Vessel Stiffness Research Articles

Optimization of stent designs regarding the thrombosis risk using computational fluid dynamics

Abstract In-stent thrombosis is a major complication of stent implantations. Unlike pathological occurrences as in-stent restenosis for instance, thrombosis represents an acute event associated with high mortality rates. Experiments show that low wall shear stress promotes undirected endothelial cell coverage of the vessel wall and therefore increases the risk of thrombus formation. Stent design represents a crucial factor influencing the surface areas of low wall shear stress and thus the incidence of acute in-stent thrombosis. In this study, we present an optimization method for stent designs with minimized thrombosis risk. A generic stent design was developed, based on five different stent design parameters. Optimization was conducted based on computational fluid dynamics analysis and the gradient-free Nelder-Mead approach. For each optimization step, a numerical fluid simulation was performed in a vessel with a reference vessel diameter of 2.70 mm with stent-overexpansion ratio of 1.0:1.1. For each numerical fluid simulation a physiological Reynolds number of 250, resulting in a mean velocity of 0.331 m/s at the inlet and a laminar flow as well as stiff vessel walls were assumed. The impact of different stent designs was analyzed based on the wall shear stress distribution. As a basis for the comparison of different stent designs, a dimensionless thrombosis risk number was calculated from the area of low wall shear stress and the overall stented area. The first two optimization steps already provide a decrease of thrombosis risk of approximately 83%. In conclusion, computational fluid dynamic analyses and optimization methods usind the Nelder-Mead approach represent a useful tool for the development of hemodynamically optimized stent designs with minimized thrombosis risk.

Vessel stiffness, calcification and osteoporosis. Common pathogenetic components

Atherosclerosis and osteoporosis until recently were regarded as the diseases of modern society, and their simultaneous development was explained just by the increased chances with longevity. Currently, there are studies showing evidence on these diseases in ancient populations, regardless the age and gender. The diseases found in younger age, with the early Egyptian civilization, witness on the common genetic and behavioral risk factors and pathogenetic components, than simple age-related chance. Scientific publications show more and more data on common properties of these diseases and pathogenetic mechanisms. High risk of premature death from atherosclerosis and osteoporosis complications facilitates the search for individual and general predictors of the disorders with the aim of on-time prevention. Treatment of atherosclerosis and osteoporosis presentation events in one patient demands for a range of medications that leads to polypragmasia. The review is focused on common mechanisms of vascular stiffness development, calcification and bone density decrease. Profound understanding might make it to open novel targets for one drug to both diseases, with decreased rate of complications.

Fabrication of Hydrogel Tubes with Vascular Mimicked Stiffness for Construction of in Vitro Vascular Models.

Stiffness of blood vessels is one of the most important parameters involving in vascular diseases. However, no vascular model well mimics the stiffness of native blood vessels, and thus, the effects of vascular stiffness on endothelial cells cannot be studied in vitro. For this purpose, we fabricated the gelatin/carboxybetaine (CBMA) interpenetrating network (IPN) hydrogel tubes to exactly present the stiffness of soft (i.e., physical) and stiff (i.e., pathological) arteries in human. The vascular models are then constructed via endothelial cell culture inside the gel tubes under a cardiac-like pulsatile perfusion. As found, the velocity magnitude and wall shear stress in the stiff gel tube are much higher than those in the soft one. Correspondingly, the endothelial cells in the soft gel tube (i.e., physical model) express higher vascular functions than those in the stiff one (i.e., pathological model). Moreover, a pathological model was more sensitive to ethanol-induced vascular injury than the physical model. Thus, the new vascular models with a tunable stiffness provide a useful tool to investigate the stiffness involved mechanism in vascular diseases under in vivo mimicked microenvironments.

