Windkessel Effect Research Articles

Nonlinear biomechanical behaviour of extracranial carotid artery aneurysms in the framework of Windkessel effect via FSI technique

Extracranial carotid artery aneurysms (ECCA) lead to rupture and neurologic symptoms from embolisation, with potentially fatal outcomes. Investigating the biomechanical behaviour of EECA with blood flow dynamics is crucial for identifying regions more susceptible to rupture. A coupled three-dimensional (3D) Windkessel-framework and hyperelastic fluid-structure interaction (FSI) analysis of ECCAs with patient-specific geometries, was developed in this paper with a particular focus on hemodynamic parameters and the arterial wall's biomechanical response. The blood flow has been modelled as non-Newtonian, pulsatile, and turbulent. The biomechanical characteristics of the aneurysm and artery are characterised employing a 5-parameter Mooney-Rivlin hyperelasticity model. The Windkessel effect is also considered to efficiently simulate pressure profile of the outlets and to capture the dynamic changes over the cardiac cycle. The study found the aneurysm carotid artery exhibited the high levels of pressure, wall shear stress (WSS), oscillatory shear index (OSI), and relative residence time (RRT) compared to the healthy one. The deformation of the arterial wall and the corresponding von Mises (VM) stress were found significantly increased in aneurysm cases, in comparison to that of no aneurysm cases, which strongly correlated with the hemodynamic characteristics of the blood flow and the geometric features of the aneurysms. This escalation would intensify the risk of aneurysm wall rupture. These findings have critical implications for enhancing treatment strategies for patients with extracranial aneurysms.

Role of Vascular Function in the Prognosis of Heart Failure Patients.

Background: Blood vessels have the Windkessel effect and are involved in blood circulation. The breakdown of this mechanism is also involved in the pathogenesis of heart failure (HF); however, the relationship between vascular dysfunction and HF prognosis is not fully understood. Methods: We evaluated 214 patients hospitalized for HF at our institution who underwent a cardio-ankle vascular index (CAVI), which evaluates vascular function, between January 2012 and July 2018. To investigate factors (including CAVI) associated with major adverse cardiac events (MACE) during 1 year after patients with HF were discharged, we evaluated clinical profiles, blood tests, chest X-P, 12-lead electrocardiography, and transthoracic echocardiographic findings. MACE was defined as cardiovascular death or readmission for HF. Results: The severity of HF between the MACE and non-MACE was not significantly different. Previous HF and chronic kidney disease were significantly more common in the MACE group. CAVI and % mean atrial pressure in the MACE group were statistically higher than those in the non-MACE group. The cardiac shadow as shown by chest X-P and left ventricular size in the MACE group were significantly bigger, and HF preserved ejection fraction (EF) (EF > 50%) was significantly more common in the MACE group. In multivariate analysis, CAVI was an independent predictive factor for the occurrence of MACE (model 1; hazard ratio (HR): 1.33, 95% confidence interval (CI): 1.05-1.68, p = 0.018; model 2; HR: 1.31, 95% CI: 1.07-1.60, p = 0.009). Conclusions: Because high CAVI is associated with poor prognosis of HF, these patients require more careful treatment.

From sucking worms to Windkessel: The physics of an early eighteenth century firefighting device

We describe the physics of the “Windkessel effect” and its role in smoothing the output of water produced by piston-driven pumps found in early fire engines and modern residential well houses. We also construct a simple, analytical model of its operation and apply this model to the Windkessel in Richard Newsham's 1725 fire engine. We find that Newsham's Windkessel reduces the variations in the pump output stream from a high of 80% to a low of 16%.

The Pathogenesis and Impact of Arterial Stiffening in Hypertension: The 2023 John H. Laragh Research Award.

