Relevant bibliographies by topics / Hemodynamic loading

Academic literature on the topic 'Hemodynamic loading'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Hemodynamic loading.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Hemodynamic loading"

1

Fujimoto, Naoki, Barry A. Borlaug, Gregory D. Lewis, Jeffrey L. Hastings, Keri M. Shafer, Paul S. Bhella, Graeme Carrick-Ranson, and Benjamin D. Levine. "Hemodynamic Responses to Rapid Saline Loading." Circulation 127, no. 1 (January 2013): 55–62. http://dx.doi.org/10.1161/circulationaha.112.111302.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Granton, John. "Cardiopulmonary Interactions during Positive Pressure Ventilation." Canadian Respiratory Journal 3, no. 6 (1996): 380–85. http://dx.doi.org/10.1155/1996/253907.

Full text
Abstract:
Positive pressure ventilation (PPV) may lead to significant hemodynamic alterations. The cardiocirculatory effects of PPV occur through alterations in the loading conditions of the right and left ventricle and are mediated by changes in intrathoracic pressures and in lung volume. However, the net effect of PPV on cardiac output and hemodynamics is not always predictable. PPV may lead to either a decrease or an increase in cardiac performance. The cardiac consequences of PPV are also dependent on baseline loading conditions and contractile function of the heart.
APA, Harvard, Vancouver, ISO, and other styles
3

Gefke, Maria, Niels Juel Christensen, Per Bech, Erik Frandsen, Morten Damgaard, Ali Asmar, and Peter Norsk. "Hemodynamic responses to mental stress during salt loading." Clinical Physiology and Functional Imaging 37, no. 6 (April 6, 2016): 688–94. http://dx.doi.org/10.1111/cpf.12360.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rissanen, Joonas Antero, Keijo Häkkinen, Jari Antero Laukkanen, and Arja Häkkinen. "Acute Hemodynamic Responses to Combined Exercise and Sauna." International Journal of Sports Medicine 41, no. 12 (June 29, 2020): 824–31. http://dx.doi.org/10.1055/a-1186-1716.

Full text
Abstract:
AbstractThis study investigated acute hemodynamic, plasma volume and immunological responses to four loading protocols: sauna only, and sauna after endurance, strength or combined endurance and strength exercise. Twenty-seven healthy, slightly prehypertensive men (age 32.7±6.9 years) were measured at PRE, MID (after exercise), POST, POST30min and POST24h. The measurements consisted systolic and diastolic blood pressure, heart rate, body temperature and concentrations of high-sensitive C-reactive protein, white blood cells and plasma volume measurements. Endurance+sauna showed significant decreases in systolic blood pressure at POST (–8.9 mmHg), POST30min (–11.0 mmHg) and POST24h (–4.6 mmHg). At POST30min, significant decreases were also observed in sauna (–4.3 mmHg) and combined+sauna (–7.5 mmHg). Diastolic blood pressure decreased significantly from -5.4 to –3.9 mmHg at POST in all loadings. Plasma volume decreased significantly at MID in all exercise loadings and at POST in endurance+sauna and strength+sauna. Plasma volume increased significantly (p < 0.01) in endurance+sauna and combined+sauna at POST24h. White blood cells increased following all exercise+sauna loadings at MID, POST and POST30min, whereas high sensitive C-reactive protein showed no changes at any measurement point. The combination of endurance exercise and sauna showed the greatest positive effects on blood pressure. Both loadings including endurance exercise increased plasma volume on the next day.
APA, Harvard, Vancouver, ISO, and other styles
5

Ramo, P., R. Kettunen, and L. Hirvonen. "Hemodynamic effects of endurance training on canine left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 1 (January 1, 1987): H7—H13. http://dx.doi.org/10.1152/ajpheart.1987.252.1.h7.

