Cardiovascular Lesions and their Genetic Features in Patients with Gout

Abstract

Uric acid (UA) is the final product of purine nucleotide metabolism in the human body. Hyperuricemia is an abnormally high level of uric acid in the blood, which can lead to arthritis and gout. The prevalence of hyperuricemia is growing worldwide. Epidemiological studies have shown that UA levels positively correlate with cardiovascular diseases (CVD), including hypertension, atherosclerosis, atrial fibrillation (AF), and heart failure (HF). Hyperuricemia contributes to the onset and progression of CVD by regulating molecular signals such as inflammatory responses, oxidative stress, insulin resistance/diabetes, endoplasmic reticulum stress, and endothelial dysfunction. Despite extensive research, the underlying molecular mechanisms remain unclear. It has been demonstrated that allopurinol, a xanthine oxidase (XO) inhibitor, improves cardiovascular outcomes in patients with HF, coronary artery disease (CAD), type 2 diabetes (T2D), and left ventricular hypertrophy (LVH). However, whether febuxostat, another XO inhibitor, can similarly improve cardiovascular outcomes remains controversial. Furthermore, it is uncertain whether urate-lowering therapy (ULT) can benefit patients with asymptomatic hyperuricemia. This review focuses on the latest cellular and molecular data regarding hyperuricemia-associated cardiovascular diseases and clinical data on the effectiveness of ULT in CVD patients.