterial stiffness and 10-year cardiovascular risk in the general population. From the perspective of predictive, preventive, and personalized medicine (PPPM/3PM), we assumed that combined assessment of Hcy and UA provides a better tool for targeted prevention and personalized intervention of cardiovascular diseases via suppressing arterial stiffness. This study consisted of 17,697 participants from Beijing Health Management Cohort, who underwent health examination between January 2012 and December 2019. Brachial-ankle pulse wave velocity (baPWV) was used as an index of arterial stiffness. Individuals with both high Hcy and UA had the highest baPWV, compared with those with low Hcy and low UA (β: 30.76, 95% CI: 18.36–43.16 in males; β: 53.53, 95% CI: 38.46–68.60 in females). In addition, these individuals owned the highest 10-year cardiovascular risk (OR: 1.49, 95% CI: 1.26–1.76 in males; OR: 7.61, 95% CI: 4.63–12.68 in females). Of note, males with high homocysteine and low uric acid were significantly associated with increased cardiovascular risk (OR: 1.30, 95% CI: 1.15–1.47), but not the high uric acid and low homocysteine group (OR: 1.02, 95% CI: 0.90–1.16). This study found the significantly mutual effect of Hcy and UA on arterial stiffness and cardiovascular risk using a large population and suggested the clinical importance of combined evaluation and control of Hcy and UA for promoting cardiovascular health. The adverse effect of homocysteine on arteriosclerosis should be addressed beyond uric acid, especially for males. Monitoring of the level of both Hcy and UA provides a window opportunity for PPPM/3PM in the progression of arterial stiffness and prevention of CVD. Hcy provides a novel predictor beyond UA of cardiovascular health to identify individuals at high risk of arterial stiffness for the primary prevention and early treatment of CVD. In the progressive stage of arterial stiffness, active control of Hcy and UA levels from the aspects of dietary behavior and medication treatment is conducive to alleviating the level of arterial stiffness and reducing the risk of CVD. Further studies are needed to evaluate the clinical effect of Hcy and UA targeted intervention on arterial stiffness and cardiovascular health.

Tài liệu tham khảo

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