Mechanical programming of arterial smooth muscle cells in health and ageing

Arterial smooth muscle cells (ASMCs), the predominant cell type within the arterial wall, detect and respond to external mechanical forces. These forces can be derived from blood flow (i.e. pressure and stretch) or from the supporting extracellular matrix (i.e. stiffness and topography). The healthy arterial wall is elastic, allowing the artery to change shape in response to changes in blood pressure, a property known as arterial compliance. As we age, the mechanical forces applied to ASMCs change; blood pressure and arterial wall rigidity increase and result in a reduction in arterial compliance. These changes in mechanical environment enhance ASMC contractility and promote disease-associated changes in ASMC phenotype. For mechanical stimuli to programme ASMCs, forces must influence the cell’s load-bearing apparatus, the cytoskeleton. Comprised of an interconnected network of actin filaments, microtubules and intermediate filaments, each cytoskeletal component has distinct mechanical properties that enable ASMCs to respond to changes within the mechanical environment whilst maintaining cell integrity. In this review, we discuss how mechanically driven cytoskeletal reorganisation programmes ASMC function and phenotypic switching.     

Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves

Understanding how arterial remodeling changes the mechanical behavior of pulmonary arteries (PAs) is important to the evaluation of pulmonary vascular function. Early and current efforts have focused on the arteries' histological changes, their mechanical properties under in vitro mechanical testing, and their zero-stress and no-load states. However, the linkage between the histology and mechanical behavior is still not well understood. To explore this linkage, we investigated the geometry, residual stretch, and histology of proximal PAs in both adult rat and neonatal calf hypoxic models of pulmonary hypertension (PH), compared their changes due to chronic hypoxia across species, and proposed a two-layer mechanical model of artery to relate the opening angle to the stiffness ratio of the PA outer to inner layer. We found that the proximal PA remodeling in calves was quite different from that in rats. In rats, the arterial wall thickness, inner diameter, and outer layer thickness fraction all increased dramatically in PH and the opening angle decreased significantly, whereas in calves, only the arterial wall thickness increased in PH. The proposed model predicted that the stiffness ratio of the calf proximal PAs changed very little from control to hypertensive group, while the decrease of opening angle in rat proximal PAs in response to chronic hypoxia was approximately linear to the increase of the stiffness ratio. We conclude that the arterial remodeling in rat and calf proximal PAs is different and the change of opening angle can be linked to the change of the arterial histological structure and mechanics.     

Murine Model of Femoral Artery Wire Injury with Implantation of a Perivascular Drug Delivery Patch

Percutaneous interventions including balloon angioplasty and stenting have been used to restore blood flow in vessels with occlusive vascular disease. While these therapies lead to the rapid restoration of blood flow, these technologies remain limited by restenosis in the case of bare metal stents and angioplasty, or reduced healing and possibly enhanced risk of thrombosis in the case of drug eluting stents. A key pathophysiological mechanism in the formation of restenosis is intimal hyperplasia caused by the activation of vascular smooth muscle cells and inflammation due to arterial stretch and injury. Surgeries that induce arterial injury in genetically modified mice are useful for the mechanistic study of the vascular response to injury but are often technically challenging to perform in mouse models due to the their small size and lack of appropriate sized devices. We describe two approaches for a surgical technique that induces endothelial denudation and arterial stretch in the femoral artery of mice to produce robust neointimal hyperplasia. The first approach creates an arteriotomy in the muscular branch of the femoral artery to obtain vascular access. Following wire injury this arterial branch is ligated to close the arteriotomy. A second approach creates an arteriotomy in the main femoral artery that is later closed through localized cautery. This method allows for vascular access through a larger vessel and, consequently, provides a less technically demanding procedure that can be used in smaller mice. Following either method of arterial injury, a degradable drug delivery patch can be placed over or around the injured artery to deliver therapeutic agents.     

