Elevated Uric Acid Is Associated With New-Onset Atrial Fibrillation: Results From the Swedish AMORIS Cohort.

Background The role of uric acid is gaining increasing importance in the evaluation of cardiovascular disease, but its relationship with atrial fibrillation (AF) is unclear. This study aims to investigate the association between uric acid levels and risk of new-onset AF. Methods and Results A total of 339 604 individuals 30 to 60 years of age and free from cardiovascular disease at baseline (1985-1996) in the Swedish AMORIS (Apolipoprotein-Mortality Risk) cohort were followed until December 31, 2019 for incident AF. Cox regression models were used to examine the association between uric acid and AF, adjusting for potential confounders and stratifying by incident cardiovascular disease. Over a mean follow-up of 25.9 years, 46 516 incident AF cases occurred. Compared with the lowest uric acid quartile, each of the upper 3 quartiles were associated with an increased risk of AF in a dose-response manner. Adjusted hazard ratios were 1.09 (95% CI, 1.06-1.12) for second quartile, 1.19 (95% CI, 1.16-1.23) for third quartile, and 1.45 (95% CI, 1.41-1.49) for fourth quartile. The association was similar among individuals with and without incident hypertension, diabetes, heart failure, or coronary heart disease. The dose-response pattern was further supported in a subsample of individuals with repeated measurements of uric acid. Conclusions Elevated uric acid was associated with an increased risk of AF, not only among people with cardiovascular disease and cardiovascular risk factors but also among those without. Future investigations are needed to examine whether lowering uric acid is relevant for AF prevention.

Impaired fasting glucose: a risk factor for atrial fibrillation and heart failure.

BACKGROUND: Dysglycaemia is associated with overall cardiovascular disease even at prediabetes levels. The aim of this study was to explore the association between glucose levels and future risk of developing atrial fibrillation and heart failure, respectively. METHODS: In this prospective cohort study subjects from the Swedish AMORIS-cohort with fasting glucose from health examinations 1985-1996 without previous cardiovascular disease (N = 294,057) were followed to 31 December 2011 for incident atrial fibrillation or heart failure. Cox proportional hazard models with attained age as timescale and adjustments for sex, cholesterol, triglycerides, and socioeconomic status were used to estimate hazard ratios by glucose categorized groups (normal glucose 3.9-6.0 mmol/L, impaired fasting glucose; 6.1-6.9 mmol/L, undiagnosed diabetes ≥ 7.0 mmol/L, and diagnosed diabetes). RESULTS: During a mean follow-up time of 19.1 years 28,233 individuals developed atrial fibrillation and 25,604 developed heart failure. The HR for atrial fibrillation was 1.19 (95% confidence interval 1.13-1.26) for impaired fasting glucose, 1.23 (1.15-1.32) for undiagnosed diabetes and 1.30 (1.21-1.41) for diagnosed diabetes. Corresponding figures for heart failure were; 1.40 (1.33-1.48), 2.11 (1.99-2.23), 2.22 (2.08-2.36) respectively. In a subset with BMI data (19%), these associations were attenuated and for atrial fibrillation only remained statistically significant among subjects with diagnosed diabetes (HR 1.25; 1.02-1.53). CONCLUSIONS: Fasting glucose at prediabetes levels is associated with development of atrial fibrillation and heart failure. To some extent increased BMI may drive this association.