Fifty years ago, Dr. John Laragh brought forward the "vasoconstriction-volume hypothesis" of hypertension. This is Ohm's Law in blood pressure regulation, explicating hypertension as a consequence of increased peripheral vascular resistance, cardiac output, or both. Resistance vessels, those of a diameter less than 200 μm, determines mean arterial pressure by controlling peripheral vascular resistance. In comparison, large capacitance arteries, particularly the aorta, confines the systolic and diastolic blood pressure in physiological range through the "windkessel effect." Loss of this cushioning function results in aortic stiffening and isolated systolic hypertension, both of which are independently associated with increased risk for coronary, cerebral, and renal diseases. Aortic stiffening is both a cause and a consequence of hypertension. On one hand, aortic stiffness precedes the onset of hypertension in populations and experimental models, and hemodynamic derangements related to aortic stiffening contributes to the development of hypertension by promoting renal dysfunction. On the other hand, the vasculature itself is a hypertensive target organ and hypertensive mechanical stretch directly induces the pathogenesis of aortic adventitial remodeling. Various cell types, including bone marrow-derived circulating fibrocytes, vascular stem cell antigen-1 positive progenitors, and endothelial to mesenchymal transition, and to a lesser extent resident fibroblasts, contribute to adventitial matrix deposition and aortic stiffening in hypertension. Vascular smooth muscle stiffness is another important contributor of aortic stiffening. Understanding the roles of immune components and specific signal pathways in the pathogenesis aortic stiffening paves the path to novel antihypertensive and anti-fibrosis therapies.

Biomechanics of abdominal aortic aneurysm in the framework of Windkessel effect and fully-developed inflow velocity via two-way non-linear FSI

Abdominal aortic aneurysm (AAA) is a pathological condition characterised by localised dilation of the infrarenal aorta, which can be fatal if rupture occurs. Current diagnostic criteria for repair are not patient-specific, but computational modelling may help to predict the potential growth and risk of AAA rupture accurately. This paper highlights how important using the Windkessel effect and fully-developed inflow velocity framework for the biomechanical analysis of AAA is; in other words, this research investigates how different boundary conditions in modelling methods affect the ability to correctly represent the biomechanics of AAA with complex non-linear parameters using a two-way fluid–structure interaction (FSI) technique. Time-averaged wall shear stress (TAWSS) is highly sensitive to boundary conditions, so unrealistic or simplified boundary conditions can lead to very different TAWSS results. This study also revealed that the use of outflow 3-element Windkessel boundary conditions on pulsatile pressure affects the flow pattern and increases the flow recirculation period. By accounting for the Windkessel effect and preventing backflow in numerical studies of AAA, the maximum displacement found in the distal branches can also be reduced. Models assuming plug velocity profiles overestimate peak wall stress by approximately 20% compared with models using fully developed parabolic inlet velocity profiles. This study incorporated a three-layer anisotropic material model and non-Newtonian fluid properties into the simulation, providing a more realistic representation of the effect of boundary condition selection on AAA mechanics. The results summarised from the parametric study could contribute to better prediction of AAA growth and rupture risk, and have important implications for the development of improved treatment strategies for AAA patients.

Early vertebral artery thrombosis presenting as subclavian steal by virtue of windkessel and venturi effect

Reversed flow in elastic vessels, especially if partially obstructed, is a common phenomenon. Spectral Doppler ultrasound can assess underlying flow dynamics but is technician dependent and needs clinical correlation to avoid misdiagnosis. Vertebral artery backflow can be explained by Windkessel effect, Venturi effect or true Steal syndrome.

Modifying the ICP pulse wave: effects on parenchymal blood flow pulsatility.

Pulsation of the cerebral blood flow (CBF) produces intercranial pressure (ICP) waves. The aim of this study is to determine whether externally modifying ICP pulsatility alters parenchymal blood flow pulsatility. A cardiac-gated inflatable device was inserted in the lateral epidural space of 12 anesthetized canines (canis familiaris) and used to cause reduction, inversion, and augmentation of the ICP pulse. CBF in each hemisphere was measured using laser Doppler velocimetry. A significant increase in both mean CBF and its amplitude was observed for reduction as well as inversion of the ICP pulse, with larger changes observed for the inversion protocol. Significant increases in the mean CBF were also observed ipsilaterally for the augmentation protocol together with indications of reduced CBF amplitude contralaterally. External alteration of the ICP pulse thus caused significant changes in parenchymal blood flow pulsatility. The inverse relationship between the ICP and CBF amplitude suggests that the changes did not occur via modification of the intracranial Windkessel mechanism. Thus, the effects likely occurred in the low-pressure vessels, i.e., capillaries and/or venules, rather than the high-pressure arteries. Future MRI studies are however required to map and quantify the effects on global cerebral blood flow.NEW & NOTEWORTHY This study demonstrated that external modification of ICP pulsatility, using a cardiac-gated inflatable device implanted epidurally in canines, alters brain tissue blood flow pulsatility. Specifically, decreasing systolic ICP increased blood flow pulsatility in brain tissue. The results suggest that the altered CBF pulsatility is unlikely to depend on modification of the Windkessel effect on the feeding arterial system but was rather an effect directly on tissue and the lower pressure distal vessels.