The Role of Type VIII Collagen in Arterial Vessel Stiffening

The Role of Type VIII Collagen in Arterial Vessel Stiffening

MUSCULAR ARTERIAL TONE IS A DETERMINANT OF PERIPHERAL MUSCULAR ARTERY STIFFNESS

Objective: Due the practical weaknesses of cuff based methods for arterial blood pressure (BP) measurement, efforts are made to establish non-invasive and continuous PB measurement by using alternative methods. One of them is based on the determination of the pulse transit time and pulse wave velocity (PWV), respectively. Arterial BP and PWV correlate, which opens the possibility of the determination of arterial BP by measuring the pulse transit time (PTT). Recent validation studies revealed usefulness of this method in clinical practice. The accuracy of this method depends on the transfer function (model) between arterial BP and PWV. Since PWV is mainly determined by the arterial elasticity (stiffness), knowledge about the contribution of different components and to the arterial stiffness as well as their modulation is important. We hypothesize that the vascular smooth muscle (VSM) tone significantly determines arterial stiffness in muscular arteries and thus may contribute to the PWV-BP relation. Design and method: We used the pressurized artery method and investigated the influence of inherent and pharmacologically modified VSM tone on measures of arterial stiffness. We first characterized passive and active components of arterial stiffness by calculating pressure-diameter-relation, stress-strain-relation, and the stiffness parameter beta in vessels with spontaneous tone and in vessel after calcium depletion. Further, the effect of norepinephrine in different concentrations on the measures of stiffness was investigated. Results: Vessels with spontaneous myogenic tone showed left shifted pressure-diameter- and stress-strain-relations compared to passive vessels, expressing an increased vascular stiffness. Norepinephrine in higher concentration further shifted these curves to the left and consequently increased vessel stiffness. The stiffness parameter beta was also increased. Conclusions: The data suggest that the myogenic tone and the action of norepinephrine increases arterial stiffness in muscular arteries of rats. This effect may contribute the PWV in muscular arterioles and thus influences to the PWV-BP relation.

Children with kawasaki disease present elevated stiffness of great arteries: Phase-contrast MRI study.

Patients with diagnosed Kawasaki disease (KD) are known to develop extracardiac vascular lesions and are prone to accelerated stiffening of medium-size arteries. To noninvasively evaluate great vessel (central aorta and main pulmonary artery (MPA)) stiffness using phase-contrast MRI (PC-MRI). Retrospective review. Thirty-three patients with previously diagnosed KD and 15 control subjects underwent PC-MRI evaluation. A free-breathing PC-MRI sequence was applied with Cartesian encoding and retrospective sorting using a 1.5 or 3.0T system. We evaluated regionally specific vessel stiffness using pulse-wave velocity (PWV) and relative area change (RAC) at the ascending aorta, descending aorta, and MPA. Hemodynamics among patients with KD and controls were compared using Student's t-test, Wilcoxon Rank-sum, and χ2 . Additional group-specific comparisons were performed using Kruskal-Wallis or one-way analysis of variance (ANOVA). Patients with KD showed elevated PWV in both ascending (5.0 ± 1.2 vs. 2.4 ± 0.5, P < 0.001) and descending aorta (4.4 ± 2.1 vs. 2.8 ± 0.8, P < 0.001). RAC was correspondingly reduced in both segments (both P < 0.01). PWV measured in MPA was increased in KD patients (2.2 ± 0.5 vs. 1.5 ± 0.6, P = 0.045) while the RAC was reduced (34 ± 6 vs. 47 ± 3, P = 0.045). There were no associations between considered vessel stiffness indices and respective ventricular size and function, functional indices, and no correlations were observed with KD severity markers. Patients with KD have elevated great vessel stiffness measured at the chronic stage of the disease. Accelerated stiffness process does not appear to affect biventricular function in youth Level of Evidence: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:1228-1236.

Beneficial Effects of Exercise on Subendothelial Matrix Stiffness are Short-Lived.

Aerobic exercise helps to maintain cardiovascular health in part by mitigating age-induced arterial stiffening. However, the long-term effects of exercise regimens on aortic stiffness remain unknown, especially in the intimal extracellular matrix layer known as the subendothelial matrix. To examine how the stiffness of the subendothelial matrix changes following exercise cessation, mice were exposed to an 8 week swimming regimen followed by an 8 week sedentary rest period. Whole vessel and subendothelial matrix stiffness were measured after both the exercise and rest periods. After swimming, whole vessel and subendothelial matrix stiffness decreased, and after 8 weeks of rest, these values returned to baseline. Within the same time frame, the collagen content in the intima layer and the presence of advanced glycation end products (AGEs) in the whole vessel were also affected by the exercise and the rest periods. Overall, our data indicate that consistent exercise is necessary for maintaining compliance in the subendothelial matrix.

