Lower Wall Stress Research Articles

The Influence of Wall Stress on AAA Growth and Biomarkers

Objectives This study investigated the relation between abdominal aortic aneurysm (AAA) wall stress, AAA growth rate and biomarker concentrations. With increasing wall stress, more damage may be caused to the AAA wall, possibly leading to progression of the aneurysm and reflection in up- or downregulation of specific circulating biomarkers. Levels of matrix metalloproteinase-9, tissue inhibitor of matrix metalloproteinase-1, C-reactive protein and alpha 1-antitrypsin were therefore evaluated. Methods Thirty-seven patients (maximum AAA diameter 41–55 mm) with two, three or four consecutive computed tomography angiography (CTA) scans were prospectively included. Diameter growth rate in mm/year was determined between each pair of two sequential CTA scans. AAA wall stress was computed by finite element analysis, based on the first of the two sequential CTA scans only ( n = 69 pairs). Biomarker information was determined in 46 measurements in 18 patients. The relation between AAA diameter and wall stress was determined and the AAA's were divided into three equally sized groups (relative low, medium and high stress). Growth rate and biomarker concentrations were compared between these groups. Additionally, correlation coefficients were computed between absolute wall stress, AAA growth and biomarker concentrations. Results A relative low AAA wall stress was associated with a lower aneurysm growth rate. Growth rate was also positively related to MMP-9 plasma concentration ( r = 0.32). The average MMP-9 and CRP concentrations increased with increasing degrees of relative wall stress, although the absolute and relative wall stress did not correlate with any of the biomarkers. Conclusion Although lower relative wall stress was associated to a lower AAA growth rate, no relation was found between biomarker concentrations and wall stress. Future research may focus on more and extensive biomarker measurements in relation to AAA wall stress.

Finite element analysis of wall stress in the equine pulmonary artery

Arterial calcification is found frequently in the pulmonary artery of racehorses, but the aetiology is unknown. Calcification might be associated with increased wall stress due to arterial geometry (shape) and exercise-induced hypertension. High wall stress levels are found in the regions associated with calcified lesion formation, exacerbated as transluminal pressure increases to levels associated with exercise. The pulmonary arteries of 5 horses, unaffected by calcification, were dissected and pressurised to resting and exercising physiological transluminal pressures and scanned with MRI. Arterial geometries were reconstructed to form 3D computer models and finite element analyses performed. Wall stress levels were measured in 4 regions of interest: the arterial trunk and bifurcation, the wall ipsilateral and contralateral to the bifurcation. Measurements were made for arterial transluminal pressures of 25, 50 and 100 mmHg. High wall stress levels were consistently found at the pulmonary artery bifurcation and wall ipsilateral to the bifurcation, where calcified lesions typically form. Lower wall stress levels were found along the trunk and the wall contralateral to the bifurcation where lesions are less frequently found. Wall stress levels increased 5-fold over a 4-fold increase in pressure. The wall stress levels ranged 10 kPa in the wall of the branch contralateral to the bifurcation at 25 mmHg to 400 kPa in the bifurcation at 100 mmHg. Wall stress from arterial geometry and increased pulmonary artery transluminal pressure are factors that may be associated with calcification of the equine pulmonary artery. Arterial calcification may increase the risk of arterial wall failure in racing horses.

The mechanical role of thrombus on the growth rate of an abdominal aortic aneurysm

In the decision for surgical repair of abdominal aortic aneurysms (AAAs), the maximum diameter is the main factor. Several studies have concluded that the diameter may not be reliable as rupture risk criterion for the individual patient and wall stress was found to have a higher sensitivity and specificity. The AAA wall stress may also be an influential factor in growth of the AAA. This study investigates the effect of intraluminal thrombus on the wall stress and growth rate of aneurysms, using both idealized and patient-specific AAA models in wall stress computations. Idealized AAA models were created for wall stress analysis. Thrombus was modeled as an incompressible linear elastic material and was fixed to the wall. The reduction in wall stress for a range of thrombus volumes and shear moduli was computed. For 30 patient-specific AAA models with varying thrombus volumes, the wall stress was computed with and without thrombus. The diameter growth rate was compared for AAAs with a small and large thrombus volume. The results were compared between the idealized and patient-specific models. The thrombus caused a reduction in wall stress, which was stronger for larger thrombi and higher elastic moduli. Any AAAs with a large thrombus were found to have significant stronger growth in diameter than aneurysms with a small thrombus (P < .01). The stress reduction due to the thrombus showed the same trend for the idealized and patient-specific models, although the effect was overestimated by the idealized models and a considerable variation between patients was observed. A larger thrombus in AAA was associated with a higher AAA growth rate, but also with a lower wall stress. Therefore, weakening of the AAA wall, under the influence of thrombus, may play a more imminent role in the process of AAA growth than the stress acting on the wall.

