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The local pulse wave velocity (PWV) from large elastic arteries and its pressure-dependent changes within a cardiac cycle are potential biomarkers for cardiovascular risk stratification. However, pulse wave reflections can impair the accuracy of local PWV measurements. We propose a method to measure pressure-dependent variations in local PWV while minimizing the influence of pulse wave reflections. The PWV is computed from the pulse transit time between two forward-traveling pulse waveforms obtained across known path length, after measured/modelled flow-based wave separation analysis (WSA). An in-vivo study of 60 participants (24 female), was conducted to compare inter- and intra-cycle variations in PWV obtained from measured and forward pulse waves. For this, proximal and distal diameter waveforms from the carotid artery, along with carotid tonometry, were recorded using a custom bi-modal arterial probe. The carotid blood flow for WSA was captured with an ultrasound imaging system. The reference PWV was derived from the Bramwell-Hill equation. After WSA, the reliability of PWV measurement improved with coefficient of variation reducing from 25% to 10% near the peak of the pulse waves and matched the reference PWV with no statistically significant difference. The average PWV at foot of the pulse wave before and after WSA were comparable to the reference PWV with no statistically significant difference. The coherence of carotid pulse pressure obtained from the mean values of PWV within a cardiac cycle after WSA with that of the carotid pulse pressure from tonometry, substantiates the results obtained for reflection-free PWV. The reliability of measuring local PWV and its pressure dependent variations within a cardiac cycle is improved by combining transit-time approach with WSA.

Subjects with amputation of the lower limbs are at increased risk of cardiovascular mortality and morbidity. We hypothesize that amputation-induced alterations in the arterial tree negatively impact arterial biomechanics, blood pressure and flow behavior. These changes may interact with other biological factors, potentially increasing cardiovascular risk. To evaluate this hypothesis regarding the purely mechanical impact of amputation on the arterial tree, we used a simulation computer model including a detailed one-dimensional (1D) arterial network model (143 arterial segments) coupled with a zero-dimensional (0D) model of the left ventricle. Our simulations included five settings of the arterial network: (1) 4-limbs control, (2) unilateral amputee (right lower limb), (3) bilateral amputee (both lower limbs), (4) trilateral amputee (lower-limbs and right upper-limb), and (5) quadrilateral amputee (lower and upper limbs). Analysis of regional stiffness, as calculated by pulse wave velocity (PWV) for large-, medium- and small-sized arteries, showed that, while aortic stiffness did not change with increasing degree of amputation, stiffness of medium and smaller-sized arteries increased with greater amputation severity. Despite a staged decrease in cardiac output, the systolic and diastolic blood pressure values increased, resulting in an increase in both central and peripheral pulse pressures but with an attenuation of pulse pressure amplification. The most significant increase in peak systolic pressure and decrease in peak systolic blood flow was observed at the site of the abdominal aorta. Wave separation analysis indicated no changes in the shape of the forward and backward wave components. However, the results from wave intensity analysis showed that with extended amputation, there was an increase in peak forward wave intensity and a rise in the inverse peak of the backward wave intensity, suggesting potential alterations in cardiac hemodynamic load. In conclusion, this simulation study showed that biomechanical and hemodynamic changes in the arterial network geometry could interact with additional risk factors to increase the cardiovascular risk in patients with amputations.

Purpose of Review Arterial pulse waveform analysis has a long tradition but has not pervaded medical routine yet. This review aims to answer the question whether the methodology is ready for prime time use. The current methodological consensus is assessed, existing technologies for waveform measurement and pulse wave analysis are discussed, and further needs for a widespread use are proposed. Recent Findings A consensus document on the understanding and analysis of the pulse waveform was published recently. Although still some discrepancies remain, the analysis using both pressure and flow waves is favoured. However, devices which enable pulse wave measurement are limited, and the comparability between devices is not sufficiently given. Summary Pulse waveform analysis has the potential for prime time. It is currently on a way towards broader use, but still needs to overcome challenges before settling its role in medical routine.

