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Browsing by Author "Bark, David, advisor"

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    Alternative heart assistance pump
    (Colorado State University. Libraries, 2021) Sharifi, Alireza, author; Bark, David, advisor; James, Susan, advisor; Scansen, Brian, committee member; Popat, Ketul, committee member; Gao, Xinfeng, committee member
    On average, the human heart beats around 115,000, and pumps around 2,000 gallons of blood daily. This essential organ may undergo systolic or diastolic dysfunction in which the heart cannot properly contract or relax, respectively. To help hearts pump effectively should these types of failures occur, ventricular assist devices (VAD) are implemented as a temporary or permanent solution. The most common VAD is the left ventricular assist device (LVAD) which supports the left ventricle in pumping the oxygen-rich blood from the heart to the aorta, and ultimately to the rest of the body. Although current VADs are an important treatment for advanced heart failure, generally VADS come with many complications and issues after implantation. These complications include incidents of hemolysis (tearing of the blood cells), thrombosis (clotting of the blood), bleeding (especially in the gastrointestinal tract), and infection at the driveline site. Specifically, the current continuous flow pumps are associated with a much higher incidence of gastrointestinal bleeding, myocardial perfusion, kidney problems, among others, compared with the earlier generation pulsatile pumps. However, the presence of several moving mechanical components made the pulsatile pumps less durable, bulky, and prone to malfunction, ultimately leading to favor toward continuous flow designs. The goal of the present study is to develop a novel heart assist pump, overcoming drawbacks to current commercially available pumps, by improving hemodynamic (blood flow) performance, pulsatility, and eliminating bleeding disorders. Our design will overcome the current pumps which suffer from non-physiological flow, and blood damage. The impact of this work goes beyond heart assist devices and would be applicable to other blood pumps. The fundamental biological and physical principles of designing a blood pump will be reviewed in chapter one. In addition, recent studies on current LVADs and the motivation behind these studies will also be discussed. Then, the idea of using a contractive tubular heart as an alternative pump will be presented in chapter two. To understand the pumping mechanism of the tubular heart, a detailed study on the embryonic heart is presented in this chapter. Subsequently, the effect of flow forces on blood cells will be studied in chapter 3. Moreover, the relation between flow regime and bleeding disorders have been studied in the same chapter. A discussion of our design, including the pump design, testing set up, experimental results will be presented in chapter 4. Finally, the limitations of the present study and future work will be presented in chapter 5.
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    Biomechanical analysis of hypoplastic left heart syndrome and calcific aortic stenosis: a statistical and computational study
    (Colorado State University. Libraries, 2021) Zebhi, Banafsheh, author; Bark, David, advisor; Gao, Xinfeng, committee member; Wang, Zhijie, committee member; Scansen, Brian, committee member
    Cardiovascular diseases are a leading cause of death in the United States. In this dissertation, a congenital heart disease (CHD) and a valvular disease are discussed. CHDs occur in ~5% of live births. Structural CHDs can be complex and difficult to treat, such as hypoplastic left heart syndrome (HLHS) in which the left ventricle is generally underdeveloped, representing ~9% of all congenital heart diseases. Calcific aortic stenosis is one of the most common valvular diseases in which valves thicken and stiffen, and in some cases nodular deposits form, limiting valve function that may result in flow regurgitation and outflow obstruction. The overarching hypothesis of this research is that patient-specific heart geometry and valve characteristics are linked to cardiovascular diseases and may play an important role in regulating hemodynamics within the heart. This hypothesis is studied through three specific aims. In specific aim 1, a computational fluid dynamics study was developed to quantify the hemodynamic characteristics within the right ventricles of healthy fetuses and fetuses with HLHS, using 4D patient-specific ultrasound scans. In these simulations, we find that the HLHS right ventricle exhibits a greater cardiac output than normal; yet, hemodynamics are relatively similar between normal and HLHS right ventricles. Overall, this study provides detailed quantitative flow patterns for HLHS, which has the potential to guide future prevention and therapeutic interventions, while more immediately providing additional functional detail to cardiologists to aid in decision making. The specific aim 2 is a comprehensive review in which we highlight underlying molecular mechanisms of acquired aortic stenosis calcification in relation to hemodynamics, complications related to the disease, diagnostic methods, and evolving treatment practices for calcific aortic stenosis and, bioprosthetic or native aortic scallop intentional laceration (BASILICA) procedure to free coronary arteries from obstruction. In specific aim 3, we use statistical trends and relationships to identify the role of patient-specific aortic valve characteristics in post-BASILICA coronary obstruction. The findings of this study shows that in addition to direct anatomical measurements of the aortic valve, the aspect ratios of the anatomical features are important in determining the cause of post-BASILICA coronary obstruction. The overall significance of this dissertation is that computational and statistical analysis of patient's specific flow hemodynamics and geometric characteristics can provide more insight into the cardiovascular disease and treatment approaches which can ultimately assist surgeons with procedural planning.
