Intensive blood pressure control in heart failure with preserved ejection fraction: a symptom-modifying strategy.

Patients with heart failure with preserved ejection fraction (HFpEF) account for over half of heart failure (HF) cases globally and the presence of HFpEF is closely linked with systemic hypertension, which contributes to the structural, hemodynamic, and symptomatic burden of the disease. HFpEF is a heterogeneous syndrome in which concentric remodeling/hypertrophy and diastolic dysfunction commonly arise from chronic pressure overload (often hypertension) and/or age-related arterial stiffening, metabolic comorbidity, and other myocardial substrates. This review critically examines the rationale for intensive blood pressure (BP) management in HF, particularly HFpEF, emphasizing its dual role in disease prevention and symptom alleviation. Drawing from landmark trials and mechanistic studies, the review demonstrates how acute and sustained BP reductions can improve hemodynamic profiles, reverse remodeling, and enhance functional capacity. It further explores the pathophysiologic underpinnings of hypertensive HFpEF, including left ventricular remodeling, arterial stiffness, pulmonary hypertension, right ventricular dysfunction, and metabolic-renal comorbidities; all of which amplify symptomatic burden. In addition, this review evaluates pharmacologic agents with antihypertensive and HF benefits, such as mineralocorticoid receptor antagonists (MRAs), angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor blockers (ARBs), and sodium–glucose cotransporter 2 inhibitors (SGLT2i). It also presents emerging evidence for renal denervation (RDN) as a novel adjunctive therapy, particularly in patients with resistant hypertension or autonomic imbalance. Preclinical and early clinical findings suggest that RDN may reduce sympathetic overactivity, enhance arterial compliance, and promote reverse cardiac remodeling in HFpEF. Ultimately, this review highlights BP modulation as a modifiable target capable of altering the trajectory of HFpEF, advocating for earlier and more intensive intervention strategies to improve both clinical and patient-reported outcomes.