Abstract
Introduction: Hyponatremia is a common electrolyte abnormality in heart failure and has been consistently associated with worse clinical outcomes. While its prognostic value is well established in heart failure with reduced ejection fraction, its significance in heart failure with preserved ejection fraction remains less clearly defined. Increasing evidence suggests that hyponatremia may reflect advanced neurohormonal activation, congestion, and cardiorenal dysfunction in this population. Methods: This study was conducted as a narrative review of the literature examining the pathophysiology, clinical implications, and management of hyponatremia in heart failure with preserved ejection fraction. Electronic databases including PubMed, EMBASE, Cochrane Library, Scopus, and Google Scholar were searched for relevant publications between 2010 and 2025. Eligible sources included clinical trials, observational studies, registry analyses, guideline documents, and review articles focusing on sodium disorders in heart failure populations. The findings were synthesized qualitatively to provide an integrated overview of the mechanisms, prognostic significance, and therapeutic considerations. Results: Available evidence indicates that hyponatremia occurs frequently in patients with heart failure with preserved ejection fraction and is associated with increased risks of mortality, rehospitalization, and cardiovascular events. The underlying mechanisms involve complex interactions between neurohormonal activation, impaired renal free water excretion, and therapeutic factors such as diuretic exposure. Hyponatremia appears to function primarily as a marker of disease severity rather than a direct mediator of adverse outcomes. Current management strategies primarily rely on general heart failure treatment principles, including optimizing diuretic therapy, managing fluid balance, and selectively using vasopressin antagonists. Conclusions: Hyponatremia represents an important biomarker of adverse prognosis in heart failure with preserved ejection fraction. Despite its clinical relevance, evidence guiding phenotype-specific management remains limited. Future research should focus on clarifying pathophysiologic mechanisms, improving risk stratification, and determining whether targeted correction of hyponatremia can improve clinical outcomes in this growing patient population.