Sex differences in the role of the smooth muscle cell mineralocorticoid receptor in cardiovascular aging

Vascular aging is a process that involves the development of vasomotor dysfunction and vessel stiffening, which leads to cardiovascular disease (CVD). Clinical data supports that differential mechanisms may be involved in the progression of vascular aging in males compared to females. We have previously demonstrated that male mice with smooth muscle cell (SMC)‐specific deletion of the mineralocorticoid receptor (MR‐KO), a steroid hormone receptor known to regulate renal sodium handling, have lower blood pressure, vascular tone, and vasoconstriction as they age. The purpose of this study was to determine whether there are sex differences in the role of SMC‐MR in vascular aging. We demonstrated that vascular MR expression increases and miR‐155 decreases from 3 to 12 months of age in male mice. Additional studies revealed that SMC‐MR transcriptionally represses vascular miR‐155, which then promotes an increase in expression of miR‐155 target genes, Cav1.2, the pore‐forming subunit of the L‐type calcium channel (LTCC) and the angiotensin II type 1 receptor (AT1R) at 12 months of age in male mice. When compared directly to males, aging female mice do not display an increase in vascular MR expression until 18 months of age, accompanied by a decrease in miR‐155. Similarly, 12 month old female mice do not have altered vascular expression of Cav1.2 or AT1R compared to young females. Further, LTCC function is increased at 12 months of age in males and decreased at 12 months of age in females and then ultimately rose in females by 18 months of age. Additionally, Ang II‐mediated vasoconstriction increases at 12 months of age in males and is attenuated by SMC‐MR‐KO, however, in females, Ang II constriction is unaltered at 12 months of age and then surpasses the male Ang II constriction response at 18 months of age. We also observed an increase in vascular stiffness, measured by aortic pulse wave velocity, in male mice at 12 months of age that persists at 18 months of age and is prevented by SMC‐MR‐KO. In contrast, female mice do not exhibit increases in stiffness until 18 months of age, which is also attenuated by SMC‐MR‐KO. To explore potential mechanisms of vascular stiffness, we performed atomic force microscopy studies in 16–19 month old male and female mice. Females exhibited significantly more SMC‐stiffness than males, and SMC‐MR‐KO partially restored the aging‐associated stiffness. We also examined cardiac function, measured by echocardiography, and found that systolic and diastolic cardiac function declines with age in both males and females, but is modulated by SMC‐MR‐KO in females only. Further, we found that exercise capacity, measured by a graded exercise test, declines in both males and females with age, but is modulated by SMC‐MR‐KO in males only. Together, these results suggest that the mechanisms and time course of cardiovascular aging are distinct between males and females, and that SMC‐MR appears to play a differential role in males versus females. Furthermore, these studies suggest that sex‐specific therapies may be essential to improve CVD outcomes in the aging population.Support or Funding InformationSupported by HL095590‐05, HL119290, and AHA15POST21300000.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Type 2 Diabetic Coronary Vascular Smooth Muscle Cells Exhibit Decreased Stiffness and Decreased Adhesion

We previously reported that type 2 diabetic (T2D) coronary resistance microvessels (CRMs) undergo early inward hypertrophic remodeling with reduced vessel stiffness that is associated with a proliferative VSMC phenotype. We also previously revealed that there is no difference in stiffness of decellularized CRMs from diabetic (db/db) and normal (Db/db) mice, suggesting that the decreased stiffness of the intact diabetic CRM is not due to alterations in the extracellular matrix (ECM) of those microvessels. Given that diabetic CRMs are less stiff and this decreased stiffness does not appear to be due differences in the mechanical strength of the surrounding ECM, the aim of the current study was to determine whether a reduction in cellular mechanical stiffness between Db/db and db/db CRM vascular smooth muscle cells (VSMCs) may be responsible. VSMCs were isolated from 16 week old Db/db and db/db mice and passage 1 cells were used for all experiments (n=6–7 for all groups). Using an atomic force microscope with probes coated with fibronectin (FN), a nano‐indentation protocol was used to measure cellular stiffness and adhesion to FN. Elastic modulus, a measurement of cellular stiffness, was reduced in diabetic coronary VSMCs compared to normal (Db/db: 6.74 ± 0.40 kPa vs. db/db: 4.96 ± 0.35 kPa, p = 0.004). By comparison, there were no significant differences in elastic modulus between normal and diabetic aortic VMSCs (Db/db: 5.39 ± 0.79 kPa vs. db/db: 5.18 ± 0.87 kPa, p = 0.861). Additionally, diabetic coronary VSMCs had reduced adhesive force to fibronectin compared to normal coronary VSMCs (Db/db: 54.78 ± 5.49 vs. db/db: 39.8 ± 3.43 pN, p = 0.03). In a separate experiment, qPCR was performed on mRNA from normal and diabetic CRM VSMCs. Alpha‐smooth muscle actin trended lower in db/db CRM VSMCs (p=0.07), indicating a de‐differentiated phenotype. Cell cycle regulator, p53, had significantly reduced mRNA expression in the diabetic coronary VSMCs over control VSMCs (Db/db 1.00±0.06 vs. db/db 0.63±0.08, p&lt;0.01). These data show that reductions in cellular stiffness and adhesion to the ECM of diabetic CRM VSMCs may underlie ex vivo whole microvessel mechanical properties to account for reduced CRM stiffness. The changes in diabetic coronary VSMC stiffness and adhesion may be the result of VMSC phenotypic switching to a more de‐differentiated/proliferative phenotype.Support or Funding InformationSupport: NIH R00 HL116769 and S10 OD023438 and Nationwide Children's Hospital to AJTThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Age-related changes in cerebrovascular reactivity and their relationship to cognition: A four-year longitudinal study

Although cerebrovascular factors are the second leading cause of cognitive impairment and dementia in elderly, the precise spatial and temporal trajectories of vascular decline in aging have not been fully characterized. With an advanced cerebrovascular reactivity (CVR) MRI technique that specifically informs vascular stiffness and dilatory ability of cerebral vessels, we present four-year longitudinal CVR data measured in 116 healthy individuals (20–88 years of age). Our data revealed a spatial heterogeneity in vascular decline in aging (p = 0.003), in that temporal lobe showed the fastest rate of longitudinal CVR decline, followed by parietal and frontal lobes. The rate of CVR decline was also age-dependent. Middle age, not older age, manifested the fastest rate of longitudinal CVR decline (p < 0.05). Longitudinal changes in CVR were associated with changes in processing speed (p = 0.031) and episodic memory (p = 0.022), but not with working memory or reasoning. The rate of longitudinal CVR change was not different between hypertensive and normotensive participants. However, cross-sectionally, individuals with hypertension revealed in a lower CVR compared to normotensive participants (p = 0.016). These findings help elucidate age-related decline in brain hemodynamics and support CVR as a non-invasive biomarker in evaluating cerebrovascular conditions in elderly individuals.

ARTERIAL STIFFNESS IN YOUNG PATIENTS WITH CHRONIC GLOMERULONEPHRITIS

Aim. To study the presence of the phenomenon of stiffness of the arterial vessels in young patients with chronic glomerulonephritis. Materials and methods. The parameters of malleolar-brachial index (while chronic kidney disease (CKD) progression) were studied in 47 young patients with chronic glomerulonephritis and 24 comparable by age healthy volunteers. Results. There was detected the elevation of malleolar-brachial index in young patients with chronic glomerulonephritis, when having stage 3-5 CKD. Conclusions. Malleolar-brachial index, as an index of arterial stiffness, grows with CKD progression, that is a marker of early aging of vessels and cardiovascular remodeling in young patients with chronic glomerulonephritis.

Micro-piezoelectric pulse diagnoser and frequency domain analysis of human pulse signals

BackgroundThe theory of pulse diagnosis is to assess the physiological condition of the human body using radial pulse. However, pulses can vary markedly from person to person. Further, pulse diagnosis is difficult to learn and requires one-on-one teaching. MethodsTo address this problem, we built a home-made pulse diagnoser and measured human pulses for studying the standardization of pulse diagnosis. Our pulse diagnoser was composed of a piezoelectric transducer, differential amplifier, data acquisition instrument, and a Matlab analysis program. The measured pulses were converted into electronic signals by a piezoelectric transducer and saved on a computer. The digitalized data were then refined and analyzed by fast Fourier transform for frequency analysis. Simulations were performed to assess the factors that affected the pulse, including phase shifts of reflected pulse waves (generate sub-peaks in pulses), inconsistent heart rates (deform pulse waves), the vessel stiffness (alter harmonic frequencies of the pulses), and the wave amplitudes (determined by the pulse strength). ResultsBy comparing a published report and our simulation findings, we characterized the pulse types and the effects of various factors, and then applied the findings to study actual pulses in patients. Three types of pulses were determined from the frequency spectrum—choppy pulse (Se mai) without apparent harmonic peaks, the harmonic frequencies of wiry pulse (Xian mai) that are non-integer multiples of the fundamental frequency, and surging pulse (Hong mai) that exhibit strong amplitudes in the spectrum of frequency. A normal pulse and a slippery pulse were differentiated by a phase shift, but not by assessing the frequency spectrum. ConclusionThese findings confirm that frequency domain analysis can avoid ambiguity arising in assessing the three types of pulses in the time domain. Further studies of other pulses in the frequency domain are required to develop a precise electronic pulse diagnoser.

