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Vascular aging (VA) involves structural and functional changes in blood vessels that contribute to cardiovascular disease. Several noninvasive pulse wave (PW) indices have been proposed to assess the arterial stiffness component of VA in the clinic and daily life. This study investigated 19 of these indices, identified in recent review articles on VA, by using a database comprising 3,837 virtual healthy subjects aged 25-75 yr, each with unique PW signals simulated under various levels of artificial noise to mimic real measurement errors. For each subject, VA indices were calculated from filtered PW signals and compared with the precise theoretical value of aortic Young's modulus (EAo). In silico PW indices showed age-related changes that align with in vivo population studies. The cardio-ankle vascular index (CAVI) and all pulse wave velocity (PWV) indices showed strong linear correlations with EAo (Pearson's rp > 0.95). Carotid distensibility showed a strong negative nonlinear correlation (Spearman's rs < -0.99). CAVI and distensibility exhibited greater resilience to noise compared withPWVindices.Blood pressure-related indices and photoplethysmography (PPG)-based indices showed weaker correlations with EAo (rp and rs < 0.89, ΙrpΙ and ΙrsΙ < 0.84, respectively). Overall, blood pressure-related indices were confounded by more cardiovascular properties (heart rate, stroke volume, duration of systole, large artery diameter, and/or peripheral vascular resistance) compared with other studied indices, and PPG-based indices were most affected by noise. In conclusion, carotid- femoral PWV, CAVI and carotid distensibility emerged as the superior clinical VA indicators, with a strong EAo correlation and noise resilience. PPG-based indices showed potential for dailyVAmonitoring underminimized noise disturbances. [ABSTRACT FROM AUTHOR]

Arterial pulse waves (PWs) such as blood pressure and photoplethysmogram (PPG) signals contain a wealth of information on the cardiovascular (CV) system that can be exploited to assess vascular age and identify individuals at elevated CV risk. We review the possibilities, limitations, complementarity, and differences of reduced-order, biophysical models of arterial PW propagation, as well as theoretical and empirical methods for analyzing PW signals and extracting clinically relevant information for vascular age assessment. We provide detailed mathematical derivations of these models and theoretical methods, showing how they are related to each other. Finally, we outline directions for future research to realize the potential of modeling and analysis of PW signals for accurate assessment of vascular age in both the clinic and in daily life. [ABSTRACT FROM AUTHOR]

Another type of natural wave, traced from longitudinal wall motion and propagation along the artery, is observed in our in vivo human carotid artery experiments. We coin it as extension wave (EW) and hypothesize that EW velocity (EWV) is associated with arterial longitudinal stiffness. The EW is thus assumed to complement the pulse wave (PW), whose velocity (PWV) is tracked from the radial wall displacement and linked to arterial circumferential stiffness through the Moens-Korteweg equation, as indicators for arterial mechanical anisotropy quantification by noninvasive high-frame-rate ultrasound. The relationship between directional arterial stiffnesses and the two natural wave speeds was investigated in wave theory, finite-element simulations based on isotropic and anisotropic arterial models, and in vivo human common carotid artery (n = 10) experiments. Excellent agreement between the theory and simulations showed that EWV was 2.57 and 1.03 times higher than PWV in an isotropic and an anisotropic carotid artery model, respectively, whereas in vivo EWV was consistently lower than PWV in all 10 healthy human subjects. A strong linear correlation was substantiated in vivo between EWV and arterial longitudinal stiffness quantified by a well-validated vascular-guided wave imaging technique (VGWI). We thereby proposed a novel index calculated as EWV2/PWV2 as an alternative to assess arterial mechanical anisotropy. Simulations and in vivo results corroborated the effect of mechanical anisotropy on the propagation of spontaneous waves along the arterial wall. The proposed anisotropy index demonstrated the feasibility of the concurrent EW and PW imaged by high frame-rate ultrasound in grading of arterial wall anisotropy. NEW & NOTEWORTHY An extension wave formed by longitudinal wall displacements was observed by high-frame-rate ultrasound in the human common carotid artery in vivo. A strong correlation between extension wave velocity and arterial longitudinal stiffness complements the well-established pulse wave, which is linked to circumferential stiffness, to noninvasively assess direction-dependent wall elasticity of the major artery. The proposed anisotropy index, which directly reflects arterial wall microstructure and function, might be a potential risk factor for screening (sub-) clinical cardiovascular diseases. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Exercise markedly influences pulse wave morphology, but the mechanism is unknown. We investigated whether effects of exercise on the arterial pulse result from alterations in stroke volume or pulse wave velocity (PWV)/large artery stiffness or reduction of pressure wave reflection. Healthy subjects (n = 25) performed bicycle ergometry. with workload in- creasing from 25 to 150 W for 12 mm. Digital arterial pressure waveforms were recorded using a servo-controlled finger cuff. Radial arterial pressure waveforms and carotid-femoral PWV were deter- mined by applanation tonometry. Stroke volume was measured by echocardiography, and brachial and femoral artery blood flows and diameters were measured by ultrasound. Digital waveforms were recorded continuously. Other measurements were made before and after exercise. Exercise markedly reduced late systolic and diastolic augmentation of the peripheral pressure pulse. At 15 mm into recovery, stroke volume and PWV were similar to baseline values, but changes in pulse wave morphology persisted. Late systolic augmentation index (radial pulse) was reduced from 54 ± 3.9% at baseline to 42 ± 3.7% (P < 0.01), and diastolic augmentation index (radial pulse) was reduced from 37 ± 1.8% to 25 ± 2.9% (P < 0.001). These changes were accompanied by an increase in femoral blood flow (from 409 ± 44 to 773 ± 48 mI/mm, P < 0.05) and an increase in femoral artery diameter (from 8.2 ± 0.4 to 8.6 ± 0.4 mm, P < 0.05). In conclusion, exercise dilates muscular arteries and reduces arterial pressure augmentation, an effect that will enhance ventricular-vascular coupling and reduce load on the left ventricle. [ABSTRACT FROM AUTHOR]

Using a frequency-domain Womersley-type model, we previously simulated pulsatile blood flow throughout the coronary arterial tree. Although this model represents a good approximation for the smaller vessels, it does not take into account the nonlinear convective energy losses in larger vessels. Here, using Womersley's theory, we present a hybrid model that considers the nonlinear effects for the larger epicardial arteries while simulating the distal vessels (down to the 1st capillary segments) with the use of Womersley's Theory. The main trunk and primary branches were discretized and modeled with one-dimensional Navier-Stokes equations, while the smaller-diameter vessels were treated as Womersley-type vessels. Energy losses associated with vessel bifurcations were incorporated in the present analysis. The formulation enables prediction of impedance and pressure and pulsatile flow distribution throughout the entire coronary arterial tree down to the first capillary segments in the arrested, vasodilated state. We found that the nonlinear convective term is negligible and the loss of energy at a bifurcation is small in the larger epicardial vessels of an arrested heart. Furthermore, we found that the flow waves along the trunk or at the primary branches tend to scale (normalized with respect to their mean values) to a single curve, except for a small phase angle difference. Finally, the model predictions for the inlet pressure and flow waves are in excellent agreement with previously published experimental results. This hybrid one-dimensional/Womersley model is an efficient approach that captures the essence of the hemodynamics of a complex large-scale vascular network. The present model has numerous applications to understanding the dynamics of coronary circulation. [ABSTRACT FROM AUTHOR]