Dynamic Impedance Mismatch as the Physical Basis of Heart Failure with Preserved Ejection Fraction: A Vascular Network Degradation Model

Heart failure with preserved ejection fraction (HFpEF) remains a paradox: patients present with the full syndrome of heart failure despite normal left ventricular ejection fraction (LVEF). The prevailing pump-centric framework offers no unified explanation. We propose a physical principle: pump efficiency depends not only on the pump but also on its interaction with the downstream network. The healthy vascular tree operates as a distributed impedance matching network, with terminal arterioles continuously adjusting resistance to local metabolic demand. In HFpEF, endothelial dysfunction impairs this dynamic matching, and the vascular tree transitions from dynamic load matching to rigid impedance allocation. Using a terminal-load formulation based on transmission-line theory, we show that this transition alone—with central pump function held constant—reproduces the characteristic hemodynamic signature of HFpEF: increased wave reflection, reduced energy transmission efficiency, increased perfusion heterogeneity, and augmented central pulse pressure. We define a clinically measurable index, the Dys-Matching Index (DMI), as the normalized ratio of large-artery stiffness to microvascular dynamic dilatory reserve, estimating its empirical range at approximately 1.1 from published OptimEx-Clin data. The framework explains why HFpEF is a network failure rather than a pump failure, why exercise training improves symptoms without repairing the network, and why future therapy must restore the dynamic range of the vascular impedance matching system.