Why don't ventricles dilate in pseudotumor cerebri? A circuit model of the cerebral windkessel.

Pseudotumor cerebri is a disorder of intracranial dynamics characterized by elevated intracranial pressure (ICP) and chronic cerebral venous hypertension without structural abnormalities. A perplexing feature of pseudotumor is the absence of the ventriculomegaly found in obstructive hydrocephalus, although both diseases are associated with increased resistance to cerebrospinal fluid (CSF) resorption. Traditionally, the pathophysiology of ventricular dilation and obstructive hydrocephalus has been attributed to the backup of CSF due to impaired absorption, and it is unclear why backup of CSF with resulting ventriculomegaly would not occur in pseudotumor. In this study, the authors used an electrical circuit model to simulate the cerebral windkessel effect and explain the presence of ventriculomegaly in obstructive hydrocephalus but not in pseudotumor cerebri. The cerebral windkessel is a band-stop filter that dampens the arterial blood pressure pulse in the cranium. The authors used a tank circuit with parallel inductance and capacitance to model the windkessel. The authors distinguished the smooth flow of blood and CSF and the pulsatile flow of blood and CSF by using direct current (DC) and alternating current (AC) sources, respectively. The authors measured the dampening notch from ABP to ICP as the band-stop filter of the windkessel. In obstructive hydrocephalus, loss of CSF pathway volume impaired the flow of AC power in the cranium and caused windkessel impairment, to which ventriculomegaly is an adaptation. In pseudotumor, venous hypertension affected DC power flow in the capillaries but did not affect AC power or the windkessel, therefore obviating the need for adaptive ventriculomegaly. In pseudotumor, the CSF spaces are unaffected and the windkessel remains effective. Therefore, ventricles remain normal in size. In hydrocephalus, the windkessel, which depends on the flow of AC power in patent CSF spaces, is impaired, and the ventricles dilate as an adaptive process to restore CSF pathway volume. The windkessel model explains both ventriculomegaly in obstructive hydrocephalus and the lack of ventriculomegaly in pseudotumor. This model provides a novel understanding of the pathophysiology of disorders of CSF dynamics and has significant implications in clinical management.

Mechanical response in elastic fluid flow networks

Compliance in fluid carrying vessels is the capability of interacting with flow and attenuating waves via mechanisms such as the Windkessel effect. In this paper we investigate how vessel compliance impacts the dynamics of flow and pressure in the transient regime shortly after changes in boundary conditions. We show that individual vessels as well as networks composed of many such vessels can exist in one of two possible regimes, one in which transient dynamics are fast and one in which it is slow. These results can be used to analyze the response capabilities of biological flow networks such as the animal vasculature.

Is It Good to Have a Stiff Aorta with Aging? Causes and Consequences.