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    Stress, structure, and function of the embryonic heart
    (Colorado State University. Libraries, 2023) Gendernalik, Alex L., author; Bark, David, advisor; Garrity, Deborah, committee member; Puttlitz, Christian, committee member; Heyliger, Paul, committee member
    Embryonic heart development is a complex process that requires the coordination of hemodynamic stress and tissue morphogenesis. Improperly timed or distorted mechanical cues can cause reverberating malformations that result in congenital heart defects (CHDs) or embryo death. CHDs occur in ~1% of live births. Only ~20% have a known genetic origin. Altered mechanical signaling or hemodynamics is likely a common contributor to CHD prevalence. Significant research using animal models has shown that altered hemodynamics causes varied malformations. Mechanical properties describe the underlying tissue architecture, which dictates how the heart transmits and reacts to stress. This work aims to quantify and map the mechanical properties to understand how they direct the formation of specific heart structures and function. Furthermore, we seek to understand how mechanical properties change in response to altered hemodynamics. We hypothesize that mechanical properties indicate regions of eventual structure formation, are sensitive to altered hemodynamics, and dictate the pumping method that the heart uses to drive blood flow. We test this hypothesis through three aims. In aim 1, we describe a novel technique in which we use controlled pressurization to deform the embryonic zebrafish heart. We measure deformation in two-dimensions and identify constitutive models of the embryonic heart tissue. Finite element analysis is used to validate our findings in three dimensions. In this aim, we establish that controlled pressurization is a valid technique for inducing measured deformation of the heart. Through this, we determine that the zebrafish myocardial stiffness is on the order of 10 kPa. In aim 2, we further develop our pressurization technique by measuring deformation in three dimensions using confocal microscopy. Furthermore, we use a morpholino antisense oligonucleotide (MO), gata1, to alter embryonic zebrafish heart hemodynamics by blocking development of red blood cells, thus decreasing the viscosity and arterial pressure based on Poiseuille's law. Upon mapping strain in three dimensions, we find that strain throughout the heart is variable, with specific regions of low and high strain from 2 to 3 days post-fertilization (dpf). Low arterial pressure in gata1 MO embryos resulted in significantly increased strain compared to controls, indicating that altered hemodynamics cause altered mechanical properties in the developing embryonic heart. In aim 3, we seek to determine if the zebrafish early embryonic heart tube drives blood flow through peristalsis or impedance-type pumping. We attempt to directly induce impedance pumping by cannulating the atrial inlet of the heart tube after halting contractions and applying a controlled pressure pulse. Additionally, we use precisely controlled temperatures to increase heart rate, thus increasing arterial pressure. As temperature is increased, we use high speed imaging to analyze the contractile motion and resulting blood flow in the tube heart. Furthermore, we describe a previously unknown response whereby the traveling endocardial closure shortens with increased arterial pressure. In this aim, we fail to find evidence of impedance-type pumping but cannot preclude it contributes to blood flow. In summary, our pressurization technique can be used to map strain in the zebrafish embryonic heart; altering hemodynamics by reducing arterial pressure results in decreased stiffness of the embryonic heart myocardium, and endocardial closure length in the embryonic zebrafish heart tube shortens as arterial pressure and heart rate increase.
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    Understanding and leveraging mechanical forces in haemostasis
    (Colorado State University. Libraries, 2023) Macleod Briongos, Iain, author; Bark, David, advisor; Olver, Christine, committee member; Popat, Ketul, committee member; Henry, Charles, committee member
    Cardiovascular disease accounts for one third of deaths worldwide, of which over 75% are in low- and middle-income countries. Platelets and von Willebrand Factor play a central role in haemostasis and in cardiovascular diseases, being involved in both excess clotting that causes heart attacks and strokes, and excess bleeding. Herein, we outline a method for leveraging paper microfluidics with the aim of developing a WHO ASSURED criteria compliant point-of-care device for the diagnosis of von Willebrand Disease, as well as work to increase the understanding of mechanical force generation by platelets through Traction Force Microscopy.