Full text
Abstract:
To investigate the effects of endurance training on myocardial performance seven beagle dogs (exercise group, EG) were trained by treadmill running for 6–7 wk. Before and after experimental period the EG and control group (CG, n = 7) underwent a standard submaximal exercise test (SMT), and hemodynamic status was checked during anesthesia by catheterization technique exposing the animals to different loadings: pacing, volume loading, and isoproterenol infusion. The increase of heart rate during SMT was about 30 beats/min less in the EG than in the CG. A highly linear relationship between stroke work and end-diastolic volume was observed within the groups (for EG r = 0.953, for CG r = 0.846), but the slope of the regression line obtained for EG appeared to be significantly (P less than 0.001) greater. In EG isoproterenol induced increases in end-diastolic (27%), end-systolic (37%), and stroke volumes (19%), but, on the contrary, decreases of these volumes in CG (19, 15, and 22%, respectively); ejection fraction remained unchanged for both EG and CG. Ventricular stroke work was significantly greater in EG. Systemic vascular resistance decreased in EG in every loading test. The results indicate an improved pump performance, which is related not only to the heterometric autoregulatory adjustments, but also to extracardial adaptations.
APA, Harvard, Vancouver, ISO, and other styles
6

Sedmera, David. "HLHS: Power of the Chick Model." Journal of Cardiovascular Development and Disease 9, no. 4 (April 11, 2022): 113. http://dx.doi.org/10.3390/jcdd9040113.

Full text
Abstract:
Background: Hypoplastic left heart syndrome (HLHS) is a rare but deadly form of human congenital heart disease, most likely of diverse etiologies. Hemodynamic alterations such as those resulting from premature foramen ovale closure or aortic stenosis are among the possible pathways. Methods: The information gained from studies performed in the chick model of HLHS is reviewed. Altered hemodynamics leads to a decrease in myocyte proliferation causing hypoplasia of the left heart structures and their functional changes. Conclusions: Although the chick phenocopy of HLHS caused by left atrial ligation is certainly not representative of all the possible etiologies, it provides many useful hints regarding the plasticity of the genetically normal developing myocardium under altered hemodynamic loading leading to the HLHS phenotype, and even suggestions on some potential strategies for prenatal repair.
APA, Harvard, Vancouver, ISO, and other styles
7

Rogers, Aaron J., Ramaswamy Kannappan, Hadil Abukhalifeh, Mohammed Ghazal, Jessica M. Miller, Ayman El-Baz, Vladimir G. Fast, and Palaniappan Sethu. "Hemodynamic Stimulation Using the Biomimetic Cardiac Tissue Model (BCTM) Enhances Maturation of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Cells Tissues Organs 206, no. 1-2 (2018): 82–94. http://dx.doi.org/10.1159/000496934.

Full text
Abstract:
Human induced pluripotent stem cell (hiPSC)-derived cardio­myocytes (hiPSC-CMs) hold great promise for cardiovascular disease modeling and regenerative medicine. However, these cells are both structurally and functionally ­immature, primarily due to their differentiation into cardiomyocytes occurring under static culture which only reproduces biomolecular cues and ignores the dynamic hemo­dynamic cues that shape early and late heart development during cardiogenesis. To evaluate the effects of hemodynamic stimuli on hiPSC-CM maturation, we used the biomimetic cardiac tissue model to reproduce the hemodynamics and pressure/volume changes associated with heart development. Following 7 days of gradually increasing stimulation, we show that hemodynamic loading results in (a) enhanced alignment of the cells and extracellular matrix, (b) significant increases in genes associated with physiological hypertrophy, (c) noticeable changes in sarcomeric organization and potential changes to cellular metabolism, and (d) a significant increase in fractional shortening, suggestive of a positive force frequency response. These findings suggest that culture of hiPSC-CMs under conditions that accurately reproduce hemodynamic cues results in structural orga­nization and molecular signaling consistent with organ growth and functional maturation.
APA, Harvard, Vancouver, ISO, and other styles
8

Napoli, Anthony M. "Physiologic and Clinical Principles behind Noninvasive Resuscitation Techniques and Cardiac Output Monitoring." Cardiology Research and Practice 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/531908.

Full text
Abstract:
Clinical assessment and vital signs are poor predictors of the overall hemodynamic state. Optimal measurement of the response to fluid resuscitation and hemodynamics has previously required invasive measurement with radial and pulmonary artery catheterization. Newer noninvasive resuscitation technology offers the hope of more accurately and safely monitoring a broader range of critically ill patients while using fewer resources. Fluid responsiveness, the cardiac response to volume loading, represents a dynamic method of improving upon the assessment of preload when compared to static measures like central venous pressure. Multiple new hemodynamic monitors now exist that can noninvasively report cardiac output and oxygen delivery in a continuous manner. Proper assessment of the potential future role of these techniques in resuscitation requires understanding the underlying physiologic and clinical principles, reviewing the most recent literature examining their clinical validity, and evaluating their respective advantages and limitations.
APA, Harvard, Vancouver, ISO, and other styles
9

Ogilvie, Leslie M., Brittany A. Edgett, Jason S. Huber, Mathew J. Platt, Hermann J. Eberl, Sohrab Lutchmedial, Keith R. Brunt, and Jeremy A. Simpson. "Hemodynamic assessment of diastolic function for experimental models." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 5 (May 1, 2020): H1139—H1158. http://dx.doi.org/10.1152/ajpheart.00705.2019.