Biomechanical and morphometric properties of the arterial wall referenced to the zero-stress state in experimental diabetes

Morphometric and passive biomechanical properties were studied in isolated segments of the thoracic and abdominal aorta, left common carotid artery, left femoral artery and the left pulmonary artery in 20 non-diabetic and 28 streptozotocin (STZ)-induced diabetic rats. The diabetic and non-diabetic rats were divided into groups living 1, 4, 8, and 12 weeks after the induction of diabetes (n = 7 for each diabetic group) or sham injection (n = 5 for each group). The mechanical test was performed as a distension experiment where the proximal end of the arterial segment was connected via a tube to the container used for applying pressures to the segment and the distal end was left free. The vessel diameter and length were obtained from digitized images of the arterial segments at pre-selected pressures and at no-load and zero-stress states. Circumferential and longitudinal stresses (force per area) and strains (deformation) were computed from the length, diameter and pressure data and from the zero-stress state data. The zero-stress state was obtained by cutting vessel rings radially causing the rings to open up into a sector. Diabetes was associated with pronounced morphometric changes, e.g., wall thickness. With respect to the biomechanical data, the opening angle increased and reached a plateau in 4 weeks after which it decreased again (p < 0.05). The opening angle was smallest in the thoracic aorta and largest in the pulmonary artery. Furthermore, it was found that the circumferential stiffness of the arteries studied increased with the duration of diabetes. In the longitudinal direction significant differences were found 8 weeks after injection of STZ in all arteries except the pulmonary artery. In the 12 weeks group, the femoral artery was stiffest in the circumferential direction whereas the thoracic aorta was stiffest in the longitudinal direction. The accumulated serum glucose level correlated with the arterial wall thickness and elastic modulus (correlation coefficient between 0.56 and 0.81).     

Can the modified Allen's test always detect sufficient collateral flow in the hand? A computational study

Blood flow in the largest arteries of the arm up to the digital arteries is numerically modelled using the one-dimensional equations of pressure and flow wave propagation in compliant vessels. The model can be applied to different anatomies of arterial networks and can simulate compression of arteries, these allowing us to simulate the modified Allen's test (MAT) and to assess its suitability for the detection of sufficient collateral flow in the hand if radial blood supply is interrupted. The test measures blood flow in the superficial palmar arch before and during compression of the radial artery. The absence of reversal flow in the palmar arch with the compression indicates insufficient collateral flow and is referred to as a positive MAT. This study shows that small calibres of the superficial palmar arch and insufficient compression of the radial artery can lead to false-positive results. Measurement of the drop in digital systolic pressures with compression of the radial artery has proved to be a more sensitive test to predict the presence of sufficient ulnar collateral flow in networks with small calibres of the superficial palmar arch. However, this study also shows that digital pressure measurements can fail in detecting enough collateral flow if the radial artery is insufficiently compressed.     

Can the modified Allen's test always detect sufficient collateral flow in the hand? A computational study

Blood flow in the largest arteries of the arm up to the digital arteries is numerically modelled using the one-dimensional equations of pressure and flow wave propagation in compliant vessels. The model can be applied to different anatomies of arterial networks and can simulate compression of arteries, these allowing us to simulate the modified Allen's test (MAT) and to assess its suitability for the detection of sufficient collateral flow in the hand if radial blood supply is interrupted. The test measures blood flow in the superficial palmar arch before and during compression of the radial artery. The absence of reversal flow in the palmar arch with the compression indicates insufficient collateral flow and is referred to as a positive MAT. This study shows that small calibres of the superficial palmar arch and insufficient compression of the radial artery can lead to false-positive results. Measurement of the drop in digital systolic pressures with compression of the radial artery has proved to be a more sensitive test to predict the presence of sufficient ulnar collateral flow in networks with small calibres of the superficial palmar arch. However, this study also shows that digital pressure measurements can fail in detecting enough collateral flow if the radial artery is insufficiently compressed.     

Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats

Chronic smoking and secondhand tobacco smoke exposure are major risk factors for cardiovascular disease that are known to adversely alter the structural and mechanical properties of arteries. The objective of this study was to determine the effects of subchronic secondhand tobacco smoke exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in conscious, unsedated radiotelemetry-implanted rats. Pulse wave change in pressure over time (dP/dt) was used an indicator of arterial stiffness and was compared with both structural (wall thickness) and functional (nitric oxide production and bioactivity and endothelin-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver was examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450, specifically CYP1A1). Subchronic secondhand tobacco smoke exposure altered the circadian pattern of heart rate and blood pressure, with a loss in the normal dipping pattern of blood pressure during sleep. Secondhand tobacco smoke exposure also increased pulse wave dP/dt in the absence of any structural modifications in the arterial wall. Furthermore, although nitric oxide production and endothelin-1 levels were not altered by secondhand tobacco smoke, there was increased inactivation of nitric oxide as indicated by peroxynitrite production. Increased lung neutrophils or pulmonary CYP1A1 may be responsible for the increase in oxidative stress in rats exposed to secondhand tobacco smoke. In turn, this may be related to the observed failure of blood pressure to dip during periods of sleep and a possible increase in arterial stiffness.     

A biomechanical model of artery buckling

The stability of arteries under blood pressure load is essential to the maintenance of normal arterial function and the loss of stability can lead to tortuosity and kinking that are associated with significant clinical complications. However, mechanical analysis of arterial bent buckling is lacking. To address this issue, this paper presents a biomechanical model of arterial buckling. Using an elastic cylindrical arterial model, the mechanical equations for arterial buckling were developed and the critical buckling pressure was found to be a function of the wall stiffness (Young's modulus), arterial radius, length, wall thickness, and the axial strain. Both the model equations and experimental results demonstrated that the critical pressure is related to the axial strain. Arteries may buckle and become tortuous due to reduced (subphysiological) axial strain, hypertensive pressure, and a weakened wall. These results are in accordance with, and provide a possible explanation to the clinical observations that hypertension and aging are the risk factors for arterial tortuosity and kinking. The current model is also applicable to veins and ureters.     

The Local Forces Acting on the Mechanotransduction Channel in Hair Cell Stereocilia

In hair cells, mechanotransduction channels are located in the membrane of stereocilia tips, where the base of the tip link is attached. The tip-link force determines the system of other forces in the immediate channel environment, which change the channel open probability. This system of forces includes components that are out of plane and in plane relative to the membrane; the magnitude and direction of these components depend on the channel environment and arrangement. Using a computational model, we obtained the major forces involved as functions of the force applied via the tip link at the center of the membrane. We simulated factors related to channels and the membrane, including finite-sized channels located centrally or acentrally, stiffness of the hypothesized channel-cytoskeleton tether, and bending modulus of the membrane. Membrane forces are perpendicular to the directions of the principal curvatures of the deformed membrane. Our approach allows for a fine vectorial picture of the local forces gating the channel; membrane forces change with the membrane curvature and are themselves sufficient to affect the open probability of the channel.     

A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS.     

Pulmonary circulation in embolic pulmonary edema

The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism.     

The Local Forces Acting on the Mechanotransduction Channel in Hair Cell Stereocilia

In hair cells, mechanotransduction channels are located in the membrane of stereocilia tips, where the base of the tip link is attached. The tip-link force determines the system of other forces in the immediate channel environment, which change the channel open probability. This system of forces includes components that are out of plane and in plane relative to the membrane; the magnitude and direction of these components depend on the channel environment and arrangement. Using a computational model, we obtained the major forces involved as functions of the force applied via the tip link at the center of the membrane. We simulated factors related to channels and the membrane, including finite-sized channels located centrally or acentrally, stiffness of the hypothesized channel-cytoskeleton tether, and bending modulus of the membrane. Membrane forces are perpendicular to the directions of the principal curvatures of the deformed membrane. Our approach allows for a fine vectorial picture of the local forces gating the channel; membrane forces change with the membrane curvature and are themselves sufficient to affect the open probability of the channel.     