Aortic stiffness increases with advancing age, more than doubling during the human life span, and is a robust predictor of cardiovascular disease (CVD) clinical events independent of traditional risk factors. The aorta increases in diameter and length to accommodate growing body size and cardiac output in youth, but in middle and older age the aorta continues to remodel to a larger diameter, thinning the pool of permanent elastin fibers, increasing intramural wall stress and resulting in the transfer of load bearing onto stiffer collagen fibers. Whereas aortic stiffening in early middle age may be a compensatory mechanism to normalize intramural wall stress and therefore theoretically "good" early in the life span, the negative clinical consequences of accelerated aortic stiffening beyond middle age far outweigh any earlier physiological benefit. Indeed, aortic stiffness and the loss of the "windkessel effect" with advancing age result in elevated pulsatile pressure and flow in downstream microvasculature that is associated with subclinical damage to high-flow, low-resistance organs such as brain, kidney, retina, and heart. The mechanisms of aortic stiffness include alterations in extracellular matrix proteins (collagen deposition, elastin fragmentation), increased arterial tone (oxidative stress and inflammation-related reduced vasodilators and augmented vasoconstrictors; enhanced sympathetic activity), arterial calcification, vascular smooth muscle cell stiffness, and extracellular matrix glycosaminoglycans. Given the rapidly aging population of the United States, aortic stiffening will likely contribute to substantial CVD burden over the next 2-3 decades unless new therapeutic targets and interventions are identified to prevent the potential avalanche of clinical sequelae related to age-related aortic stiffness.

Deletion of type VIII collagen reduces blood pressure, increases carotid artery functional distensibility and promotes elastin deposition

Arterial stiffening is a significant predictor of cardiovascular disease development and mortality. In elastic arteries, stiffening refers to the loss and fragmentation of elastic fibers, with a progressive increase in collagen fibers. Type VIII collagen (Col-8) is highly expressed developmentally, and then once again dramatically upregulated in aged and diseased vessels characterized by arterial stiffening. Yet its biophysical impact on the vessel wall remains unknown. The purpose of this study was to test the hypothesis that Col-8 functions as a matrix scaffold to maintain vessel integrity during extracellular matrix (ECM) development. These changes are predicted to persist into the adult vasculature, and we have tested this in our investigation. Through our in vivo and in vitro studies, we have determined a novel interaction between Col-8 and elastin. Mice deficient in Col-8 (Col8−/−) had reduced baseline blood pressure and increased arterial compliance, indicating an enhanced Windkessel effect in conducting arteries. Differences in both the ECM composition and VSMC activity resulted in Col8−/− carotid arteries that displayed increased crosslinked elastin and functional distensibility, but enhanced catecholamine-induced VSMC contractility. In vitro studies revealed that the absence of Col-8 dramatically increased tropoelastin mRNA and elastic fiber deposition in the ECM, which was decreased with exogenous Col-8 treatment. These findings suggest a causative role for Col-8 in reducing mRNA levels of tropoelastin and the presence of elastic fibers in the matrix. Moreover, we also found that Col-8 and elastin have opposing effects on VSMC phenotype, the former promoting a synthetic phenotype, whereas the latter confers quiescence. These studies further our understanding of Col-8 function and open a promising new area of investigation related to elastin biology.

Microstructural and mechanical characterization of the layers of human descending thoracic aortas

The mechanical properties of human aortas are linked to the layered tissue and its microstructure at different length scales. Each layer has specific mechanical and structural properties. While the ground substance and the elastin play an important role in tissue stiffness at small strain, collagen fibers carry most of the load at larger strains, which corresponds to the physiological conditions of the aorta at maximum pulsatile blood pressure. In fact, collagen fibers are crimped in the unloaded state. Collagen fibers show different orientation distributions when they are observed in a plane that is tangent to the aortic wall (in-plane section) or along a direction orthogonal to it (out-of-plane section). This was systematically investigated using large images (2500 × 2500 µm) with high resolution obtained by second harmonic generation (SHG) in order to homogenize tissue heterogeneity after a convergence analysis, which is a main goal of the study. In addition, collagen fibers show lateral interactions due to entanglements and the presence of transverse elastin fibers, observed on varying length scales using atomic force microscopy and a three-dimensional rendering obtained by stacking a sequence of SHG and two-photon fluorescence images; this is another important contribution. Human descending thoracic aortas from 13 heartbeat donors aged 28 to 66 years were examined. Uniaxial tensile tests were carried out on the longitudinal and circumferential strips of the aortic wall and the three separated layers (intima, media and adventitia). A structurally-motivated material model with (i) a term to describe the combined response of ground substance and elastin and (ii) terms to consider four families of collagen fibers with different directions was applied. The exclusion of compressed fibers was implemented in the fitting process of the experimental data, which was optimized by a genetic algorithm. The results show that a single fiber family with directional and dispersion parameters measured from SHG images can describe the mechanical response of all 39 layers (3 layers for each of the 13 aortas) with very good accuracy when a second (auxiliary) family of aligned fibers is introduced in the orthogonal direction to account for lateral fiber interaction. Indeed, all observed distributions of collagen directions can be accurately fitted by a single bivariate von Mises distribution. Statistical analysis of in-plane and out-of-plane dispersion of fiber orientations reveals structural differences between the three layers and a change of collagen dispersion parameters with age. Statement of significanceThe stiffness of healthy young aortas is adjusted so that a diameter expansion of about 10 % is possible during the heartbeat. This creates the Windkessel effect, which smooths out the pulsating nature of blood flow and benefits organ perfusion. The specific elastic properties of the aorta that are required to achieve this effect are related to the microstructure of the aortic tissue at different length scales. An increase in the aortic stiffness, in addition to reducing cyclic expansion and worsening perfusion, is a risk factor for clinical hypertension. The present study relates the microstructure of healthy human aortas to the mechanical response and examines the changes in microstructural parameters with age, which is a key factor in increasing stiffness.