Microbubble Expansion in a Flexible Tube

We have utilized a computational model of the expansion of a microbubble in a liquid-filled flexible tube to investigate the potential for acoustic vaporization of perfluorocarbon droplets to damage blood vessels during a novel gas embolotherapy technique for the potential treatment of tumors. This model uses a fixed grid, multi-domain, interface tracking, direct numerical simulation method that treats all interfaces and boundaries as sharp discontinuities for high accuracy. In the current work, we examined effects of initial bubble size on the flows and wall stresses that result from droplet vaporization. The remaining dimensionless parameters that govern the system response (Reynolds, Weber, and Strouhal numbers, initial bubble pressure, and wall stiffness and tension) were selected to model an arteriole. The results for a flexible tube are significantly different from those for a rigid tube. Two major flow regimes occur due to the combined effect of bubble and tube deformation: in flow at the tube ends and out flow near the bubble surface. The flexibility of the tube largely dissipates the extreme pressure that develops in the rigid tube model. Both the magnitude and the overall expansion time of the rapidly changing pressure are greatly reduced in the flexible tube. Smaller initial bubble diameters, relative to the vessel diameter, result in lower wall stresses. This study indicates that wall flexibility can significantly influence the wall stresses that result from acoustic vaporization of intravascular perfluorocarbon droplets, and suggests that acoustic activation of droplets in larger, more flexible vessels may be less likely to damage or rupture vessels than activation in smaller and stiffer vessels.

Focalized Contractile Impairment at Hypertrophied Myocardium Proven in Consideration of Wall Stress in Patients With Hypertrophic Cardiomyopathy

In hypertrophic cardiomyopathy (HCM) a hyperkinetic state is sometimes observed in spite of impaired systolic function in the hypertrophied myocardium. The aim of the present study was to determine the mechanism of this paradox. Seventeen patients with HCM and 10 normal subjects underwent cine magnetic resonance (MR) imaging to measure percent systolic wall thickening and percent fractional shortening. The ratio of systolic radial wall stress of the LV at the hypertrophied myocardium over that at the nonhypertrophied myocardium was evaluated to describe the focal advantageous condition for wall thickening. The ratio was 0.66 +/- 0.36 at the start of contraction and 0.78 +/- 0.31 at early-systole, indicating consistently smaller radial wall stress at the hypertrophied myocardium. Although the condition for contraction was favorable (a ratio less than 1.00), percent systolic wall thickening at the hypertrophied myocardium (23.0 +/- 11.8%) was smaller than that at the nonhypertrophied myocardium (70.5 +/- 32.3%). Smaller end-diastolic dimension (HCM group; 45.2 +/- 4.2 mm, reference group; 48.9 +/- 4.1 mm, P = 0.04) with a statistically identical value of systolic decrease in intraventricular dimension (HCM group; 19.7 +/- 3.9 mm, reference group; 18.9 +/- 3.2 mm, P = 0.60) yielded high percent fractional shortening in patients with HCM (43.5 +/- 7.6%). Although contractile impairment was proven at the hypertrophied region with low radial wall stress in the HCM group, the smaller end-diastolic dimension in this group resulted in high percent fractional shortening.

Oesophageal wall stress and muscle hypertrophy in high amplitude oesophageal contractions§

Excessive wall stress is a known stimulus for muscle growth. We recently reported a thickened muscularis propria in patients with high amplitude oesophageal contractions (HAEC). The goal of this study was to determine oesophageal wall stress in normal subjects and patients with HAEC. A manometry catheter equipped with a high frequency ultrasound (US) transducer was used to record pressure and US images simultaneously in 10 healthy subjects and 11 patients with HAEC. Recordings were obtained at 2 and 10 cm above the lower oesophageal sphincter during water swallows. The changes in circumferential wall stress during oesophageal contraction in both groups are relatively small because of an increase in the wall thickness-to-radius ratio during contraction. Patients show a greater muscle thickness than normal subjects at rest and at the peak of contraction. The wall stress in patients is elevated at the 2 cm but not at the 10-cm level as compared to normal subjects. Wall strain is not different between the two groups. Increase in wall thickness during oesophageal contraction maintains low wall stress. A greater wall stress in patients with HAEC may be a stimulus for the increased wall thickness.

