Instantaneous blood flow, impedance and elastic properties computed in man from aortic pulse waves

A mathematical model of the pressure-flow relationship in the arterial circulation and its possible use in routine hemodynamics in man are described. The instantaneous blood flow velocity in the ascending aorta can be calculated from two pressure curves simultaneously recorded 5 cm apart. The mechanical aortic input impedance is computed from the recorded pressure and the calculated blood flow velocity curves. Projection of the pulse waves on a time-length plane leads to the determination of the pulse wave velocity and then an estimation of the elastic modulus of the aortic wall.     

An ultrasound-based method for determining pulse wave velocity in superficial arteries

In this paper, we present a method for estimating local pulse wave velocity (PWV) solely from ultrasound measurements: the area-flow (QA) method. With the QA method, PWV is estimated as the ratio between change in flow and change in cross-sectional area (PWV = dQ/dA) during the reflection-free period of the cardiac cycle. In four anaesthetized dogs and 21 human subjects (age 23-74) we measured the carotid flow and cross-sectional area non-invasively by ultrasound. As a reference method we used the Bramwell-Hill (BH) equation which estimates PWV from pulse pressure and cross-sectional area. Additionally, we therefore measured brachial pulse pressure by oscillometry in the human subjects, and central aortic pulse pressure by micro-manometry in the dogs. As predicted by the pressure dependency of arterial stiffness, the estimated PWV decreased when the aortic pressure was lowered in two of the dogs. For the human subjects, the QA and BH estimates were correlated (R=0.43, p<0.05) and agreed on average (mean difference of -0.14 m/s). The PWV by the BH method increased with age (p<0.01) whereas the PWV by the QA method tended to increase with age (p<0.1). This corresponded to a larger residual variance (residual = deviation of the estimated PWV from the regression line) for the QA method than for the BH method, indicating different precisions for the two methods. This study illustrates that the simple equation PWV = dQ/dA gives estimates correlated to the PWV of the reference method. However, improvements in the basic measurements seem necessary to increase the precision of the method.     

Increased aortic stiffness assessed by pulse wave velocity in apolipoprotein E-deficient mice

Atherosclerosis develops and progresses spontaneously in apolipoprotein E-knockout (apoE-KO) mice. A direct consequence of atherosclerosis is an increase in vascular stiffness. Pulse wave velocity (PWV) has been used to assess the stiffness of large vessels and was found to be increased in patients with atherosclerosis. In the present study, aortic stiffness was assessed by PWV in 4- and 13-mo-old apoE-KO mice and age-matched controls (C57BL/6J). In 13-mo-old apoE-KO mice with extensive atherosclerotic lesions in the aorta (61 +/- 4%), PWV increased significantly (3.8 +/- 0.2 m/s) compared with controls (2.9 +/- 0.2 m/s). Endothelial nitric oxide (EDNO)-mediated vasorelaxation in response to ACh was markedly diminished in the aortic rings isolated from 13-mo-old apoE-KO mice compared with age-matched controls. In contrast, in 4-mo-old apoE-KO mice with only moderate atherosclerotic lesions in the aorta (23 +/- 5%), there were no significant changes in PWV and EDNO-mediated relaxation compared with controls. Blood pressure was not different among the four groups of mice. There were no significant differences in endothelium-independent vascular responses to sodium nitroprusside among different groups investigated. Histological evaluation revealed focal fragmentation of the elastic laminae in the aortic walls of 13-mo-old apoE-KO mice. These results demonstrate for the first time that aortic stiffness determined by PWV increases in 13-mo-old apoE-KO mice. Endothelial dysfunction and elastic destruction in vascular wall caused by atherosclerosis may have contributed.     

Coupling between MRI-assessed regional aortic pulse wave velocity and diameters in patients with thoracic aortic aneurysm: a feasibility study

Aims

Thoracic aortic aneurysm (TAA) is potentially life-threatening and requires close follow-up to prevent aortic dissection. Aortic stiffness and size are considered to be coupled. Regional aortic stiffness in patients with TAA is unknown. We aimed to evaluate coupling between regional pulse wave velocity (PWV), a marker of vascular stiffness, and aortic diameter in TAA patients.