Ascending aorta mechanics and dimensions in aortopathy - from science to application.

The ascending aorta has a unique microstructure and biomechanical properties that allow it to absorb energy during systole and return energy during diastole (Windkessel effect). Derangements in aortic architecture can result in changes to biomechanics and inefficiencies in function. Ultimately biomechanical failure may occur resulting in aortic dissection or rupture. By measuring aortic biomechanics with either in vivo or ex vivo methods, one may be able to predict tissue failure in patients with aortic disease such as aneurysms. An understanding of the biomechanical changes that lead to these tissue-level failures may help guide therapy, disease surveillance, surgical intervention, and aid in the development of new treatments for this deadly condition.

The Incidence of Transverse Sinus Stenosis in Multiple Sclerosis: Further Evidence of Pulse Wave Encephalopathy

BackgroundMultiple sclerosis (MS) is associated with a breakdown in the intracranial pulse wave dampening or windkessel effect. This is manifest by an increase in the arterial stroke volume and a decrease in the dampening afforded by both the CSF displaced into the spinal canal and the blood displaced by the venous sinus pulsation. There is evidence that the reduction in compliance of the sagittal and straight sinuses in MS is caused by an increase in venous pressure despite the jugular bulb pressures being normal. This implies MS patients have a venous outflow stenosis somewhere between the torcular and jugular bulbs. The purpose of the current study is to define the site, significance and cause of these stenoses. Methods50 patients with MS were prospectively recruited from an MS clinic and compared to 50 matched control patients. Using 3DT1 post contrast images, a survey of the venous sinuses was performed looking for the narrowest portion of the sinuses in each of 4 segments from the sagittal sinus to jugular bulbs. The cross sectional areas and wetted circumferences of the venous sinuses were measured at each site to calculate the minimum hydraulic and effective diameters. The BMI, optic nerve sheath diameters and pituitary heights were measured. Statistical analysis was performed using non-parametric methods and was assessed using α≤0.05. ResultsCompared to controls, the MS patients’ sagittal sinuses were 24% larger in cross-section (p=0.0001) with an 18% larger wetted circumference (p=0.0001). The MS patients’ transverse sinuses had an average effective stenosis of 38% by area (p<0.0001) with 8/50 patients having a high grade stenosis of >65% by area and 16/50 a low grade stenosis of between 40-65% by area compared to 1/50 low grade stenoses in this segment in the controls. The commonest cause of the stenosis was a giant arachnoid granulation. The optic nerve sheaths were larger in MS than controls (p=0.0006). Comparing MS patients with transverse sinus stenosis to those without, the pituitary height was 16% smaller and BMI 25% larger (p=0.02 and 0.003 respectively) ConclusionIn patients with MS, the reduction in venous sinus compliance is associated with venous outflow stenoses in the transverse sinuses which increases the upstream venous pressure and dilates the sagittal sinuses. This finding suggests a continuum exists between MS and idiopathic intracranial hypertension.

Mimicking "J-Shaped" and Anisotropic Stress-Strain Behavior of Human and Porcine Aorta by Fabric-Reinforced Elastomer Composites.