Computational simulation of flow-induced arterial remodeling of the pancreaticoduodenal arcade associated with celiac artery stenosis

Arterial remodeling of the pancreaticoduodenal arcade, which enables collateral flow to the liver, spleen, and stomach, is a well-recognized clinical sign of celiac artery (CA) stenosis. However, the hemodynamic changes due to remodeling are poorly understood, despite their importance in surgical procedures such as pancreaticoduodenectomy. In this study, a framework to simulate remodeling of the arterial network following pathological flow alterations was developed and applied to investigate the hemodynamic characteristics of patients with CA stenosis. A one-dimensional–zero-dimensional cardiovascular model was used for blood flow simulation. After introducing CA stenosis into the normal network, arterial remodeling was simulated by iteratively changing the diameter of each artery until time-averaged wall shear stress reached its value under normal conditions. A representative case was simulated to validate the present framework, followed by simulation cases to investigate the impact of stenosis severity on remodeling outcome. A markedly dilated arcade was observed whose diameter agreed well with the corresponding values measured in subjects with CA stenosis, confirming the ability of the framework to predict arterial remodeling. A series of simulations clarified how the geometry and hemodynamics after remodeling change with stenosis severity. In particular, the arterial remodeling and resulting blood flow redistribution were found to maintain adequate organ blood supply regardless of stenosis severity. Furthermore, it was suggested that flow conditions in patients with CA stenosis could be estimated from geometric factors, namely, stenosis severity and arcade diameter, which can be preoperatively and non-invasively measured using diagnostic medical images.     

Causes of experimental pulmonary hypertension in rats.

Experimental pulmonary hypertension was induced in young male rats by means of tracheoconstriction and repeated injections of aqueous bean (Phaseolus vulg.) extract into the trachea. After 120 days, the blood pressure of the experimental and control animals was measured in the pulmonary artery with a shaped polyethylene catheter, without opening the chest. In all the experimental animals the blood pressure in the pulmonary artery was higher than in the controls. The mean pressure in the pulmonary artery of the experimental rats was 25 +/- 1 torr and in the controls 16 +/- 0.4 torr. The right ventricle of the experimental animals was larger than in the controls. No difference was found between the systemic blood pressure values, measured in the femoral artery, in the experimental animals and the controls. The experimental animals had a faster heart rate. Cardiac output, measured by the dye dilution method, was the same in the control and experimental animals and there was likewise no difference in the PO2 PCO2 and pH values in the arterial blood. The inhalation of oxygen instead of air did not affect the blood pressure in the pulmonary artery. The pulmonary blood vessels were evaluated quantitatively in histological sections of the experimental and control animal's lungs. There was no different between the thickness of the media of the distal pulmonary vessels, expressed as a percentage of the outer diameter of the vessel, in the experimental animals and the controls. A media thicker than 7% was found in 15% of the evaluated vessels from experimental animals and in 8% of those from the controls. No correlation between the mean thickness of the media and the mean blood pressure in the pulmonary artery was found in any of the animals.     

