Journal of cardiology · 2026
Uric Acid and the Risk of Aortic Aneurysm and Dissection: Insights from a Long-Term Prospective Cohort Study of 468,223 Participants in the UK Biobank.
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Yang Peng, Zhang Xiaoyang, Dong Wentao, Chen Suwei, Hu Haiou, Qiao Zhiyu, Li Chengnan, Ge Yipeng, Zhu Junming
Аннотация
BACKGROUND: Uric acid (UA) is a routinely measured biomarker linked to cardiovascular and metabolic disorders, but its role in the development of aortic aneurysm (AA) and aortic dissection (AD) remains unclear. This study aimed to evaluate the association between UA levels and incident AA/AD.
METHODS: We included 468,223 participants without baseline AA/AD from the UK Biobank prospective cohort. Baseline UA was measured and categorized by quartiles. The primary outcome was incident AA/AD. Cox proportional hazards models and restricted cubic spline (RCS) analyses were employed. Subgroup analyses were performed by age, sex, smoking status, blood pressure status, and history of coronary artery or cerebrovascular disease.
RESULTS: During a median follow-up of 15.1 years, 4,504 AA/AD events were recorded. At baseline, elevated UA levels were significantly associated with decreased estimated glomerular filtration rate and increased C-reactive protein levels. AA/AD incidence increased across UA quartiles. In fully adjusted models, hazard ratios (HRs) for AA/AD were 1.00 (reference), 1.03 (95% CI 0.92-1.15), 1.04 (95% CI 0.92-1.16), and 1.17 (95% CI 1.04-1.31) from lowest to highest UA quartile. RCS analyses indicated a linear association between UA and AA/AD risk. The association was significant for AA (Q4 vs Q1: HR 1.15, 95% CI 1.02-1.31), but not for AD (Q4 vs Q1: HR 1.30, 95% CI 0.90-1.86). Subgroup analyses showed stronger associations in participants younger than 60 years, previous smokers, and those without prior coronary artery or cerebrovascular disease. Notably, the association remained statistically significant even in participants with clinically normal blood pressure.
CONCLUSIONS: Elevated UA levels are independently associated with a higher risk of AA/AD, particularly AA. This association persists independently of hypertension and may be linked to inflammatory mechanisms and renal dysfunction. These findings support the role of UA as a potential biomarker for risk assessment and prevention of AA, especially in high-risk populations.
METHODS: We included 468,223 participants without baseline AA/AD from the UK Biobank prospective cohort. Baseline UA was measured and categorized by quartiles. The primary outcome was incident AA/AD. Cox proportional hazards models and restricted cubic spline (RCS) analyses were employed. Subgroup analyses were performed by age, sex, smoking status, blood pressure status, and history of coronary artery or cerebrovascular disease.
RESULTS: During a median follow-up of 15.1 years, 4,504 AA/AD events were recorded. At baseline, elevated UA levels were significantly associated with decreased estimated glomerular filtration rate and increased C-reactive protein levels. AA/AD incidence increased across UA quartiles. In fully adjusted models, hazard ratios (HRs) for AA/AD were 1.00 (reference), 1.03 (95% CI 0.92-1.15), 1.04 (95% CI 0.92-1.16), and 1.17 (95% CI 1.04-1.31) from lowest to highest UA quartile. RCS analyses indicated a linear association between UA and AA/AD risk. The association was significant for AA (Q4 vs Q1: HR 1.15, 95% CI 1.02-1.31), but not for AD (Q4 vs Q1: HR 1.30, 95% CI 0.90-1.86). Subgroup analyses showed stronger associations in participants younger than 60 years, previous smokers, and those without prior coronary artery or cerebrovascular disease. Notably, the association remained statistically significant even in participants with clinically normal blood pressure.
CONCLUSIONS: Elevated UA levels are independently associated with a higher risk of AA/AD, particularly AA. This association persists independently of hypertension and may be linked to inflammatory mechanisms and renal dysfunction. These findings support the role of UA as a potential biomarker for risk assessment and prevention of AA, especially in high-risk populations.