Hyperuricemia in heart failure with preserved ejection fraction: pathophysiological insights and therapeutic...

Heart failure with preserved ejection fraction (HFpEF) constitutes a growing burden worldwide, with hyperuricemia emerging as a prominent comorbidity. This review explores the prevalence, pathophysiological mechanisms, and therapeutic implications of hyperuricemia in HFpEF. Epidemiological studies consistently demonstrate that elevated serum uric acid (SUA) levels are associated with an increased risk of cardiovascular events, hospitalizations, and mortality. Mechanistic insights highlight endothelial dysfunction, oxidative stress, myocardial fibrosis, and systemic inflammation as key contributors linking hyperuricemia to adverse cardiac remodeling. Pharmacological interventions, including xanthine oxidase inhibitors, uricosuric agents, and SGLT2 inhibitors, show promise in mitigating hyperuricemia and improving HFpEF outcomes. Despite emerging evidence, critical knowledge gaps persist regarding causality, therapeutic efficacy, and optimal patient selection. Future research should focus on targeted interventions, dynamic SUA monitoring, and the interplay between hyperuricemia, diabetes, and left ventricular dysfunction to enhance the management of HFpEF patients.