Full text
Abstract:
Traditionally, the evaluation of cardiac function has focused on systolic function; however, there is a growing appreciation for the contribution of diastolic function to overall cardiac health. Given the emerging interest in evaluating diastolic function in all models of heart failure, there is a need for sensitivity, accuracy, and precision in the hemodynamic assessment of diastolic function. Hemodynamics measure cardiac pressures in vivo, offering a direct assessment of diastolic function. In this review, we summarize the underlying principles of diastolic function, dividing diastole into two phases: 1) relaxation and 2) filling. We identify parameters used to comprehensively evaluate diastolic function by hemodynamics, clarify how each parameter is obtained, and consider the advantages and limitations associated with each measure. We provide a summary of the sensitivity of each diastolic parameter to loading conditions. Furthermore, we discuss differences that can occur in the accuracy of diastolic and systolic indices when generated by automated software compared with custom software analysis and the magnitude each parameter is influenced during inspiration with healthy breathing and a mild breathing load, commonly expected in heart failure. Finally, we identify key variables to control (e.g., body temperature, anesthetic, sampling rate) when collecting hemodynamic data. This review provides fundamental knowledge for users to succeed in troubleshooting and guidelines for evaluating diastolic function by hemodynamics in experimental models of heart failure. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/assessment-of-diastolic-function/ .
APA, Harvard, Vancouver, ISO, and other styles
10

Losser, Marie-Reine, Catherine Bernard, Jean-Louis Beaudeux, Christophe Pison, and Didier Payen. "Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits." Journal of Applied Physiology 83, no. 5 (November 1, 1997): 1566–74. http://dx.doi.org/10.1152/jappl.1997.83.5.1566.

Full text
Abstract:
Losser, Marie-Reine, Catherine Bernard, Jean-Louis Beaudeux, Christophe Pison, and Didier Payen. Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits. J. Appl. Physiol. 83(5): 1566–1574, 1997.—Glucose is important for vascular and immunocompetent cell functions. We hypothesized that modifications in glucose metabolism (normal feeding, 24-h fasting, glucose loading) may influence the hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide administration (LPS; 600 μg/kg iv) in rabbits. Aortic (ABFV), hepatic artery (HABFV), and portal vein blood flow velocities (PVBFV) (pulsed Doppler), plasma tumor necrosis factor (TNF) and nitrites were measured. Fasting depleted hepatic glycogen content, and intraportal glucose load (2 g/kg) partially restored it. LPS induced a similar hypotension (−20%, P < 0.05) in three groups of animals. In fed animals, systemic vasoconstriction occured with low ABFV and PVBFV (−40%, P < 0.05), together with lactacidemia and hyperglycemia. In fasted animals, ABFV and PVBFV were maintained, without metabolic acidosis or hyperglycemia. Glucose loading induced hemodynamic and metabolic patterns comparable to those observed in fed animals, although significantly more severe. TNF release was amplified fourfold by glucose loading, with no impact on nitrite levels. In conclusion, glucose metabolism interferes with hemodynamic, metabolic, and inflammatory responses to LPS.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Hemodynamic loading"

1

Beneš, Jan. "Hemodynamika v časné fázi kritických stavů a perioperační medicíně." Doctoral thesis, 2012. http://www.nusl.cz/ntk/nusl-308510.

