The Role of Uric Acid in the Pathogenesis of Heart Failure With Preserved Ejection Fraction.

With advancing age and the development of risk factors such as hypertension, type 2 diabetes, obesity, and atrial fibrillation, the incidence of heart failure with preserved ejection fraction (HFpEF) has shown a year-on-year increase and is projected to become the most common form of heart failure in the near future. Uric acid (UA) is the end product of purine metabolism in the body and is closely associated with metabolic syndrome. Studies indicate that elevated serum uric acid levels constitute an independent risk factor for the onset, progression, and prognosis of HFpEF. UA can directly participate in the pathophysiological process of HFpEF by inducing oxidative stress, activating the inflammasome and pro-inflammatory signaling pathways, and impairing both cardiomyocyte function and microvascular endothelial integrity. This systematic review examines the epidemiological association between UA and HFpEF, the underlying mechanisms of UA involvement in HFpEF, and the potential benefits of urate-lowering therapy, including xanthine oxidase inhibitors and sodium-glucose cotransporter 2 inhibitors, for patients with HFpEF. It aims to enhance awareness of serum uric acid management in HFpEF patients and promote further exploration of pharmacological interventions in this field.