Parametric uncertainty analysis of pulse wave propagation in a model of a human arterial network

Accepted versio

Non-invasive evaluation of left ventricular afterload, part 2 : arterial pressure-flow and pressure-volume relations in humans

The mechanical load imposed by the systemic circulation to the left ventricle is an important determinant of normal and abnormal cardiovascular function. Left ventricular afterload is determined by complex time-varying phenomena, which affect pressure and flow patterns generated by the pumping ventricle. Left ventricular afterload is best described in terms of pressure-flow relations, allowing for quantification of various components of load using simplified biomechanical models of the circulation, with great potential for mechanistic understanding of the role of central hemodynamics in cardiovascular disease and the effects of therapeutic interventions. In the second part of this tutorial, we review analytic methods used to characterize left ventricular afterload, including analyses of central arterial pressure-flow relations and windkessel modeling (pressure-volume relations). Conceptual descriptions of various models and methods are emphasized over mathematical ones. Our review is aimed at helping researchers and clinicians obtain and interpret results from analyses of left ventricular afterload in clinical and epidemiological settings

Time domain computational modelling of 1D arterial networks in monochorionic placentas

Published versio

A new approach to investigate wave dissipation in viscoelastic tubes: Application of wave intensity analysis

Wave dissipation in elastic and viscoelastic medium has been investigated extensively in the frequency domain. The aim of this study is to examine the pattern of wave dissipation in the time-domain using wave intensity analysis. A single semi-sinusoidal pulse was generated in 8 mm and 16 mm diameter tubes; each is of 200 cm in length. Pressure and flow measurements were taken at intervals of 5 cm along the tube. In order to examine the effect of the wall mechanical properties on wave dissipation, we also modified the wall of the 16 mm tube; a thread of strong cotton was wound with a pitch of approximately 30deg around the circumference of the tube in the longitudinal direction. The separated forward pressure, wave intensity and wave energy were calculated using wave intensity analysis. The amplitudes of the forward pressure wave, wave intensity and wave energy dissipated exponentially with distance. In the 8 mm diameter tube, the dissipation of forward pressure, wave intensity and wave energy were greater than those in 16 mm tube. For the same sized of tube, there was no significant difference in the dissipation of forward pressure, wave intensity and wave energy between the modified and normal wall tubes. It is concluded that the size of tube has a significant effect on the wave dissipation but the mechanical properties of the wall do not have a discernable effect on wave dissipatio

Observation of natural flexural pulse waves in retinal and carotid arteries for wall elasticity estimation

The risk of cardiovascular events is linked to arterial elasticity that can be estimated from the pulse wave velocity. This symmetric wave velocity is related to the wall elasticity through the Moens-Korteweg equation. However, ultrasound imaging techniques need improved accuracy, and optical measurements on retinal arteries produce inconsistent results. Here, we report the first observation of an antisymmetric pulse wave: the flexural pulse wave. An optical system performs in vivo wave velocity measurements on retinal arteries and veins. Velocity estimation ranges between 1 and 10 millimeter per second. The theory of guided waves confirms the existence of this wave mode and its low velocity. Natural flexural waves can also be detected at the bigger scale of a carotid artery using ultrafast ultrasound imaging. This second natural pulse wave has great potential of becoming a biomarker of blood vessel aging

On-chip laser Doppler vibrometer for arterial pulse wave velocity measurement

Pulse wave velocity (PWV) is an important marker for cardiovascular risk. The Laser Doppler vibrometry has been suggested as a potential technique to measure the local carotid PWV by measuring the transit time of the pulse wave between two locations along the common carotid artery (CCA) from skin surface vibrations. However, the present LDV setups are still bulky and difficult to handle. We present in this paper a more compact LDV system integrated on a CMOS-compatible silicon-on-insulator substrate. In this system, a chip with two homodyne LDVs is utilized to simultaneously measure the pulse wave at two different locations along the CCA. Measurement results show that the dual-LDV chip can successfully conduct the PWV measurement

Optimising the assessment of cerebral autoregulation from black box models

Cerebral autoregulation (CA) mechanisms maintain blood flow approximately stable despite changes in arterial blood pressure. Mathematical models that characterise this system have been used extensively in the quantitative assessment of function/impairment of CA. Using spontaneous fluctuations in arterial blood pressure (ABP) as input and cerebral blood flow velocity (CBFV) as output, the autoregulatory mechanism can be modelled using linear and non-linear approaches, from which indexes can be extracted to provide an overall assessment of CA. Previous studies have considered a single – or at most a couple of measures, making it difficult to compare the performance of different CA parameters. We compare the performance of established autoregulatory parameters and propose novel measures. The key objective is to identify which model and index can best distinguish between normal and impaired CA. To this end 26 recordings of ABP and CBFV from normocapnia and hypercapnia (which temporarily impairs CA) in 13 healthy adults were analysed. In the absence of a ‘gold’ standard for the study of dynamic CA, lower inter- and intra-subject variability of the parameters in relation to the difference between normo- and hypercapnia were considered as criteria for identifying improved measures of CA. Significantly improved performance compared to some conventional approaches was achieved, with the simplest method emerging as probably the most promising for future studies

Vascular smooth muscle Sirtuin-1 protects against aortic dissection during Angiotensin II-induced hypertension

BACKGROUND: Sirtuin-1 (SirT1), a nicotinamide adenine dinucleotide(+)-dependent deacetylase, is a key enzyme in the cellular response to metabolic, inflammatory, and oxidative stresses; however, the role of endogenous SirT1 in the vasculature has not been fully elucidated. Our goal was to evaluate the role of vascular smooth muscle SirT1 in the physiological response of the aortic wall to angiotensin II, a potent hypertrophic, oxidant, and inflammatory stimulus. METHODS AND RESULTS: Mice lacking SirT1 in vascular smooth muscle (ie, smooth muscle SirT1 knockout) had drastically high mortality (70%) caused by aortic dissection after angiotensin II infusion (1 mg/kg per day) but not after an equipotent dose of norepinephrine, despite comparable blood pressure increases. Smooth muscle SirT1 knockout mice did not show any abnormal aortic morphology or blood pressure compared with wild-type littermates. Nonetheless, in response to angiotensin II, aortas from smooth muscle SirT1 knockout mice had severely disorganized elastic lamellae with frequent elastin breaks, increased oxidant production, and aortic stiffness compared with angiotensin II-treated wild-type mice. Matrix metalloproteinase expression and activity were increased in the aortas of angiotensin II-treated smooth muscle SirT1 knockout mice and were prevented in mice overexpressing SirT1 in vascular smooth muscle or with use of the oxidant scavenger tempol. CONCLUSIONS: Endogenous SirT1 in aortic smooth muscle is required to maintain the structural integrity of the aortic wall in response to oxidant and inflammatory stimuli, at least in part, by suppressing oxidant-induced matrix metalloproteinase activity. SirT1 activators could potentially be a novel therapeutic approach to prevent aortic dissection and rupture in patients at risk, such as those with hypertension or genetic disorders, such as Marfan's syndrome.R01 HL098028 - NHLBI NIH HHS; HL098028 - NHLBI NIH HHS; HL105287 - NHLBI NIH HHS; T32 HL07224 - NHLBI NIH HH

Integration of anatomical and hemodynamical information in magnetic resonance angiography

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