Full text
Abstract:
Beneš J.: HEMODYNAMIKA V ČASNÉ FÁZI KRITICKÝCH STAVŮ A PERIOPERAČNÍ MEDICÍNĚ - Využití méně invazivních monitorovacích prostředků k cílené hemodynamické péči ABSTRACT Hemodynamic instability occurs very often in critically ill patients and during the perioperative period. Insufficiency in the preload, contractility and afterload contribute in major part to this phenomenon. Hemodynamic monitoring allows clinicians to recognize and to intervene early the underlying cause. Due to new technologies development in recent years it is possible to provide continuous monitoring of hemodynamic parameters with diminished invasivity. Hemodynamic optimization and goal directed therapy show treatment benefit in some groups of critically ill patients and mainly during the perioperative period. Aim of hemodynamic optimizations is to attain the best obtainable hemodynamic conditions with use of fluid loading and inotropic support. In many studies in recent years goal-directed therapy was associated with morbidity and mortality reduction. According to the results of our clinical research hemodynamic optimization using stroke volume variation and minimally invasive device based on the pressure wave analysis is feasible and show the same results as other works with more invasive devices. Key words Hemodynamic monitoring,...
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Hemodynamic loading"

1

Pijls, Nico H. J., and Bernard De Bruyne. "Independence of Fractional Flow Reserve of Hemodynamic Loading Conditions." In Coronary Pressure, 167–89. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-015-9564-3_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Pijls, Nico H. J., and Bernard De Bruyne. "Independence of Fractional Flow Reserve of Hemodynamic Loading Conditions." In Coronary Pressure, 157–78. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-015-8834-8_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Akioka, K., M. Kohno, T. Nishikimi, M. Teragaki, M. Yasuda, H. Oku, K. Takeuchi, and T. Takeda. "Influence of Nisoldipine on Hemodynamics and Atrial Natriuretic Polypeptides at Exercise Loading in Hypertensive Patients." In Nisoldipine 1987, 159–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73010-8_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Chirinos, Julio A. "Myocardial wall stress and the systolic loading sequence." In Textbook of Arterial Stiffness and Pulsatile Hemodynamics in Health and Disease, 255–68. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91391-1.00016-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Hemodynamic loading"

1

Le, Trung Bao, and Fotis Sotiropoulos. "Vortex Dynamics in Sidewall Aneurysms: Hemodynamic Transition During Growth and Clinical Implications." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3406.

Full text
Abstract:
Recent works have suggested that aneurysm size and shape might not be the only indicators to predict aneurysm rupture. Rather, the long-term interaction between hemodynamics and aneurysmal wall via the loading condition (i.e shear stress and pressure) may also be important. In this work, we investigate the impact of flow pulsatility on the hemodynamic patterns on aneurysmal dome during its growth using numerical simulation.
APA, Harvard, Vancouver, ISO, and other styles
2

Qaiser, K. N., A. Almoushref, A. K. Mehta, M. Alkhayyat, J. E. Lane, and A. R. Tonelli. "Fluid Loading During the Hemodynamic Evaluation of Pulmonary Hypertension: Response and Outcomes." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3590.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Rathan, Swetha, Choon Hwai Yap, Elizabeth Morris, Sivakkumar Arjunon, Hanjoong Jo, and Ajit P. Yoganathan. "Low and Unsteady Shear Stresses Upregulate Calcification Response of the Aortic Valve Leaflets." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53946.

Full text
Abstract:
Aortic Valve (AV) calcification is a degenerative disease that results in AV sclerosis and is one of the major causes of death. AV is subjected to mechanical conditions such as fluid shear stress, transvalvular pressure and membrane tension1. Normal hemodynamic conditions constantly renew and remodel the valve, whereas altered mechanical loading has been implicated to be the cause of AV disease2. Studies have shown that adverse hemodynamics such as hypertension and altered shear stress can cause tissue inflammation that leads to calcification and stenosis3, 4, and ultimately result in valve failure. However, the molecular and cellular processes that lead to calcification are not very well understood.
APA, Harvard, Vancouver, ISO, and other styles
4

Wang, Yajuan, Onur Dur, Michael J. Patrick, Joseph P. Tinney, Kimimasa Tobita, Kerem Pekkan, and Bradley B. Keller. "Hemodynamic Investigation of Normal Developing Aortic Arch in the Chick Embryo." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193264.

