The Impact of Hyperuricemia on the Progression of Atherosclerotic Cardiovascular Disease
Hyperuricemia refers to elevated levels of serum uric acid (SUA) beyond the normal physiological range in men and women. It is caused by increased endogenous synthesis, decreased renal clearance, or a combination. While hyperuricemia has long been associated with gout, new evidence suggests that it is a significant risk factor in the pathophysiology of a variety of cardiovascular and metabolic disorders, including hypertension, metabolic syndrome, coronary artery disease, heart failure, type 2 diabetes mellitus, and chronic kidney disease. The increasing global frequency of hyperuricemia has sparked scientific and clinical interest in the possible mechanistic relationship between elevated SUA levels and cardiovascular morbidity. Hyperuricemia's pathological mechanisms, including oxidative stress, endothelial dysfunction, and systemic inflammation, may lead to vascular remodeling, atherosclerotic plaque progression, and increased cardiovascular mortality. This case report emphasizes the need for increased clinical awareness of the cardiovascular dangers associated with asymptomatic hyperuricemia. Its purpose is to investigate the potential link between elevated SUA and the severity of coronary artery involvement, emphasizing the importance of early detection and treatment of hyperuricemia as a modifiable cardiovascular risk factor.
Authors
- Kakha Nadaraia (ORCID: https://orcid.org/0000-0003-1937-8719)
- Lali Gujejiani
- Marika Mdivnishvili
- Ketino Virkovi
- Vakhtang Chumburidze
- Maia Kharebashvili
Institutions
- Tbilisi State University (GE)
- Caucasus University (GE)
- National Heart Foundation of Australia (AU)
- Caucasus International University (GE)
- Open Society (CZ)
- Tbilisi State Medical University (GE)
- EU Business School, Geneva (CH)
Publication Details
- Journal
- Cureus
- Published
- 2025-10-11
- DOI
- https://doi.org/10.7759/cureus.94371
- Primary Topic
- Gout, Hyperuricemia, Uric Acid
- Type
- article
- Field-Weighted Citation Impact
- 0.00