Methods

In 40 TAA patients (59 ± 13 years, 28 male), regional aortic diameters and regional PWV were assessed by 1.5 T MRI. The incidence of increased diameter and PWV were determined for five aortic segments (S1, ascending aorta; S2, aortic arch; S3, thoracic descending aorta; S4, suprarenal and S5, infrarenal abdominal aorta). In addition, coupling between regional PWV testing and aortic dilatation was evaluated and specificity and sensitivity were assessed.

Results

Aortic diameter was 44 ± 5 mm for the aortic root and 39 ± 5 mm for the ascending aorta. PWV was increased in 36 (19 %) aortic segments. Aortic diameter was increased in 28 (14 %) segments. Specificity of regional PWV testing for the prediction of increased regional diameter was ≥ 84 % in the descending thoracic to abdominal aorta and ≥ 68 % in the ascending aorta and aortic arch.

Conclusion

Normal regional PWV is related to absence of increased diameter, with high specificity in the descending thoracic to abdominal aorta and moderate results in the ascending aorta and aortic arch.     

Systems engineering analysis of aortic root blood pressure

This paper describes the aortic blood pressure as a function of aortic blood flow and the parameters of the blood and circulatory system. The method of performance involves the analogue of a multi-branched electrical to hydraulic transmission line applying graphical convolution to the blood flow-transform impedance relationship resulting in a theoretical pressure curve for the infinite aorta. The difference between the single pressure pulse and the computed adjusted infinite aorta pressure curve is described as the reflected wave. This reflected wave is then shown to be of reasonable configuration in time and velocity. The blood pressure is thus finally described completely by the physical parameters of the blood and the circulatory system and the blood flow.     

Measurement of aortic input impedance in mice: effects of age on aortic stiffness

Mice are used with increasing frequency as models of human cardiovascular diseases, but significant gaps exist in our knowledge of vascular function in the aging mouse. We determined aortic input impedance spectra, pulse wave velocity, and augmentation index in adult (8-mo-old) and old (29-mo-old) mice to determine whether arterial stiffening occurred with age in mice as it does in humans. Pressure and blood velocity signals measured simultaneously from the same location in the ascending aorta were used to determine input impedance spectra (0-10 harmonics). The first minimum of the impedance modulus occurred at the second harmonic in adult mice but shifted to the fourth harmonic in old mice. Characteristic impedance (average of 2nd-10th harmonic) was 57% higher in old mice: 471 +/- 62 vs. 299 +/- 10 (SE) dyn.s.cm-3 (P < 0.05). Pulse pressure and augmentation index, determined from the aortic pressure signals, were also higher in old mice: 42 +/- 2.2 vs. 29 +/- 4.9 mmHg (P < 0.05) and 37 +/- 5 vs. 14 +/- 2% (P < 0.005). Aortic pulse wave velocity measured from the timing of upstrokes of the Doppler velocity signals was 45% higher in old mice: 416 +/- 22 vs. 286 +/- 14 cm/s (n = 3, P < 0.01). These results reproduce age-related findings reported in humans and confirm that mice may be used as models of age-related vascular stiffening.     

Use of simultaneous pressure and velocity measurements to estimate arterial wave speed at a single site in humans

It has not been possible to measure wave speed in the human coronary artery, because the vessel is too short for the conventional two-point measurement technique used in the aorta. We present a new method derived from wave intensity analysis, which allows derivation of wave speed at a single point. We apply this method in the aorta and then use it to derive wave speed in the human coronary artery for the first time. We measured simultaneous pressure and Doppler velocity with intracoronary wires at the left main stem, left anterior descending and circumflex arteries, and aorta in 14 subjects after a normal coronary arteriogram. Then, in 10 subjects, serial measurements were made along the aorta before and after intracoronary isosorbide dinitrate. Wave speed was derived by two methods in the aorta: 1) the two-site distance/time method (foot-to-foot delay of pressure waveforms) and 2) a new single-point method using simultaneous pressure and velocity measurements. Coronary wave speed was derived by the single-point method. Wave speed derived by the two methods correlated well (r = 0.72, P < 0.05). Coronary wave speed correlated with aortic wave speed (r = 0.72, P = 0.002). After nitrate administration, coronary wave speed fell by 43%: from 16.4 m/s (95% confidence interval 12.6-20.1) to 9.3 m/s (95% confidence interval 6.5-12.0, P < 0.001). This single-point method allows determination of wave speed in the human coronary artery. Aortic wave speed is correlated to coronary wave speed. Finally, this technique detects the prompt fall in coronary artery wave speed with isosorbide dinitrate.     

Increasing pulse wave velocity in a realistic cardiovascular model does not increase pulse pressure with age

The mechanism of the well-documented increase in aortic pulse pressure (PP) with age is disputed. Investigators assuming a classical windkessel model believe that increases in PP arise from decreases in total arterial compliance (C(tot)) and increases in total peripheral resistance (R(tot)) with age. Investigators assuming a more sophisticated pulse transmission model believe PP rises because increases in pulse wave velocity (c(ph)) make the reflected pressure wave arrive earlier, augmenting systolic pressure. It has recently been shown, however, that increases in c(ph) do not have a commensurate effect on the timing of the reflected wave. We therefore used a validated, large-scale, human arterial system model that includes realistic pulse wave transmission to determine whether increases in c(ph) cause increased PP with age. First, we made the realistic arterial system model age dependent by altering cardiac output (CO), R(tot), C(tot), and c(ph) to mimic the reported changes in these parameters from age 30 to 70. Then, c(ph) was theoretically maintained constant, while C(tot), R(tot), and CO were altered. The predicted increase in PP with age was similar to the observed increase in PP. In a complementary approach, C(tot), R(tot), and CO were theoretically maintained constant, and c(ph) was increased. The predicted increase in PP was negligible. We found that increases in c(ph) have a limited effect on the timing of the reflected wave but cause the system to degenerate into a windkessel. Changes in PP can therefore be attributed to a decrease in C(tot).     

Aortic reflection coefficients and their association with global indexes of wave reflection in healthy controls and patients with Marfan's syndrome

Early return of reflected pressure waves increases the load on central arteries and may increase the risk of aortic rupture in patients with Marfan's syndrome (MFS). To assess whether wave reflection is elevated in MFS, we used ultrasound and MRI to measure central pressure and flow waveforms in 26 patients (13-54 yr of age) and 26 age- and gender-matched controls. Aortic systolic and diastolic cross-sectional areas were measured at the ascending and descending aorta (AA and DA), diaphragm (DIA), and lower abdominal aorta (AB). From these measurements, local characteristic impedance (Z(0-xx)) and local reflection coefficients (Gamma(xx-yy)) were calculated. Calculated global wave reflection indexes were the augmentation index (AIx) and the ratio of backward to forward pressure wave (P(b)/P(f)). The aorta was wider in MFS patients at AA (P < 0.01) and DA (P < 0.01). Aortic pulse wave velocity was 42 cm/s higher in MFS patients (P < 0.05). Z(0-xx) was not different between groups, except at DA, where it was lower in MFS patients. In controls, Gamma(AA-DA) was 0.31 +/- 0.08, Gamma(DA-DIA) was 0.00 +/- 0.11, and Gamma(DIA-AB) was 0.31 +/- 0.16. Mean values of Gamma(xx-yy) were not different between MFS patients and controls. In controls, aging diminished Gamma(AA-DA) but increased Gamma(DIA-AB). Clear age-related patterns were absent in MFS patients. AIx or P(b)/P(f) was not higher in MFS patients than in controls. There were indications for enhanced wave reflection in young MFS patients. Our data demonstrated that the major determinants of AIx were pulse wave velocity and the effective length of the arterial system and, to a lesser degree, HR and P(b)/P(f).     

Determination of the pulse wave velocity by a filtered cross-correlation technique

A cross-correlation technique is presented to determine the average time lag between simultaneous pulse wave tracings at two points by considering the similarity of the complete wave series. It is shown that a true average phase velocity can be meaningfully defined for a natural pulse wave by the correlation technique. The cross-correlation technique is also performed on the pulse wave series of a particular frequency component isolated from the original series with a specially designed digital band pass filter. It is shown that well defined dispersion curve of pulse wave velocity can be determined from the filtered cross-correlation technique. The conventional method to determine pulse wave velocity from a single characteristic point is discussed in the light of the findings of the present study.     