Full text
Abstract:
Governed by genetic and epigenetic feedback [1], during embryonic cardiac development, the anatomy of aortic arches demonstrates drastic three dimensional (3D) changes that interact with the function of cardiovascular system. Six major pairs of aortic arches appear at different embryonic periods and eventually form the two brachiocephalic arteries (left and right third), an aortic arch (left fourth) and pulmonary arteries and ductus arteriosus (left and right sixth) [2–4], Fig 1. Flow-driven hemodynamic loading plays a major role in this dynamic process. Morphological studies on the embryonic aortic arches began over 100 years ago while the recent remarkable developments include understanding genetic determinants such as the effects of neural crest cells [5,6]. However the relationship between hemodynamic factors and the dynamic 3D geometry changes is still limited requiring an interdisciplinary research effort [7,8].
APA, Harvard, Vancouver, ISO, and other styles
5

Sucosky, Philippe, Kartik Balachandran, Hanjoong Jo, and Ajit P. Yoganathan. "Altered Shear Stress Stimulates Upregulation of Endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-β1-Dependent Pathway." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204693.

Full text
Abstract:
Inflammation and calcification are common features of aortic valve (AV) diseases [1]. AV diseases preferentially occur in the aortic side of the valvular leaflets where they are exposed to complex and unstable hemodynamic conditions [2]. The reasons for this side-specific response, potentially associated with the local shear stress environment, are not completely understood. In addition, while it has been shown that exposure of vascular endothelial cells to oscillatory shear stress induces inflammatory responses by bone morphogenic protein (BMP)-4-dependent mechanisms [3], it is not clear whether BMP plays a role in the inflammation of AV leaflet exposed to altered mechanical environment. In the present study, we hypothesized that AV inflammation occurs preferentially in the aortic surface of AV leaflets in a BMP and TGF-β1-dependent manner due to the local hemodynamic loading conditions. This hypothesis was tested via three sets of experiments focused on the biological response of porcine AV leaflets using either a standard or pro-osteogenic medium.
APA, Harvard, Vancouver, ISO, and other styles
6

Rausch, Manuel, Wolfgang Bothe, John-Peder Escobar-Kvitting, Serdar Goktepe, Craig Miller, and Ellen Kuhl. "In-Vivo Dynamic Strains of the Ovine Anterior Mitral Valve Leaflet." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53195.

Full text
Abstract:
Throughout the cardiac cycle the Mitral Valve (MV) experiences complex mechanical and hemodynamic loading [1]. Dysfunction of the MV may have devastating consequences and has been associated with high morbidity and mortality. Surgical repair techniques are available to treat malfunctioning MVs [2]. However, it is likely that interventions such as surgical repair may cause alterations in the loading conditions and associated deformations of the MV. In consequence such alterations could result in detrimental remodeling and disturb normal valve function. It is therefore essential to characterize the MV under in-vivo conditions as accurately as possible and thereby establish a baseline of the normal valve. Even though excellent research has been conducted in-vivo [3], in-vitro [4], as well as in-silico [5], the Anterior Mitral Valve Leaflet (AMVL) has never been characterized from a mechanical perspective across its entire surface. The goal of this study is, hence, to provide a more complete picture of the deformations across the entire AMVL in the beating heart.
APA, Harvard, Vancouver, ISO, and other styles
7

Alemu, Yared, Gaurav Girdhar, Michalis Xenos, Thomas Claiborne, Jolyon Jesty, Shmuel Einav, Marvin Slepian, and Danny Bluestein. "Evaluation of Syncardia Total Artificial Heart Using Device Thrombogenicity Emulator." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53420.

Full text
Abstract:
The thrombogenicity of the left ventricle of the temporary Total Artificial Heart (TAH-t) (SynCardia Systems, Inc. Tucson, AZ) was evaluated using our device thrombogenicity emulator (DTE) methodology [1] that integrates advanced numerical modeling of the whole device combined with experimental measurements of platelet activity. The ejection phase of the cardiac cycle, including diaphragm motion, was modeled with fully-coupled fluid structure interaction (FSI) simulation. Stress loading histories of several thousand platelet trajectories were extracted from these simulations and collapsed into quantitative probability density function (PDF) distributions that represent the TAH-t thrombogenic footprint. Representative stress-loading waveforms with substantially higher stress accumulation (high propensity to cause platelet activation) were replicated in computer controlled hemodynamic shearing device (HSD), where the effect on platelet activation was measured with a modified prothrombinase assay. By determining the platelet stress accumulation distribution, the thrombogenic signature unique to specific TAH design from the results, this methodology facilitates virtual evaluation and optimization of various designs.
APA, Harvard, Vancouver, ISO, and other styles
8

Xenos, Michalis, Yared Alemu, Shmuel Einav, and Danny Bluestein. "Turbulent and Direct Numerical Simulations for Optimizing Mechanical Heart Valve Designs." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206501.