Direct Numerical Simulations of Micro-Bubble Expansion in Gas Embolotherapy

We are currently developing a novel gas embolotherapy technique that involves the selective, acoustic vaporization of liquid perfluorocarbon droplets in or near a tumor as a possible treatment for cancer The resulting bubbles can then stick within the tumor vasculature to occlude blood flow and "starve" the tumor The potential development of high stresses during droplet vaporization is a major concern for safe implementation of this technique. No prior study, either experimentally or theoretically, addresses this important issue. In this work, the acoustic vaporization procedure of the therapy is investigated by direct numerical simulations. The nonlinear, multiphase, computational model is comprised of an ideal gas bubble surrounded by liquid inside a long tube. Convective and unsteady inertia, viscosity, and surface tension affect the bubble dynamics and are included in this model, which is solved by a novel fixed-grid, sharp-interface, moving boundary method. We assess the potential for flow-induced wall stresses to rupture the vessel or damage the endothelium during vaporization under a range of operating conditions by varying dimensionless parameters--Reynolds, Weber, and Strouhal numbers, inertial energy and initial droplet size. It is found that the wall pressure is typically highest at the start of the bubble expansion, but the maximum wall shear stress occurs at a later time. Smaller initial bubble diameters, relative to the vessel diameter, result in lower wall stresses.

Paradoxical changes in brain natriuretic peptide levels and loading conditions after intravenous conscious sedation

Background Elevated filling pressure and wall stress have been proposed as stimuli for elevated brain natriuretic peptide (BNP) levels. Narcotic and benzodiazepine sedation, such as is used for transesophageal echocardiography (TEE), is known to decrease filling pressures. We hypothesized that lower filling pressure and wall stress associated with intravenous conscious sedation (IVCS) would lead to lower BNP levels. Methods We studied BNP levels, blood pressure, and echocardiographic indices of filling pressure and wall stress before and after IVCS and TEE. Results When data before and after IVCS and TEE were compared, mean blood pressure decreased (149 ± 24/83 ± 14 mm Hg vs 126 ± 29/69 ± 14; P < .01), as did mitral Doppler E wave velocity (82 ± 23 cm/s vs 76 ± 22; P < .05), right ventricular/atrial gradient (31 ± 10 mm Hg vs 29 ± 13; P < .05), and wall stress. However, BNP levels increased (195 ± 407 pg/mL vs 238 ± 458; P < .01). Conclusions In a series of patients undergoing clinically indicated TEE, BNP levels increase above baseline after IVCS. The increase in BNP occurs despite lower blood pressure, lower mitral Doppler E velocity, lower right ventricular/atrial gradient, and lower wall stress compared with baseline. The mechanism of the paradoxical increase in BNP is not entirely clear, but it may conceivably be a result of counterregulatory hormone release caused by acute decrease in blood pressure.

Is quantitative interpretation likely to increase sensitivity of dobutamine stress echocardiography? A study of false-negative results

Background False-negative interpretations of dobutamine stress echocardiography (DSE) may be associated with reduced wall stress. Using measurements of contraction, we sought whether these segments were actually ischemic but unrecognized or showed normal contraction. Methods We studied 48 patients (29 men; mean age 60 ± 10 years) with normal regional function on the basis of standard qualitative interpretation of DSE. At coronary angiography within 6 months of DSE, 32 were identified as having true-negative and 16 as having false-negative results of DSE. Three apical views were used to measure regional function with color Doppler tissue, integrated backscatter, and strain rate imaging. Cyclic variation of integrated backscatter was measured in 16 segments, and strain rate and peak systolic strain was calculated in 6 walls at rest and peak stress. Results Segments with false-negative results of DSE were divided into 2 groups with and without low wall stress according to previously published cut-off values. Age, sex, left ventricular mass, left ventricular geometric pattern, and peak workload were not significantly different between patients with true- and false-negative results of DSE. Importantly, no significant differences in cyclic variation and strain parameters at rest and peak stress were found among segments with true- and false-negative results of DSE with and without low wall stress. Stenosis severity had no influence on cyclic variation and strain parameters at peak stress. Conclusions False-negative results of DSE reflect lack of ischemia rather than underinterpretation of regional left ventricular function. Quantitative markers are unlikely to increase the sensitivity of DSE.

Functional correlates of central arterial geometric phenotypes.

We have assessed the functional correlates of common carotid artery (CCA) arterial geometry, derived by combining a measure of vascular mass (VM) with the wall-to-lumen (W/L) ratio in both untreated hypertensive (HT) and normotensive (NT; blood pressure <140/90 mm Hg) subjects of a broad age span (30 to 79 years) of both genders. Brachial systolic, diastolic, and pulse (SBP, DBP, PP) pressures; CCA SBP and PP; CCA diameter (D); intima-media thickness (IMT); relative distensibility; circumferential wall stress (MBPxW/L); fluid shear stress (FSS); strain; augmentation index (AGIh); and aortic pulse wave velocity (PWV) were measured in 680 NT and 635 untreated HT Taiwanese men and women. Carotid geometric phenotypes (CGPs) were derived from ultrasonographic measures of VM and W/L ratio. A normal CGP (CGP1) was defined as that within the 95th NT percentile of age- and gender-specific VM and W/L means. Three "deviant" CGPs were defined as follows: CGP2 or remodeling, ie, a normal VM coupled with an increased W/L; CGP3 or hypertrophy, ie, an increase in both VM and W/L; and CGP4 or hypertrophy with dilation, ie, an increased VM with normal W/L. The prevalence of specific CGPs in the total sample was 83.4% for CGP1, 5.5% for CGP2, 2.2% for CGP3, and 8.9% for CGP4. Compared with CGP1, all deviant CGPs had increased carotid resistance, had higher CCA circumferential wall stress, and varied in blood flow velocity. Compared with CGP1, CGP2 subjects were more likely to be women (69.3% versus 45.9%), were on average 10 years older, and had similar central and brachial BP levels, PWV, and AGIh but had increased strain, higher distensibility, lower flow, and a higher FSS. CGP3 subjects did not differ in age or gender but had a higher prevalence of HT; higher circumferential stress, PWV, and distensibility; and lower flow, as well as a trend toward higher SBP, PP, and AGIh and lower FSS. CGP4 subjects did not differ in age or gender but exhibited higher AGIh and aortic PWV, lower distensibility and FSS, and unchanged strain and flow. CGP4 was the only deviant CGP in which the average brachial or central arterial pressures were significantly increased. CGP4 subjects also had the highest prevalence of HT among all the CGPs (77.8% versus 45% in CGP1). CGPs exhibit some common mechanical or functional properties but each also exhibits a unique profile. Although differing quantitatively in NT and HT and at young and older age, the characteristic functional profile of a given CGP is preserved, regardless of age or BP status. A normal CGP is characterized by a low circumferential wall stress and high FSS. Each deviant CGP is characterized by a unique combination of increased circumferential wall stress, with variable FSS, strain, distensibility, central BP, and late pressure augmentation. The interplay among these factors, particularly circumferential wall and FSS, likely determines the CGP; conversely, the resultant CGP may modulate the FSS and wall stress for a given pressure and flow.

Familial hypertrophic cardiomyopathy. Cardiac ultrasonic abnormalities in genetically affected subjects without echocardiographic evidence of left ventricular hypertrophy.

It is not known whether the apparent normality of echocardiographic examination results, in subjects bearing a mutation for hypertrophic cardiomyopathy but without ultrasonic left ventricular hypertrophy, is due to incomplete phenotypic expression, or inaccurate echocardiographic criteria. The aim of this study was to search for echocardiographic abnormalities in these patients. Echocardiography was performed in 100 subjects from two families with a mutation in the beta-MHC (720) or My-BPC (714) genes. We compared genetically affected subjects with an apparently normal left ventricle (thickness < 13 mm) (20 patients), and nonaffected first-degree relatives (61 normal subjects). (1) Patients had a thicker left ventricular wall (9.7 +/- 1.4 vs 8.9 +/- 1.4 mm, P = 0.03), a greater indexed mass (107 +/- 18 vs 97 +/- 17 g. m-2, P = 0.03), a larger left atrium (27 +/- 9 vs 23 +/- 10 mm3, P = 0.09) and lower wall stress (78 +/- 11 vs 89 +/- 15 10(3) dynes. cm-2, P = 0.002); these differences were highly significant after adjustment for height, age and systolic blood pressure either for wall thickness (P = 0.000003), mass (P = 0.005) or atrial volume (P = 0.001), and the ventricular systolic dimension appeared smaller (P = 0.01); (2) results remained significant (P < 0.01) when a lower cut-off value (< or = 11 mm) or only adults (> or = 18 years) were considered; (3) a subanalysis of Family 714 (13 patients, 25 normals matched for sex, age and height) showed the same trends. In familial hypertrophic cardiomyopathy, genetically affected subjects with an apparently normal heart by echocardiography show slight ultrasonic structural and functional left ventricular modifications, suggesting that the phenotype of the disease is a continuous spectrum from normal structure to typical hypertrophy.

Cardiopulmonary interaction during partial liquid ventilation in surfactant-treated preterm lambs.

Gas ventilation following instillation of perfluorochemical (PFC) liquid, partial liquid ventilation (PLV), improves gas exchange and pulmonary mechanics in neonatal animals and humans with severe respiratory distress. The effect of PLV on cardiac contractility, performance, pulmonary blood flow and ductal shunt has not been fully described. To this end, we evaluated these indices of cardiopulmonary function in eight conventionally gas ventilated, surfactant-treated premature lambs (125 days gestation) before and during PLV. Animals were instrumented with central venous and aortic lines. Serial evaluation of arterial blood chemistry/pressure, and pulmonary mechanics was performed; cardiac contractility, performance, pulmonary blood flow and ductal shunts were serially assessed by echocardiography. As compared to conventional gas ventilation, during PLV there was a significant decrease in left ventricular meridian (22.5+/-6.6 SE vs 8.1+/-1.4 SE g/cm2, P < 0.02) and circumferential wall stress (54.1+/-16.5 vs 24.4+/-3.8 SE g/cm2, P < 0.04) at end systole. The fall in wall stress at end systole was associated with a significant decrease in left ventricular internal diameter (1.2+/-0.05 SE vs 1.04+/-0.045 SE cm; P < 0.01). There were no significant changes in heart rate, systemic arterial and central venous pressures, systemic vascular resistance, left ventricular shortening and ejection fractions during PLV. The decrease in wall stress was associated with a significant decrease in mean airway pressures (15.9+/-1.1 SE vs 9.9+/-0.2 SE cmH2O; P < 0.05) and ostensibly a change in intrathoracic pressures during PLV. There were no significant differences in blood flows (pre vs during PLV; ml/min/kg): pulmonary (226+/-62 SE vs 293+/-65 SE), aortic (237+/-36 SE vs 204+/-21 SE), and left to right ductal (119+/-25 SE vs 105.5+/-26 SE) measured before and during PLV. Cardiac output and pulmonary blood flow do not change significantly during PLV and therefore do not appear to contribute to improved gas exchange. This stable cardiac performance occurs at lower wall stress and thereby more advantageous energetic conditions.

Ventricular wall stress revisited. A keystone of cardiology.

Wall stress has been used as one of the parameters of myocardial mechanics. The present review focuses on recently developed data on ventricular wall stress, especially in relation to other newly developed areas in cardiology. In hypertensive hearts, there is a broad continuous spectrum in the structural and functional changes: those with low wall stress (inappropriate hypertrophy), those with normal wall stress (appropriate hypertrophy) and those with high wall stress (inadequate hypertrophy). Among them, the responses to neurohumoral stimuli are various, and their clinical features and courses also varied. These differences in wall stress among the different categories of hypertensive hearts may be caused by the variable influences of non-mechanical factors, such as molecular, metabolic and neurohumoral ones. Wall stress is an essential determinant of myocardial oxygen consumption, and is also an important determinant of the myocardial contractile state and diastolic function. In contrast to excitation-contraction coupling, contraction-excitation feedback has been studied, suggesting the importance of wall stress regulating electrical phenomena. The interrelationship between mechanical factors (including wall stress) and non-mechanical factors (including molecular, metabolic, neurohumoral and genetic ones) has been investigated intensively. In conclusion, wall stress (or force on the myocardial cell) may be a keystone in cardiology, relating to each of the cardiac phenomena. If wall stress deviates from the normal range, even with compensatory mechanisms, severe cardiac events occur. The compensatory mechanisms for wall stress may act as a risk factor on the heart, especially when the wall stress remains outside the normal range.

Preoperative left ventricular wall stress, ejection fraction, and aortic valve gradient as prognostic indicators in aortic valve stenosis.

Patients with aortic valve stenosis (AS) and left ventricular (LV) dysfunction may dramatically improve after aortic valve replacement, but operative risk is high. In an earlier study, all patients with low preoperative wall stress and low ejection fraction, or with low aortic valve gradient, died or had persistent heart failure after operation. Because wall stress is difficult to calculate, we reassessed its effect and the effect of other preoperative characteristics on outcome in 66 consecutive catheterization patients with predominant aortic stenosis referred for valve replacement. Despite ejection fraction that was inordinately low compared with afterloading wall stress in nine patients, seven patients improved with surgery. All three patients with ejection fraction less than 20% improved after surgery. Two of three patients with mean aortic valve gradients of less than 30 mm Hg improved. Mortality was 33% in patients with mean gradient less than 30 mm Hg and 19% with mean gradient less than 50 mm Hg. In the 54 patients with calculated aortic valve areas of less than or equal to 0.8 cm2, 1 (2%) had continuing heart failure, while 6 of 12 (50%, P less than .01) patients with aortic valve areas of 0.9-1.2 cm2 had continued symptoms of or died of heart failure. Patients who died or failed to improve after operation were older (71 +/- 9 years) than those who improved (65 +/- 9 years, P = .02). We conclude that wall stress calculations do not predict which patients with aortic stenosis will benefit from aortic valve replacement and that poor left ventricular function and low mean aortic valve gradient do not absolutely preclude operation. On the other hand, low gradient, non-critical valve area, and advanced age are all relative contraindications to aortic valve replacement in aortic stenosis.

Left ventricular dimensions and mechanics in distance runners

We assessed heart size and mechanics at rest in highly trained distance runners. By means of two-dimensional echocardiography, we compared 62 runners (>40 miles/week) and 84 nonrunners. Left ventricular end-diastolic volume index and mass index were larger in runners than in nonrunners ( p < 0.001) and in men than in women ( p < 0.001). However, left ventricular end-diastolic and end-systolic volume/mass ratios were similar for runners and nonrunners. Noninvasive estimates of end-systolic and peak-systolic meridional and circumferential wall stresses were lower in runners than in nonrunners ( p < 0.001). Lower wall stress resulted from lower myocardial area/cavity area ratios, and thus ‘average’ radius/thickness ratios (measured from the parasternal short-axis view), in runners than in nonrunners ( p < 0.001). We detected a subtle change in ventricular shape among the distance runners. Basilar hypertrophy accounted for increased myocardial thickness with normal cavity size in the parasternal short-axis view, as might be expected in hearts working under sustained pressure elevations during prolonged training periods. However, cavity length and therefore ventricular volume were increased in the apical views, leading to a normal overall volume/mass ratio. These hearts have thus adjusted to periods of volume, as well as to pressure overload. Race performance is determined by a complex interaction between the heart, vascular, and skeletal muscle systems. In this study no parameter of myocardial size or function predicted 10 km or marathon race times, just as no physical characteristic or training record predicted left ventricular mass, end-diastolic or end-systolic volume. Myocardial adaptation and performance are unique characteristics of the individuals.

Determinants of ventricular function in pressure-overload hypertrophy in man.

Determinants of ventricular function in pressure-overload hypertrophy in man.

Dependence of wall stress in the human thoracic aorta on age and pressure.

The tangential wall stress and the tangential elasticity modulus at pressures from 0 to 200 mm Hg were calculated from pressure-volume diagrams of 27 human thoracic aortas aged 22 to 85 years. The relative volume increase of the aortas between 0 and 100 mm Hg decreased linearly from about 190% at age 20 to about 40% at age 85, whereas the elasticity modulus at 100 mm Hg increased linearly from 10 kg/cm 2 at age 20 to 42.5 kg/cm 2 at age 85. The decrease of the distensibility of the aortic wall with age was partly compensated by an increase of the internal volume of the aorta but at higher ages the distensibility was less than the theoretical values necessary for a proper buffering chamber activity. The tangential wall stress decreased linearly with age from about 2.5 kg/cm 2 at age 20 to about 1.2 kg/cm 2 at age 85. Since the pressoreceptors in the wall of the elastic vessels respond to the wall stress, this result means either that smooth muscles must increase the stress of the elastic fibers continuously, or the pressoreceptors must adapt their sensitivity throughout life to lower wall stress so that it will be kept constant. Weakness of the smooth muscles or a failure of the pressoreceptors to adapt themselves to lower stresses at higher ages may be the cause of essential hypertension.