An ex vivo heart perfusion device preserves the donor heart in a warm beating state during transfer between extraction and implantation surgeries. One of the current challenges includes the use of rigid and noncompliant plastic tubes, which causes injuries to the heart at the junction between the tissue and the tube. The compliant and rapidly strain-stiffening mechanical property that generates a "J-shaped" stress-strain behavior is necessary for producing the Windkessel effect, which ensures continuous flow of blood through the aorta. In this study, we mimic the J-shaped and anisotropic stress-strain behavior of human aorta in synthetic elastomers to replace the problematic noncompliant plastic tube. First, we assess the mechanical properties of human (n = 1) and porcine aorta (n = 14) to quantify the nonlinear and anisotropic behavior under uniaxial tensile stress from five different regions of the aorta. Second, fabric-reinforced elastomer composites were prepared by reinforcing silicone elastomers with embedded fabrics in a trilayer geometry. The knitted structures of the fabric provide strain-stiffening as well as anisotropic mechanical properties of the resulting composite in a deterministic manner. By optimizing the combination between different elastomers and fabrics, the resulting composites matched the J-shaped and anisotropic stress-strain behavior of natural human and porcine aorta. Finally, improved analytical constitutive models based on Gent's and Mooney-Rivlin's constitutive model (to describe the elastomer matrix) combined with Holzapfel-Gasser-Ogden's model (to represent the stiffer fabrics) were developed to describe the J-shaped behavior of the natural aortas and the fabric-reinforced composites. We anticipate that the suggested fabric-reinforced silicone elastomer composite design concept can be used to develop complex soft biomaterials, as well as in emerging engineering fields such as soft robotics and microfluidics, where the Windkessel effect can be useful in regulating the flow of fluids.

Multifaceted Mechanisms of Vascular Calcification in Aging.

Approximately 20% of the world's population will be around or above 65 years of age by the next decade. Out of these, 40% are suspected to have cardiovascular diseases as a cause of mortality. Arteriosclerosis, characterized by increased vascular calcification, impairing Windkessel effect and tissue perfusion, and determining end-organ damage, is a hallmark of vascular pathology in the elderly population. Risk factors accumulated during aging affect the normal physiological and vascular aging process, which contributes to the progression of arteriosclerosis. Traditional risk factors, age-associated diseases, and respective regulating mechanisms influencing vascular calcification and vascular stiffness have been extensively studied for many years. Despite the well-known fact that aging alone can induce vascular damage, specific mechanisms that implicate physiological aging in vascular calcification, contributing to vascular stiffness, are poorly understood. This review focuses on mechanisms activated during normal aging, for example, cellular senescence, autophagy, extracellular vesicles secretion, and oxidative stress, along with the convergence of premature aging models' pathophysiology, such as Hutchinson-Gilford Progeria (prelamin accumulation) and Klotho deficiency, to understand vascular calcification in aging. Understanding the mechanisms of vascular damage in aging that intersect with age-associated diseases and risk factors is crucial to foster innovative therapeutic targets to mitigate cardiovascular disease. Visual Overview- An online visual overview is available for this article.

A Flow Dynamic Rationale for Accelerated Vascularized Composite Allotransplant Rejection.

From 1996 to 2000, Diefenbeck et al. carried out six knee vascularized composite allotransplants. The allotransplants were composed of bone, soft tissue, and femoral vascular pedicle (25 to 40 cm). All rejected between 14 and 56 months. Failures were attributed to chronic rejection. In 2008, the Louisville team lost their fourth patient's hand transplant at 8 months. During the rejection workup, intraoperative findings noted a thickened arterial pedicle attributed to intimal hyperplasia with significant fibrotic perivascular tissue and a near "no-flow phenomenon." No cutaneous rejection was appreciated and failure was attributed to chronic rejection. Data were collected from two teams, one in Germany and the other in Louisville, Kentucky. The population under study consisted of the six knee and one hand transplants. The factor of interest was the long donor arterial pedicle. The outcome measurements were transplant survival time and histopathologic results. There are only seven published vascularized composite allotransplant cases where a donor artery longer than 25 cm was used. This cohort represents a 100 percent accelerated failure rate. The cause of these losses remains unexplained. The donor arteries suffered from T-cell-mediated rejection and ischemia-induced media/adventitial necrosis. We hypothesize that the donor artery rejected at an accelerated rate because of ischemia caused by disruption of the external vasa vasorum in conjunction with intimal hyperplasia induced by T-cell-mediated rejection that led to disruption of the Windkessel effect. Loss of this effect presented as intimal hyperplasia accelerated by ischemia causing an expedited transplant failure. Therapeutic, V.