Full text
Abstract:
Patients who receive mechanical heart valve (MHV) implants require mandatory anticoagulation medication after MHV implantation due to the thrombogenic potential of the devise. Optimization of MHV designs may facilitate in reducing the flow induced thrombogenic potential. To accomplish this goal highly resolved 3D geometries of different bileaflet mechanical heart valves were examined to study the contribution of distinct flow phases to platelet damage. Both turbulent and direct numerical simulations (DNS) were conducted and compared. A multiphase approach was formulated, in which the blood interacts with a large number of particles injected in the fluid domain, representing the platelets passing through the MHV. Loading histories experienced by the platelets were calculated by computing the combined effect of stress and exposure time. Platelet stress accumulation during randomized repetitive passages past the valves were calculated using a damage accumulation model. The results from the simulations were used as an input to our hemodynamic shearing device (HSD) which emulated the numerical loading waveforms, and platelet activity measured in order to quantify the thrombogenic potential of different MHVs.
APA, Harvard, Vancouver, ISO, and other styles
9

Nobili, Matteo, Jawaad Sheriff, Umberto Morbiducci, Alberto Redaelli, and Danny Bluestein. "Identification of a Mathematical Model for the Prediction of Platelet Damage Accumulation in Artificial Organs: A Preliminary Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176165.

Full text
Abstract:
Platelets are the pre-eminent cell involved in hemostasis and thrombosis. In recent years it has been demonstrated that flow-induced platelet activation is a major cause for the relatively high incidence of thromboembolic complications in mechanical heart valves (MHVs) [1,2].The platelet activation state (PAS) assay has proved to be a reliable technique for the experimental measurement of procoagulant activity [3]. A Predictive numerical model for platelets damage accumulation could provide critical information for thrombogenicity optimization of implantable prosthetic devices. This would lead to improving the safety and efficacy of implantable devices. Reliable models able to predict this phenomenon are still lacking. The aim of this work is an attempt to bridge this gap. A model for describing the activation of formed elements in blood requires establishing a correlation between mechanical loading, exposure time and the phenomenological response of these elements to it. A physically consistent phenomenological model is used [4] and genetic algorithms (GAs) [5], have been successfully applied to the tuning of the model parameters by correlating its predictions to PAS measurements conducted in a Hemodynamic Shearing Device (HSD) by exposing platelets to prescribed shear stress loading waveforms.
APA, Harvard, Vancouver, ISO, and other styles
10

Eichholz, Benjamin, Ruihang Zhang, and Yan Zhang. "Diversion of Pulsatile Flow Over a Rectangular Sidewall Cavity Using Superhydrophobic Mesh." In ASME 2020 Fluids Engineering Division Summer Meeting collocated with the ASME 2020 Heat Transfer Summer Conference and the ASME 2020 18th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/fedsm2020-20158.

Full text
Abstract:
Abstract Pulsatile flow over open cavity represents one type of physiological phenomenon related to a few common cardiovascular diseases, such as cerebral sidewall aneurysm and arrhythmia-induced thromboembolism in the left atrium appendage (LAA). In recent years, endovascular treatments using mesh-based implants have become increasingly popular. In this paper, we study the characteristics of pulsatile flow over a simplified sidewall cavity under two Reynolds/Womersley number conditions using Particle Image Velocimetry. The impacts of a regular mesh and a superhydrobobically-coated mesh on the cavity flow are investigated. Our results quantify the phase-to-phase changes of the flow fields and reveal the formation and the transport of the primary vortex over the ostium of the rectangular cavity. Results suggest the meshes diverted the main flow away from the cavity and prohibited the development of the primary vortex. A penetrated jet flow was formed near the front side of the cavity due to the presence of the mesh. The superhydrophobic mesh dramatically reduced the kinetic energy of the penetrated jet into the cavity. It indicates the mesh flow diversion is effective because of the destruction of the shear-induced vortex dynamics that causes flow stagnation on the rear cavity wall. Our results also indicate the superhydrophobic coating is potentially beneficial in terms of reducing the hemodynamic loading inside the cavity.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Hemodynamic loading' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography