The arterial pulse wave (PW) is a rich source of information on cardiovascular (CV) health. It is widely measured by both consumer and clinical devices. However, the physical determinants of the PW are not yet fully understood, and the development of PW analysis algorithms is limited by a lack of PW data sets containing reference CV measurements. Our aim was to create a database of PWs simulated by a computer to span a range of CV conditions, representative of a sample of healthy adults. The typical CV properties of 25–75 yr olds were identified through a literature review. These were used as inputs to a computational model to simulate PWs for subjects of each age decade. Pressure, flow velocity, luminal area, and photoplethysmographic PWs were simulated at common measurement sites, and PW indexes were extracted. The database, containing PWs from 4,374 virtual subjects, was verified by comparing the simulated PWs and derived indexes with corresponding in vivo data. Good agreement was observed, with well-reproduced age-related changes in hemodynamic parameters and PW morphology. The utility of the database was demonstrated through case studies providing novel hemodynamic insights, in silico assessment of PW algorithms, and pilot data to inform the design of clinical PW algorithm assessments. In conclusion, the publicly available PW database is a valuable resource for understanding CV determinants of PWs and for the development and preclinical assessment of PW analysis algorithms. It is particularly useful because the exact CV properties that generated each PW are known.NEW & NOTEWORTHY First, a comprehensive literature review of changes in cardiovascular properties with age was performed. Second, an approach for simulating pulse waves (PWs) at different ages was designed and verified against in vivo data. Third, a PW database was created, and its utility was illustrated through three case studies investigating the determinants of PW indexes. Fourth, the database and tools for creating the database, analyzing PWs, and replicating the case studies are freely available.

Aims: In hypertensive adults, first-phase ejection fraction (EF1), a measure of early ventricular contraction is reduced and associated with prolonged systolic contraction and diastolic dysfunction. Whether this is true in children with primary hypertension is unknown. Methods: Echocardiography was performed in 47 normotensive and 81 hypertensive children. Hypertensive children were stratified according to tertiles of LVMi (g/m2.7). EF1 was calculated from the fraction of LV volume ejected up to the time of peak aortic flow. E/e’ was used as a measure of diastolic function. Myocardial wall stress (MWS) was calculated in a subsample of children from LV volumes and central aortic pressure. Time to onset of relaxation (TOR) was defined as time to peak MWS over ejection time. Results: Normotensive and hypertensive children were of similar age. Hypertensive children in tertiles 2 and 3 of LVMi had higher BMI z-score than normotensives. EF1 was significantly increased in hypertensive children in tertile 1 compared with normotensive children (P < 0.001), whereas in those in tertile 3, it was significantly lower than in normotensive children (P < 0.001). EF1 was negatively associated with LVMi (β = −0.505, P < 0.001), LVM (β = −0.531, P = 0.001) and E/e’ ratio (β = −0.409, P < 0.001); in children who had MWS measured, TOR was negatively associated with EF1 (β = −0.303, P = 0.007) and positively associated with E/e’ (β = 0.459, P < 0.001). Conclusion: EF1 is preserved or enhanced in hypertensive children with similar LVMi to normotensive children but is increasingly reduced in those with greater LVMi. This reduction of EF1 is associated with prolonged myocardial wall stress and reduced diastolic function.

Objective:Central systolic blood pressure (cSBP, the peak of the central waveform) is usually regarded as the determinant of peripheral systolic blood pressure with amplification of peripheral systolic BP (pSBP) measured with reference to cSBP. However, the earlier portion of the central waveform, up to the first systolic shoulder (P1) may be the major determinant of pSBP. Methods:We performed in silicosimulation studies and examined previously acquired experimental data (n=131) in which peripheral and central blood pressure waveforms had been acquired both invasively and non-invasively to examine the determinants of pSBP. Measurements were made at baseline and during perturbation of haemodynamics by inotropic and vasoactive drugs. Results:In silicosimulations using a central-to-peripheral transfer function demonstrated that pSBP is dependent on P1 and the rate of change (dP/dt) of central pressure up to the time of P1 but not cSBP. In computational simulations, peripheral reflection in the radial artery was closely related to dP/dt and 97% of the variability in amplification as measured with reference to P1 was explained by dP/dt.In vivo, amplification of pSBP over P1 was correlated with dP/dt (R>0.75, P<0.0001 for all data sets) and P1 and dP/dt were independently correlated with pSBP explaining 90% of the variability in pSBP. Conclusion:We conclude that P1 and dP/dt are major determinants of pSBP and that pSBP and cSBP are, in part, determined by different cardiac, central and peripheral vascular properties.