Experiments on dynamic behaviour of a Dacron aortic graft in a mock circulatory loop

Woven Dacron grafts are currently used for the surgical treatment of aortic aneurysm and acute dissection, two otherwise fatal pathologies when aortic wall rupture occurs. While Dacron is chosen for aortic grafts because of characteristics such as biocompatibility and durability, few data are available about the dynamic response of Dacron prosthetic devices and about their side effects on the cardiovascular system. In this study, a Dacron graft was subjected to physiological flow conditions in a specifically-developed mock circulatory loop. Experiments were conducted at different physiological pulsation-per-minute rates. Results show that, in comparison to an aortic segment of the same length, the prosthesis is extremely stiffer circumferentially, thus limiting the dynamical radial expansion responsible for the Windkessel effect in human arteries. The prosthesis is instead excessively compliant in the axial direction and develops preferentially bending oscillations. This very different dynamic behaviour with respect to the human aorta can alter cardiovascular pressure and flow dynamics resulting in long-term implant complications.

Simulación del Corazón Izquierdo para Aplicaciones en Docencia e Investigación

Un modelo es una descripción lógica de cómo un sistema funciona o cómo se comportan sus componentes. Las herramientas de la modelización dinámica facilitan mucho la construcción de los modelos. El objetivo de este artículo es mostrar el desarrollo y los resultados del funcionamiento de un modelo interactivo de la fisiología del sistema cardiocirculatorio para el uso de estudiantes y otros interesados en la fisiología cardiovascular. El sistema de simulación está compuesto por un modelo simple de cuatro componentes, y simula las siguientes variables y parámetros: a) variaciones del volumen aurícula izquierda (AI) y ventrículo izquierdo (VI); b) variaciones presión en AI, VI y aorta (Ao); c) flujo a través de válvula mitral (VM) y válvula aórtica (VAo), y d) reproduce el “efecto Windkessel” en Ao. Se utilizó el entorno de modelización Extend el cual provee una estructura integrada para la construcción de modelos de simulación y el desarrollo de nuevas herramientas de simulación. El corazón derecho y la circulación pulmonar no son considerados. Los resultados de este modelo simulan las características generales del corazón izquierdo y de la circulación arterial, considerando distintas situaciones fisiológicas y patológicas.

Living Without a Pulse: The Vascular Implications of Continuous-Flow Left Ventricular Assist Devices.

Pulsatility seems to have a teleological role because evolutionary hierarchy favors higher ordered animals with more complex, multichamber circulatory systems that generate higher pulse pressure compared with lower ordered animals. Yet despite years of such natural selection, the modern generation of continuous-flow left ventricular assist devices (CF-LVADs) that have been increasingly used for the last decade have created a unique physiology characterized by a nonpulsatile, nonlaminar blood flow profile with the absence of the usual large elastic artery Windkessel effect during diastole. Although outcomes and durability have improved with CF-LVADs, patients supported with CF-LVADs have a high rate of complications that were not as frequently observed with older pulsatile devices, including gastrointestinal bleeding from arteriovenous malformations, pump thrombosis, and stroke. Given the apparent fundamental biological role of the pulse, the purpose of this review is to describe the normal physiology of ventricular-arterial coupling from pulsatile flow, the effects of heart failure on this physiology and the vasculature, and to examine the effects of nonpulsatile blood flow on the vascular system and potential role in complications seen with CF-LVAD therapy. Understanding these concomitant vascular changes with CF-LVADs may be a key step in improving patient outcomes as modulation of pulsatility and flow characteristics may serve as a novel, yet simple, therapy for reducing complications.