Understanding of heart failure with preserved ejection fraction (HFpEF) continues to evolve, shifting from a cardiocentric to a more encompassing paradigm inclusive of vascular and systemic pathophysiology. Among the underlying mechanisms expounded for HFpEF, one model posits structural and functional alterations in the arterial vasculature, particularly coronary microvascular rarefaction and mismatch between blood flow and oxygen demand (1, 2). Coronary microvascular dysfunction strongly associates with peripheral arterial microvascular dysfunction, collectively suggesting a systemic vascular phenotype in patients with HFpEF (3).

Paralleling this broadened scope beyond the heart, investigation of the vasculature in HFpEF is also expanding from an arterial-centric view to examine other vascular beds, including veins and, more recently, lymphatic vessels. Mechanistic studies in rodents demonstrate the significance of lymphatic vessels in regulating interstitial sodium via immune cell–mediated lymphangiogenesis(4). When lymphatic clearance is impaired in the skin, excess tissue sodium collection, interstitial volume