Arterial stiffness alone does not explain arteriovenous fistula outcomes.

Marked arterial adaptation is critical in permitting and sustaining the increased blood flow within an arteriovenous fistula (AVF). The aim of this investigation was to evaluate markers of arterial disease and their association with the early post-operative AVF outcomes. We included all patients in whom an AVF had been performed after enrolment to the Renal Impairment In Secondary Care (RIISC) study. Primary AVF failure (PFL) was defined as thrombosis at six-week review. All patients underwent BP Tru and Vicorder pulse wave analysis assessments and also had assays of advanced glycation end-products prior to AVF formation. These were correlated with the short-term AVF outcomes. One hundred and eight AVFs were created in 86 patients. The primary patency (PPT) group were found to have significantly higher body mass index (BMI) (p = 0.01). Intraluminal vein diameter was significantly greater in the PPT group than the PFL group (p≤0.01). Mean augmentation index and augmentation index 75 was significantly higher in the PPT group than the PFL group (p = 0.03 and 0.03, respectively). Aortic pulse wave velocity was slower in the PPT group at 10.2 m/s than the PFL group at 10.8 m/s (p = 0.32). Advanced glycation end-product measurements did not vary significantly between the PPT and PFL groups (p = 0.4). Logistic regression analysis provided a predictive model, which demonstrated a predictive value of 78.1% for AVF patency at 6 weeks. All patients in this end-stage renal disease cohort have significant aortic stiffness. The results for pulse wave velocity were slower in the PPT group suggesting a tendency towards stiffer vessels and PFL.

Resting spontaneous baroreflex sensitivity and cardiac autonomic control in anabolic androgenic steroid users

OBJECTIVES:Misuse of anabolic androgenic steroids in athletes is a strategy used to enhance strength and skeletal muscle hypertrophy. However, its abuse leads to an imbalance in muscle sympathetic nerve activity, increased vascular resistance, and increased blood pressure. However, the mechanisms underlying these alterations are still unknown. Therefore, we tested whether anabolic androgenic steroids could impair resting baroreflex sensitivity and cardiac sympathovagal control. In addition, we evaluate pulse wave velocity to ascertain the arterial stiffness of large vessels.METHODS:Fourteen male anabolic androgenic steroid users and 12 nonusers were studied. Heart rate, blood pressure, and respiratory rate were recorded. Baroreflex sensitivity was estimated by the sequence method, and cardiac autonomic control by analysis of the R-R interval. Pulse wave velocity was measured using a noninvasive automatic device.RESULTS:Mean spontaneous baroreflex sensitivity, baroreflex sensitivity to activation of the baroreceptors, and baroreflex sensitivity to deactivation of the baroreceptors were significantly lower in users than in nonusers. In the spectral analysis of heart rate variability, high frequency activity was lower, while low frequency activity was higher in users than in nonusers. Moreover, the sympathovagal balance was higher in users. Users showed higher pulse wave velocity than nonusers showing arterial stiffness of large vessels. Single linear regression analysis showed significant correlations between mean blood pressure and baroreflex sensitivity and pulse wave velocity.CONCLUSIONS:Our results provide evidence for lower baroreflex sensitivity and sympathovagal imbalance in anabolic androgenic steroid users. Moreover, anabolic androgenic steroid users showed arterial stiffness. Together, these alterations might be the mechanisms triggering the increased blood pressure in this population.