Waveform dispersion, not reflection, may be the major determinant of aortic pressure wave morphology

The objective of this study was to investigate the determinants of aortic pressure waveform morphology in the thoracoabdominal aorta with specific reference to features of potential prognostic value for cardiovascular disease. In particular, we aimed to determine the location of major pressure wave reflection sites within the aorta. Aortic pressure waveforms were acquired with 2-Fr Millar Mikro-tip catheter transducers in 40 subjects (26 men, 14 women), and repeated in 10 subjects, at five predetermined points within the aorta: aortic root, transverse arch, and at the levels of the diaphragm, renal arteries, and aortic bifurcation. Waveforms were analyzed for augmentation index (AI), time to inflection point (Ti), and pressure parameters. AI decreased progressively between the aortic root and bifurcation (P < 0.001), and Ti increased (P < 0.01). There was the expected progressive peripheral amplification of systolic and pulse pressures and fall in time to peak pressure (all P < 0.001). There was no difference on repeat pullback or between sexes. These data are at variance with the concept that central AI results solely from pressure wave reflection, when Ti would be expected to decrease and AI increase with distal progression. Pressure wave propagation phenomena may contribute, and the potential role of frequency dispersion merits investigation.     

Wave reflection augments central systolic and pulse pressures during facial cooling

Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 +/- 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0 degrees C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased (P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 +/- 3 vs. 15 +/- 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: -1.4 +/- 3.8 vs. 21.2 +/- 3.0 and 19.9 +/- 3.6%; PWV: 5.6 +/- 0.2 vs. 6.5 +/- 0.3 and 6.2 +/- 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.     

The velocity of the arterial pulse wave: a viscous-fluid shock wave in an elastic tube

Background

The arterial pulse is a viscous-fluid shock wave that is initiated by blood ejected from the heart. This wave travels away from the heart at a speed termed the pulse wave velocity (PWV). The PWV increases during the course of a number of diseases, and this increase is often attributed to arterial stiffness. As the pulse wave approaches a point in an artery, the pressure rises as does the pressure gradient. This pressure gradient increases the rate of blood flow ahead of the wave. The rate of blood flow ahead of the wave decreases with distance because the pressure gradient also decreases with distance ahead of the wave. Consequently, the amount of blood per unit length in a segment of an artery increases ahead of the wave, and this increase stretches the wall of the artery. As a result, the tension in the wall increases, and this results in an increase in the pressure of blood in the artery.

Methods

An expression for the PWV is derived from an equation describing the flow-pressure coupling (FPC) for a pulse wave in an incompressible, viscous fluid in an elastic tube. The initial increase in force of the fluid in the tube is described by an increasing exponential function of time. The relationship between force gradient and fluid flow is approximated by an expression known to hold for a rigid tube.

Results

For large arteries, the PWV derived by this method agrees with the Korteweg-Moens equation for the PWV in a non-viscous fluid. For small arteries, the PWV is approximately proportional to the Korteweg-Moens velocity divided by the radius of the artery. The PWV in small arteries is also predicted to increase when the specific rate of increase in pressure as a function of time decreases. This rate decreases with increasing myocardial ischemia, suggesting an explanation for the observation that an increase in the PWV is a predictor of future myocardial infarction. The derivation of the equation for the PWV that has been used for more than fifty years is analyzed and shown to yield predictions that do not appear to be correct.

Conclusion

Contrary to the theory used for more than fifty years to predict the PWV, it speeds up as arteries become smaller and smaller. Furthermore, an increase in the PWV in some cases may be due to decreasing force of myocardial contraction rather than arterial stiffness.     

Numerical modeling of arterial pulse wave propagation to characterize aortic hemodynamic: Validation using magnetic resonance data

ObjectivesArterial stiffness, which is caused by aging and other cardiovascular risk factors and primarily affects the aorta, is associated with cardiac and cerebral morbidity and mortality. The objective of our study was to non-invasively estimate local biomechanical and hemodynamic biomarkers related to proximal aortic stiffness, by combining cardiovascular magnetic resonance (CMR) data and numerical simulations.Materials and methodsTo achieve this aim, we used a numerical 1D fluid-structure model to simulate blood flow in the descending aorta, and we combined this model with clinical data (areas and velocities in three levels of the descending aorta, carotid pressures) acquired in two healthy subjects using CMR and applanation tonometry.ResultsFirst, we studied the sensibility of our model on an idealized aorta and showed that our model was able to characterize age-related arterial alterations, when compared to established physiological knowledge. Furthermore, while comparisons of simulations against clinical data revealed low errors (< 20%) in terms of aortic areas and velocities for the two subjects, more important errors were found for pulse pressures (up to 20%). Importantly, errors in terms of velocity and area were lower than their variations occurring with aging.ConclusionsThus, our fast method could enable the non-invasive estimation of aortic functional parameters and a more realistic version of our numerical model could also provide a reliable estimation of central pressure.     

