ReviewJournal of atherosclerosis and thrombosis2025
Gout, Uric Acid, and Coronary Artery Disease.
Review in Journal of atherosclerosis and thrombosis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Uric acid and subclinical atherosclerosis: distinct associations across coronary and carotid arteries.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- NMR-based metabolomics in a clinical cohort: deciphering the metabolic characteristics of gout with the dampness-heat syndrome and elucidate the efficacy of Simiao Pill.Chinese medicine · 2026Article
- Pediatric hyperuricemia: genetic basis, metabolic mechanisms, and clinical implications.Frontiers in endocrinology · 2026Review
- Hyperuricemia as an Early Indicator of Cardiovascular Risk in the General Population.Journal of clinical medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperuricemia, the biochemical precursor to gout, is usually defined as the theoretical limit of solubility of serum uric acid (UA) of ＞7.0 mg/dL. Hyperuricemia is closely associated with hypertension, diabetes mellitus, and dyslipidemia, which are well known to be related to risk factors for coronary artery disease (CAD). Furthermore, hyperuricemia has been associated with increased mortality in both the general population and individuals with cardiovascular diseases. Elevated UA in patients with CAD is accompanied by surrogate markers of atherosclerosis, including C-reactive protein, platelet activation, and endothelial dysfunction, which can contribute to possible pathogenic links between hyperuricemia and subsequent adverse cardiovascular events. Similarly, patients with gout have higher rates of cardiovascular diseases than those without it, independent of traditional cardiovascular risk factors. Gout is a disease with variable levels of inflammation, driven by deposition of monosodium urate (MSU) crystals. Recent imaging technology has revealed that deposition of MSU crystals can occur in the coronary arteries as well as the joints. However, current evidence does not support the efficacy of urate-lowering therapy on reducing cardiovascular events in patients with hyperuricemia; therefore, identifying individuals who may benefit from a sustained decrease in UA is crucial. We herein review the current understanding and future perspectives for management of hyperuricemia as a residual risk in patients with CAD.
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