Stiff vessels approached in a flexible way: Advancing quantification and interpretation of arterial stiffness

IntroductionAlthough pulse wave velocity (PWV), a proxy of arterial stiffness, is a strong predictor of cardiovascular complications, it is confounded by blood pressure (BP) and heart rate at the time of examination. Furthermore, establishing whether an artery behaves stiffer or less stiff does not inform a clinician on the cause of the stiffening. Quantification of arterial stiffnessThis paper focuses on BP as a confounder of PWV. We developed a method to patient-specifically determine the dependence of PWV on BP — on average 1 m/s per 10 mmHg diastolic BP — and used it to disentangle BP-dependent and -independent stiffening in hypertension and cancer patients. We furthermore showed that the so-called cardio-ankle vascular index (CAVI) — a measure deemed BP-independent — shows a residual BP-dependence that is readily correctable using a modified equation (CAVI0). Both developed methods are directly applicable to clinical measurements in individual patients. Interpretation of arterial stiffnessWe developed a computer modelling procedure to disentangle contributions of the individual wall components — collagen, elastin, and smooth muscle — to arterial stiffening as observed in patients. Our model-based approach shows that with ageing, the biomechanical phenotype shifts from elastin-dominated to collagen-dominated load bearing.Model-based assessment of arterial wall mechanics provides a promising tool to further improve interpretation of arterial stiffness measurements in patients. Further development of such methodology applied to various mouse models may improve the understanding and interpretation of arterial stiffening in ageing and disease.

Stiff vessels approached in a flexible way: Advancing quantification and interpretation of arterial stiffness

IntroductionAlthough pulse wave velocity (PWV), a proxy of arterial stiffness, is a strong predictor of cardiovascular complications, it is confounded by blood pressure (BP) and heart rate at the time of examination. Furthermore, establishing whether an artery is stiffened or not does not inform a clinician on the cause of the stiffening.Quantification of PWV’s confoundersThis talk will focus on BP as a confounder of PWV. We developed a method to patient-specifically determine the dependence of PWV on BP—on average 1 m/s per 10 mmHg diastolic BP—and used it to disentangle BP-dependent and -independent stiffening in hypertension and cancer patients. We furthermore showed that cardio-ankle vascular index (CAVI)—a measure that is often presented as BP-independent—shows a residual BP dependence that can be readily corrected using a modified equation (CAVI0). Both developed methods are directly applicable to clinical measurement data from individual patients.Interpretation of changes in PWVWe developed a computer modelling procedure to disentangle contributions of the individual wall components—collagen, elastin, and smooth muscle—to arterial stiffening in patient data. We used this approach to show that with ageing, the biomechanical phenotype shifted from elastin-dominated to collagen-dominated load bearing.OutlookModel-based interpretation of arterial mechanics provides a promising tool to further improve understanding of arterial stiffening. In my future career, I will use such methodology to study stiffening in various mouse models. The results of these studies can potentially be used to further improve understanding and interpretation of arterial stiffening in patients.

ЖЕСТКОСТЬ АРТЕРИАЛЬНЫХ СОСУДОВ: ОСНОВНЫЕ ДЕТЕРМИНАНТЫ, МЕТОДЫ ОЦЕНКИ И СВЯЗЬ С ОЖИРЕНИЕМ У ДЕТЕЙ (ОБЗОР ЛИТЕРАТУРЫ)

The review reflects the features of the structure and function of the arteries. The physiological mechanism of the formation of the pulse wave is described, and various levels of arterial pressure in the aorta and peripheral arteries are explained. Disorders of hemodynamics with a change in resilient-elastic properties of arterial vessels are described. Amplification and augmentation - factors modifying the pulse wave are presented. Also the paper describes the main methods of measuring arterial stiffness at the local, regional and system level, the advantage of direct measurement of the parameters related to the stiffness of the arterial wall, and the method of assessing the local and regional rigidity of the arteries. Separately, a method for determining pulse wave velocity in the carotid-femoral region was presented. Data of age impact on the structure and function of the arteries are presented. As it has been shown it is necessary to study parameters characterizing arterial rigidity in obese children, since this disease increases the incidence of cardiovascular complications in both adults and children. The relationship between the stiffness of arterial vessels and obesity children is considered. Various results of studies of arterial stiffness in children with obesity are presented. The lack of a consensus on the use of method of arterial vessels rigidity studying in childhood patients shows the need for further study of vascular remodeling and factors that may affect the structure of arteries in obese children.