The quantification of arterial wave reflection is an important area of interest in arterial pulse wave analysis. It can be achieved by wave separation analysis (WSA) if both the aortic pressure waveform and the aortic flow waveform are known. For better applicability, several mathematical models have been established to estimate aortic flow solely based on pressure waveforms. The aim of this study is to investigate and verify the model-based wave separation of the ARCSolver method on virtual pulse wave measurements. The study is based on an open access virtual database generated via simulations. Seven cardiac and arterial parameters were varied within physiological healthy ranges, leading to a total of 3325 virtual healthy subjects. For assessing the model-based ARCSolver method computationally, this method was used to perform WSA based on the aortic root pressure waveforms of the virtual patients. Asa reference, the values of WSA using both the pressure and flow waveforms provided by the virtual database were taken. The investigated parameters showed a good overall agreement between the model-based method and the reference. Mean differences and standard deviations were −0.05±0.02AU for characteristic impedance, −3.93±1.79mmHg for forward pressure amplitude, 1.37±1.56mmHg for backward pressure amplitude and 12.42±4.88% for reflection magnitude. The results indicate that the mathematical blood flow model of the ARCSolver method is a feasible surrogate for a measured flow waveform and provides a reasonable way to assess arterial wave reflection non-invasively in healthy subjects.

Pulsatile hemodynamics analyses provide important information about the ventricular‐arterial system which cannot be inferred by standard blood pressure measurements. Pulse wave analysis (PWA), wave separation analysis (WSA), and wave power analysis (WPA) characterize arterial hemodynamics with limited preclinical applications. Integrating these tools into preclinical testing may enhance understanding of disease or therapeutic effects on cardiovascular function. We used a canine rapid ventricular pacing (RVP) heart failure model to: (1) Characterize hemodynamics in response to RVP and (2) assess analyses from flow waveforms synthesized from pressure compared to those derived from measured flow. Female canines (n = 7) were instrumented with thoracic aortic pressure transducers, ventricular pacing leads, and an ascending aortic flow probe. Data were collected at baseline, 1 week, and 1 month after RVP onset. RVP progressively reduced stroke volume (SV), the PWA SV estimator, and WSA and WPA pulsatility and wave reflection indices. Indices derived from synthesized flow exhibited similar directional changes and high concordance with measured flow calculations. Our data demonstrate the value of analytical hemodynamic methods to gain deeper insight into cardiovascular function in preclinical models. These approaches can provide complementary value to standard endpoints in evaluating potential effects of pharmaceutical agents intended for human use.

Background and objectives Fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR) are the two most commonly used coronary indices of physiological stenosis severity based on pressure. To minimize the effect of wedge pressure (P wedge ), FFR is measured during hyperemia conditions, and iFR is calculated as the ratio of distal and aortic pressures (P d /P a ) in the wave-free period. The goal of this study was to predict P wedge using the backward wave (P back ) through wave separation analysis (WSA) and to reflect the effect of P wedge on FFR and iFR to identify the relationship between the two indices. Methods An in vitro circulation system was constructed to calculate P wedge . The measurements were performed in cases with stenosis percentages of 48, 71, and 88% and with hydrostatic pressures of 10 and 30 mmHg. Then, the correlation between P back by WSA and P wedge was calculated. In vivo coronary flow and pressure were simultaneously measured for 11 vessels in all patients. The FFR and iFR values were reconstructed as the ratios of forward wave at distal and proximal sites during hyperemia and at rest, respectively. Results Based on the in vitro results , the correlation between P back and P wedge was high (r = 0.990, p  < 0.0001). In vivo results showed high correlations between FFR and reconstructed FFR (r = 0.992, p  < 0.001) and between iFR and reconstructed iFR (r = 0.930, p  < 0.001). Conclusions Reconstructed FFR and iFR were in good agreement with conventional FFR and iFR. FFR and iFR can be expressed as the variation of trans-stenotic forward pressure, indicating that the two values are inferred from the same formula under different conditions.