An innovative numerical approach to resolve the pulse wave velocity in a healthy thoracic aorta model

Aortic dissection and atherosclerosis are highly fatal diseases. The development of both diseases is closely associated with highly complex haemodynamics. Thus, in predicting the onset of cardiac disease, it is desirable to obtain a detailed understanding of the flowfield characteristics in the human cardiovascular circulatory system. Accordingly, in this study, a numerical model of a normal human thoracic aorta is constructed using the geometry information obtained from a phase-contrast magnetic resonance imaging (PC-MRI) technique. The interaction between the blood flow and the vessel wall dynamics is then investigated using a coupled fluid–structure interaction (FSI) analysis. The simulations focus specifically on the flowfield characteristics and pulse wave velocity (PWV) of the blood flow. Instead of using a conventional PC-MRI method to measure PWV, we present an innovative application of using the FSI approach to numerically resolve PWV for the assessment of wall compliance in a thoracic aorta model. The estimated PWV for a normal thoracic aorta agrees well with the results obtained via PC-MRI measurement. In addition, simulations which consider the FSI effect yield a lower predicted value of the wall shear stress at certain locations in the cardiac cycle than models which assume a rigid vessel wall. Consequently, the model provides a suitable basis for the future development of more sophisticated methods capable of performing the computer-aided analysis of aortic blood flows.     

Retinal pulse wave velocity measurement using spectral‐domain optical coherence tomography

The human eyes provide a natural window for noninvasive measurement of the pulse wave velocity (PWV) of small arteries. By measuring the retinal PWV, the stiffness of small arteries can be assessed, which may better detect early vascular diseases. Therefore, retinal PWV measurement has attracted increasing attention. In this study, a jump‐scanning method was proposed for noninvasive measurement of retinal PWV using spectral‐domain optical coherence tomography (SD‐OCT). The jump‐scanning method uses the phase‐resolved Doppler OCT to obtain the pulse shapes. To realize PWV measurement, the jump‐scanning method extracts the transit time of the pulse wave from an original OCT scanning site to another through a transient jump. The measured retinal arterial PWV of a young human subject with normal blood pressure was in the order of 20 to 30 mm/s, which was consistent with previous studies. As a comparison, PWV of 50 mm/s was measured for a young human subject with prehypertension, which was in accordance with the finding of strong association between retinal PWV and blood pressure. In summary, it is believed the proposed jump‐scanning method could benefit the research and diagnosis of vascular diseases through the window of human eyes.      

Progressive resistance training without volume increases does not alter arterial stiffness and aortic wave reflection

Endurance exercise is efficacious in reducing arterial stiffness. However, the effect of resistance training (RT) on arterial stiffening is controversial. High-intensity, high-volume RT has been shown to increase arterial stiffness in young adults. We tested the hypothesis that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume would not elicit increases in either central or peripheral arterial stiffness or alter aortic pressure wave reflection in young men and women. The RT group (n = 24; 21 +/- 1 years) performed two sets of 8-12 repetitions to volitional fatigue on seven exercise machines on 3 days/week for 12 weeks, whereas the control group (n = 18; 22 +/- 1 years) did not perform RT. Central and peripheral arterial pulse wave velocity (PWV), aortic pressure wave reflection (augmentation index; AIx), brachial flow-mediated dilation (FMD), and plasma levels of nitrate/nitrite (NOx) and norepinephrine (NE) were measured before and after RT. RT increased the one-repetition maximum for the chest press and the leg extension (P < 0.001). RT also increased lean body mass (P < 0.01) and reduced body fat (%; P < 0.01). However, RT did not affect carotid-radial, carotid-femoral, and femoral-distal PWV (8.4 +/- 0.2 vs. 8.0 +/- 0.2 m/sec; 6.5 +/- 0.1 vs. 6.3 +/- 0.2 m/sec; 9.5 +/- 0.3 vs. 9.5 +/- 0.3 m/sec, respectively) or AIx (2.5% +/- 2.3% vs. 4.8% +/- 1.8 %, respectively). Additionally, no changes were observed in brachial FMD, NOx, NE, or blood pressures. These results suggest that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume does not increase central or peripheral arterial stiffness or alter aortic pressure wave characteristics in young subjects.     