Arterial pulse attenuation prediction using the decaying rate of a pressure wave in a viscoelastic material model

The present study examines the possibility of attenuating blood pulses by means of introducing prosthetic viscoelastic materials able to absorb energy and damp such pulses. Vascular prostheses made of polymeric materials modify the mechanical properties of blood vessels. The effect of these materials on the blood pulse propagation remains to be fully understood. Several materials for medical applications, such as medical polydimethylsiloxane or polytetrafluoroethylene, show viscoelastic behavior, modifying the original vessel stiffness and affecting the propagation of blood pulses. This study focuses on the propagation of pressure waves along a pipe with viscoelastic materials using the Maxwell and the Zener models. An expression of exponential decay has been obtained for the Maxwell material model and also for low viscous coefficient values in the Zener model. For relatively high values of the viscous term in the Zener model, the steepest part of the pulse can be damped quickly, leaving a smooth, slowly decaying wave. These mathematical models are critical to tailor those materials used in cardiovascular implants to the mechanical environment they are confronted with to repair or improve blood vessel function.

Robust and practical non-invasive estimation of local arterial wave speed and mean blood velocity waveforms

Objective: Local arterial wave speed, a surrogate of vessel stiffness, can be estimated via the pressure-velocity (PU) and diameter-velocity (ln(D)U) loop methods. These assume negligible early-systolic reflected waves (RWes) and require measurement of cross-sectionally averaged velocity (Umean), which is related to volumetric blood flow. However, RWes may not always be negligible and Doppler ultrasound typically provides maximum velocity waveforms or estimates of mean velocity subject to various errors (Uraw). This study investigates how these issues affect wave speed estimation and explores more robust methods for obtaining local wave speed and Umean. Approach: Using aortic phase-contrast MRI (PCMRI, n = 34) and a simulated virtual cohort (n = 3325), we assessed errors in calculated wave speed caused by RWes and use of Uraw rather than true Umean. By combining PUraw and ln(D)Uraw loop wave speed values, (i) a corrected wave speed (ln(D)P), insensitive to RWes and velocity errors, was derived; and (ii) a novel method for estimating Umean from Uraw was proposed (where Uraw can be any scaled version of Umean). Main results: Proof-of-principle was established via PCMRI data and in the ascending aorta, carotid, brachial and femoral arteries of the virtual cohort, with acceptably low wave speed and Umean errors obtained even when local pressure was estimated from diameter and mean/diastolic brachial pressures. Significance: Given a locally measured diameter waveform and brachial cuff pressures, (i) the velocity- and RWes-independent ln(D)P method can be applied non-invasively and is likely more robust than ln(D)U and PU loop methods; and (ii) Umean can be estimated from routinely-acquired Uraw.

Arterial stiffness and its association with clustering of metabolic syndrome risk factors

BackgroundMetabolic syndrome (MetS) is associated with structural and functional vascular abnormalities, which may lead to increased arterial stiffness, more frequent cardiovascular events and higher mortality. However, the role played by clustering of risk factors and the combining pattern of MetS risk factors and their association with the arterial stiffness have yet to be fully understood. Age, hypertension and diabetes mellitus seem to be strongly associated with increased pulse wave velocity (PWV). This study aimed at determining the clustering and combining pattern of MetS risk factors and their association with the arterial stiffness in non-diabetic and non-hypertensive patients.MethodsRecently diagnosed and untreated patients with MetS (n = 64, 49 ± 8 year, 32 ± 4 kg/m2) were selected, according to ATP III criteria and compared to a control group (Control, n = 17, 49 ± 6 year, 27 ± 2 kg/m2). Arterial stiffness was evaluated by PWV in the carotid-femoral segment. Patients were categorized and analyzed according MetS risk factors clustering (3, 4 and 5 factors) and its combinations.ResultsPatients with MetS had increased PWV when compared to Control (7.8 ± 1.1 vs. 7.0 ± 0.5 m/s, p < 0.001). In multivariate analysis, the variables that remained as predictors of PWV were age (β = 0.450, p < 0.001), systolic blood pressure (β = 0.211, p = 0.023) and triglycerides (β = 0.212, p = 0.037). The increased number of risk factors reflected in a progressive increase in PWV. When adjusted to systolic blood pressure, PWV was greater in the group with 5 risk factors when compared to the group with 3 risk factors and Control (8.5 ± 0.4 vs. 7.5 ± 0.2, p = 0.011 and 7.2 ± 0.3 m/s, p = 0.012). Similarly, the 4 risk factors group had higher PWV than the Control (7.9 ± 0.2 vs. 7.2 ± 0.3, p = 0.047).ConclusionsThe number of risk factors seems to increase arterial stiffness. Notably, besides age and increased systolic blood pressure, alterations in the triglycerides worsened the stiffness of large vessels, emphasizing the importance in addressing this risk factor in MetS patients.