老年肥胖型正常高值血压患者24h-动态血压变异特点及与动脉僵硬度的相关性研究

摘要 目的：探讨老年肥胖型正常高值血压患者24h-动态血压变异特点及与动脉僵硬度的相关性。方法：选择2018年1月~2020年5月期间在我院住院的老年正常高值血压患者174例作为研究对象,根据腰围分为腹型肥胖组（n=85）和非腹型肥胖组（n=89）。所有受试者监测24h-动态血压[包括24h平均收缩压（24h-SBP）、白昼平均舒张压（dDBP）、24h平均舒张压（24h-DBP）、夜间平均收缩压（nSBP）、白昼平均收缩压（dSBP）、夜间平均收缩压（nDBP）、血压变异系数（CV）]和颈-桡动脉脉搏传导速度（crPWV）,分析24h-动态血压变异性、节律性特点和crPWV的影响因素。结果：腹型肥胖组患者非杓型血压、24h-SBP-CV、24h-DBP-CV、dSBP-CV、nSBP-CV、夜间SBP下降率以及crPWV均高于非腹型肥胖组（P<0.05）,腹型肥胖组患者动脉僵硬度增高发生率高于非腹型肥胖组患者（P<0.05）。控制混杂因素后,腹型肥胖组患者腰围与夜间SBP下降率（r=0.338）、24h-SBP-CV（r=0.279）、24h-DBP-CV（r=0.259）、dSBP-CV（r=0.208）、nSBP-CV（r=0.317）、crPWV（r=0.543）呈正相关性（P<0.05）。经多元线性回归分析结果显示,腰围、LDL-C、夜间SBP下降率、24h-SBP-CV和nSBP-CV是crPWV的重要影响因素（P<0.05）。结论：腹部脂肪沉积对老年正常高值血压患者24h动态血压变异性和动脉僵硬度有显著影响,部分24h-动态血压参数与动脉僵硬度有关,控制腰围对预防动脉硬化有着重要的意义。     

Intraoperative physiologic blood flow studies in the TRAM flap.

An intraoperative study was done to establish the functional and quantitative properties of the blood supply to the TRAM flap through the assessment and manipulation of blood flow through the deep epigastric arterial system. Seventeen patients undergoing unilateral postmastectomy breast reconstruction with lower transverse rectus abdominis myocutaneous (TRAM) flaps were studied. The study is divided into two parts: (1) ultrasonic measurement of blood flow in the deep inferior epigastric artery (DIEA), and (2) direct measurement of blood pressure in the deep epigastric arterial system, after division of the deep inferior epigastric artery. With occlusion of the superior epigastric artery at the level of the upper edge of the skin flap, 71 percent of the patients had a decrease in the blood flow through the deep inferior epigastric artery, with an average decrease of 23 percent. This implies that the area of watershed perfusion in the lower TRAM flap is superior to the umbilicus, and therefore, survival of all lower TRAM flap tissues requires reversal in the normal direction of arterial flow to the flap. The blood pressure in the proximal stump of the deep inferior epigastric arterial system averaged 46 percent of the mean systemic blood pressure. Occlusion of the medial and lateral thirds of the isolated rectus muscle decreased the mean arterial blood pressure in the flap an average of 19 percent in 80 percent of the individuals studied. These data support the technique of harvesting the entire rectus muscle, avoiding muscle-splitting maneuvers that may compromise axial blood flow.     

Effects of surface tension and viscosity on airway reopening

We studied airway opening in a benchtop model intended to mimic bronchial walls held in apposition by airway lining fluid. We measured the relationship between the airway opening velocity (U) and the applied airway opening pressure in thin-walled polyethylene tubes of different radii (R) using lining fluids of different surface tensions (gamma) and viscosities (mu). Axial wall tension (T) was applied to modify the apparent wall compliance characteristics, and the lining film thickness (H) was varied. Increasing mu or gamma or decreasing R or T led to an increase in the airway opening pressures. The effect of H depended on T: when T was small, opening pressures increased slightly as H was decreased; when T was large, opening pressure was independent of H. Using dimensional analysis, we found that the relative importance of viscous and surface tension forces depends on the capillary number (Ca = microU/gamma). When Ca is small, the opening pressure is approximately 8 gamma/R and acts as an apparent "yield pressure" that must be exceeded before airway opening can begin. When Ca is large (Ca greater than 0.5), viscous forces add appreciably to the overall opening pressures. Based on these results, predictions of airway opening times suggest that airway closure can persist through a considerable portion of inspiration when lining fluid viscosity or surface tension are elevated.     

Angiotensin II contributes to arterial compliance in congestive heart failure

Arterial compliance is determined by structural factors, such as collagen and elastin, and functional factors, such as vasoactive neurohormones. To determine whether angiotensin II contributes to decreased arterial compliance in patients with heart failure, this study tested the hypothesis that administration of an angiotensin-converting enzyme inhibitor improves arterial compliance. Arterial compliance and stiffness were determined by measuring carotid artery diameter, using high-resolution duplex ultrasonography, and blood pressure in 23 patients with heart failure secondary to idiopathic dilated cardiomyopathy. Measurements were made before and after intravenous administration of enalaprilat (1 mg) or vehicle. Arterial compliance was inversely related to both baseline plasma angiotensin II (r = -0.52; P = 0.015) and angiotensin-converting enzyme concentrations (r = -0.45; P = 0.041). During isobaric conditions, enalaprilat increased carotid artery compliance from 3.0 +/- 0.4 to 5.0 +/- 0.4 x 10(-10) N(-1). m(4) (P = 0.001) and decreased the carotid artery stiffness index from 17.5 +/- 1.8 to 10.1 +/- 0.6 units (P = 0.001), whereas the vehicle had no effect. Thus angiotensin II is associated with reduced carotid arterial compliance in patients with congestive heart failure, and angiotensin-converting enzyme inhibition improves arterial elastic properties. This favorable effect on the pulsatile component of afterload may contribute to the improvement in left ventricular performance that occurs in patients with heart failure treated with angiotensin-converting enzyme inhibitors.     

Relationship between androgenic hormones and arterial stiffness, based on longitudinal hormone measurements

Circulating testosterone levels (T) decrease with age in men. Low T has been associated with coronary disease and with risk factors for atherosclerosis. This study examines the relationship in men between androgenic hormones and arterial stiffness, a major risk factor for cardiovascular events. T, sex hormone-binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEAS) were measured longitudinally over 33 yr (follow-up 11.8 +/- 8.3 yr) in 901 men from the Baltimore Longitudinal Study of Aging, of whom 206 (68.1 +/- 13.7 yr) underwent carotid duplex ultrasonography. The 901 men were used to characterize age-associated hormone levels by means of mixed-effects models. Hormone values were estimated for the 206 men at the time of ultrasonography. Free T index (FTI) was calculated by dividing T by SHBG. The arterial stiffness index was calculated from peak systolic and end diastolic diameters of the common carotid artery and simultaneous brachial artery blood pressure. T, FTI, and DHEAS were correlated negatively with age, pulse pressure (PP), and stiffness index (each P < 0.01), whereas SHBG was correlated positively with age and stiffness index (P < 0.01). However, T was the only hormone that predicted the stiffness index after adjustment for age, PP, fasting plasma glucose, body mass index, and total cholesterol. T values 5-10 yr before the carotid study also predicted the stiffness index (P < 0.05). Thus the adverse influence of low T on the cardiovascular system in men may be mediated in part via the effects of T on vascular structure and function.     

Towards early diagnosis of atherosclerosis: the finite volume method for fluid-structure interaction

Blood flow through arteries represents a very complex, fluid-structure interaction (FSI) problem. Strong coupling between the blood and artery is due to the relatively low stiffness of the artery compared to that of blood. Hence, the pressure exerted by the flowing blood on the artery wall can result in considerable deformations of the artery, and vice-versa, arterial deformations can in turn affect the blood flow. In the present work, the finite volume method is employed to solve the problem where compressible fluid, representing blood, flows in healthy arteries as well as in unhealthy, i.e., partly stiffened arteries. The stiffening of the arterial wall is assumed to be the first key stage in the development of atherosclerosis. The comparison between various deformation profiles of healthy and unhealthy arteries demonstrates significant and measurable differences, in particular in the radial direction. This is hoped to help toward establishing procedures for early diagnosis of the disease.