Background: Pulmonary arterial wave reflection (PAWR) occurs when the forward blood flow out the right ventricle is reflected by the pulmonary arterial tree, generating a backward wave. PAWR assessed by cardiac catheterization has been used to obtain information regarding pulmonary artery hemodynamics in pulmonary hypertension (PH) in people. However, diagnostic cardiac catheterization is not commonly used in small animal medicine because it is invasive and requires anesthesia. Hypothesis/Objective: To investigate whether PAWR can be assessed non-invasively in dogs with suspected PH using Doppler echocardiography, based on wave intensity analysis (WIA). In addition, the method was validated in a dog model of acute pulmonary embolism. Animals: Fifty-one client-owned dogs with tricuspid valve regurgitation were included in the clinical study (35 with suspected PH and 16 without echocardiographic evidence of PH) and eight healthy beagle dogs were included in the validation study. Methods: PAWR was assessed by separating pulmonary artery pulse pressure waveforms, which were estimated from the flow profile of tricuspid regurgitation, into forward (Pf) and backward pressures (Pb) using WIA. Reflection coefficient (RC) was defined as the ratio of peak Pb to peak Pf. We investigated the relationships between RC, cause, and survival time in dogs with suspected PH. In addition, we performed a validation study to compare PAWR obtained by cardiac catheterization and PAWR by Doppler echocardiography in dogs with experimentally-induced PH. Results: RC was significantly higher in dogs with suspected PH than in dogs without echocardiographic evidence of PH (0.18 ± 0.13 vs. 0.59 ± 0.21, P < 0.001). A characteristic reflected waveform appeared depending on the cause of PH. Kaplan-Meier survival curves showed that dogs with RC > 0.48 had a significantly shorter survival time than dogs with RC <0.48 (x 2 = 9.8, log-rank test, p = 0.0018 , median survival time 353 days vs. 110 days). In the validation study, RC obtained by Doppler echocardiography was significantly correlated with RC obtained by cardiac catheterization ( r = 0.81, P < 0.001). Conclusions: PAWR analysis performed by echocardiography seems feasible in dogs and could provide useful information for classification and prognosis in canine PH.

Background: Pulmonary arterial wave reflection provides novel information about pulmonary artery hemodynamics in pulmonary hypertension (PH). PH is common in dogs with myxomatous mitral valve disease (MMVD), though research examining the relationship between pulmonary arterial wave reflection and MMVD with PH is lacking. Hypothesis/Objective: This study investigated conventional echocardiographic parameters and pulmonary artery wave reflection parameters before and after mitral valvuloplasty in canine patients with PH due to MMVD. The parameters were backward pressure (Pb), forward pressure (Pf), and the reflection coefficient calculated as the ratio of peak Pb to peak Pf (RC). Animals: The study subjects were 10 client-owned dogs receiving mitral valvuloplasty for MMVD with PH. Methods: Conventional echocardiographic parameters and pulmonary artery wave reflection parameters were measured before and after mitral valvuloplasty. The relationships between pulmonary artery wave reflection parameters and echocardiographic parameters, estimation of pulmonary artery systolic pressure, and right atrium pressure (RAP) gained by catheter in mitral valvuloplasty were also investigated. Post-operative echocardiography and the measurement of pulmonary arterial wave reflection were performed 2 weeks after mitral valvuloplasty. Results: The parameters of normalized left ventricular internal diameter at end-diastole (LVIDDN), E velocity, and the estimation of pulmonary artery systolic pressure were significantly reduced post-operatively compared with baseline measurements ( p < 0.05). Post-operative Pb decreased significantly compared with pre-operative measurements (8.8 ± 5.9 to 5.0 ± 3.2 mmHg, p = 0.037) as did RC (0.37 ± 0.15 to 0.22 ± 0.11, p < 0.01). A statistically significant positive correlation existed between wave reflection parameters and RAP, an estimation of pulmonary artery systolic pressure. Conclusions: Results demonstrate that mitral valvuloplasty can be used to treat secondary PH caused by MMVD, resulting in the improvement of post-operative echocardiographic and wave reflection parameters and a decrease in the right afterload. In some patients, some degree of vascular admittance mismatch persisted, despite the improvement of left atrial pressure. This may be indicative of residual pulmonary arterial disease, which may continue to adversely affect interactions between the right ventricle and the vasculature.

This study examined the effects of moderate exercise-induced heat stress (EIHS) on vascular function, central hemodynamic load and indices of coronary perfusion. Vascular-hemodynamic measures were collected in 12 healthy men (aged 22±3 years) pre and post 100 minutes of moderate, intermittent exercise in two randomized conditions: heat stress (HS; wearing firefighter personal protective equipment (PPE)), and no heat stress (NHS; wearing a cooling shirt and equivalent PPE weight). Aortic blood pressure, reflected wave pressure (Pb), systolic (SPTI) and diastolic pressure time-integral (DPTI), and aortic stiffness were assessed before and after each condition. SPTI was significantly greater, and DPTI and Pb were significantly lower for HS-post compared to NHS-post (p<0.05). Pulse wave velocity was not different between conditions. In conclusion, EIHS does not affect aortic stiffness, but increases indices of myocardial work and reduces indices of coronary perfusion which may be related to chronotropic responses to EIHS. The mismatch between oxygen demand and oxygen supply may increase cardiac vulnerability to ischemia during strenuous work in the heat.