Cardioacoustic mechanical input to the arterial endothelium: a VascuQuest virtual-population dataset

This dataset is the computational record underlying the theoritical study “Cardioacoustics constitutes an endogenous mechanical input to the arterial endothelium.” It quantifies how a physiologically anchored cardiac cardioacoustic source is transformed by the arterial system into frequency-resolved mechanical input at the endothelial interface. The analysis was built with VascuQuest (version 1.0.0; commit 97db8b4c3575b1c615964b1540ceac69b97eb0ff) using the Pulse Wave Database (PWDB; Zenodo DOI 10.5281/zenodo.3275625) as the upstream virtual-artery population. A balanced final cohort of 102 physiologically eligible virtual subjects was used: 17 subjects at each age 25, 35, 45, 55, 65, and 75 years. For each subject, VascuQuest evaluates a linear frequency-domain, coupled blood–artery model over 10–40 Hz in 0.5-Hz increments and reports complex pressure, tangential traction, and wall-displacement transfer functions at five arterial sites. Healthy, partially stiffened, and globally stiff counterfactual arterial states are compared under an identical source. The cardioacoustic source construction combines invasive frequency measurements with a separate invasive A2 pressure-amplitude anchor. WP1 is retained as a transfer-only source condition; the primary absolute WP2/A2 condition is 18 Hz and 310 Pa, with sensitivity evaluations over 14.2–21.8 Hz and 190–480 Pa. The archive includes source-normalized complex transfer arrays, analytical qualification, local coupled-mode outputs, absolute endothelial pressure/traction/wall-motion exposure, wall acceleration and temporal shear-gradient derivations, paired state comparisons, spectral-shape statistics, focal-stiffness scattering outputs, endothelial evidence mapping, prospective experimental-load specifications, environment and execution provenance, and publication source-data/figure mirrors. This is a designed in silico population, not an epidemiological cohort. The dataset establishes physical source-to-endothelial-interface exposure and state-dependent spectral transformation; it does not establish biological endothelial transduction. Direct biological testing of the endogenous WP2/A2 domain remains experimentally required.