Pulsatile flow past aortic valve bioprostheses in a model human aorta

Pulsatile flow development past tissue valve prostheses in a model human aorta has been studied using qualitative flow visualization and quantitative laser-Doppler techniques. Experiments were conducted both in steady and physiological pulsatile flow situations and the measurements included the pressure drop across the valve, the instantaneous flow rate as well as the velocity profiles and turbulent stresses downstream to the valves. Our study shows that the velocity profiles with pericardial valves are closer to those measured past natural aortic valves. The porcine valves with a smaller valve opening area produce a narrower and stronger jet downstream from the valve with relatively larger turbulent axial stresses in the boundary of the jet. Our study suggests that the pericardial valves with turbulent stresses comparable to those of caged ball and tilting disc valves are preferable from a hemodynamic point of view.     

Individualization of transfer function in estimation of central aortic pressure from the peripheral pulse is not required in patients at rest

Central aortic pressure gives better insight into ventriculo-arterial coupling and better prognosis of cardiovascular complications than peripheral pressures. Therefore transfer functions (TF), reconstructing aortic pressure from peripheral pressures, are of great interest. Generalized TFs (GTF) give useful results, especially in larger study populations, but detailed information on aortic pressure might be improved by individualization of the TF. We found earlier that the time delay, representing the travel time of the pressure wave between measurement site and aorta is the main determinant of the TF. Therefore, we hypothesized that the TF might be individualized (ITF) using this time delay. In a group of 50 patients at rest, aged 28-66 yr (43 men), undergoing diagnostic angiography, ascending aortic pressure was 119 +/- 20/70 +/- 9 mmHg (systolic/diastolic). Brachial pressure, almost simultaneously measured using catheter pullback, was 131 +/- 18/67 +/- 9 mmHg. We obtained brachial-to-aorta ITFs using time delays optimized for the individual and a GTF using averaged delay. With the use of ITFs, reconstructed aortic pressure was 121 +/- 19/69 +/- 9 mmHg and the root mean square error (RMSE), as measure of difference in wave shape, was 4.1 +/- 2.0 mmHg. With the use of the GTF, reconstructed pressure was 122 +/- 19/69 +/- 9 mmHg and RMSE 4.4 +/- 2.0 mmHg. The augmentation index (AI) of the measured aortic pressure was 26 +/- 13%, and with ITF and GTF the AIs were 28 +/- 12% and 30 +/- 11%, respectively. Details of the wave shape were reproduced slightly better with ITF but not significantly, thus individualization of pressure transfer is not effective in resting patients.     

Age- and sex-dependent changes in pulse pressure in fowl aorta

Chickens (males more than females) have higher blood pressure (BP) than most mammals and spontaneously develop vascular neointimal plaques (NP) and diffuse subendothelial thickening in the lower segment of the abdominal aorta (AbA, referred to as 'NP-prone area') that partly resemble atherosclerotic lesions in mammals. NP areas, which are larger in males, have a causal relationship with incremental increases in BP during maturation. We hypothesize that decreased wall distensibility and altered hemodynamic forces at the NP-prone area may contribute to the NP formation. We measured pressure pulse wave (PW) and systolic and diastolic BP along the descending aorta in anesthetized chickens at different ages using an intravascular microtip transducer and calculated pulse pressure (PP) as an indicator for artery distensibility. At all ages examined and in both sexes, the PW showed a sharper peak at the more peripheral locations and the amplitude of the PW increased as it descended the aorta. PP, expressed as relative increases from the PP in the aortic arch (%), was 40.4+/-12.6 and 71.4+/-18.6 at the AbA and ischiadic artery, respectively, in young males (24-27 weeks); 23.5+/-8.6 and 43.8+/-16.2 in adults (72-75 weeks); and 5.4+/-3.4 and 9.1+/-4.9 in chicks (5-7 weeks). Location-dependent increases in PP were significantly higher in young males (P<0.05). The PP increases in females were not different among the three age groups. The contour of the PW in the proximal aorta changes in older birds, exhibiting steeper increases in the ascending and descending limbs, suggesting that faster wave reflection from the periphery augments peak systolic pressure. NP was most frequently seen in the lower segment of the abdominal aorta in older males. These results suggest that: (1) site-dependent increases in PP amplitude are marked in young males, possibly reflecting a reduction in arterial wall elasticity enhanced by incremental rises in BP, and (2) NP formation may contribute to the stiffness of aortic walls in the NP-prone area.