Gotowe bibliografie tematyczne / Cardiac stiffness

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Gotowa bibliografia na temat „Cardiac stiffness”

Autor: Grafiati
Data publikacji: 14 grudnia 2024

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Artykuły w czasopismach na temat "Cardiac stiffness"

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Heller, Lois Jane, David E. Mohrman i Joseph R. Prohaska. "Decreased passive stiffness of cardiac myocytes and cardiac tissue from copper-deficient rat hearts". American Journal of Physiology-Heart and Circulatory Physiology 278, nr 6 (1.06.2000): H1840—H1847. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1840.

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Passive stiffness characteristics of isolated cardiac myocytes, papillary muscles, and aortic strips from male Holtzman rats fed a copper-deficient diet for ∼5 wk were compared with those of rats fed a copper-adequate diet to determine whether alterations in these characteristics might accompany the well-documented cardiac hypertrophy and high incidence of ventricular rupture characteristic of copper deficiency. Stiffness of isolated cardiac myocytes was assessed from measurements of cellular dimensional changes to varied osmotic conditions. Stiffness of papillary muscles and aortic strips was determined from resting length-tension analyses and included steady-state characteristics, dynamic viscoelastic stiffness properties, and maximum tensile strength. The primary findings were that copper deficiency resulted in cardiac hypertrophy with increased cardiac myocyte size and fragility, decreased cardiac myocyte stiffness, and decreased papillary muscle passive stiffness, dynamic stiffness, and tensile strength and no alteration in aortic connective tissue passive stiffness or tensile strength. These findings suggest that a reduction of cardiac myocyte stiffness and increased cellular fragility could contribute to the reduced overall cardiac tissue stiffness and the high incidence of ventricular aneurysm observed in copper-deficient rats.
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Spiteri, Raymond J., i Ryan C. Dean. "Stiffness Analysis of Cardiac Electrophysiological Models". Annals of Biomedical Engineering 38, nr 12 (26.06.2010): 3592–604. http://dx.doi.org/10.1007/s10439-010-0100-9.

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Childers, Rachel C., Pamela A. Lucchesi i Keith J. Gooch. "Decreased Substrate Stiffness Promotes a Hypofibrotic Phenotype in Cardiac Fibroblasts". International Journal of Molecular Sciences 22, nr 12 (9.06.2021): 6231. http://dx.doi.org/10.3390/ijms22126231.

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A hypofibrotic phenotype has been observed in cardiac fibroblasts (CFs) isolated from a volume overload heart failure model, aortocaval fistula (ACF). This paradoxical phenotype results in decreased ECM synthesis despite increased TGF-β presence. Since ACF results in decreased tissue stiffness relative to control (sham) hearts, this study investigates whether the effects of substrate stiffness could account for the observed hypofibrotic phenotype in CFs isolated from ACF. CFs isolated from ACF and sham hearts were plated on polyacrylamide gels of a range of stiffness (2 kPa to 50 kPa). Markers related to cytoskeletal and fibrotic proteins were measured. Aspects of the hypofibrotic phenotype observed in ACF CFs were recapitulated by sham CFs on soft substrates. For instance, sham CFs on the softest gels compared to ACF CFs on the stiffest gels results in similar CTGF (0.80 vs. 0.76) and transgelin (0.44 vs. 0.57) mRNA expression. The changes due to stiffness may be explained by the observed decreased nuclear translocation of transcriptional regulators, MRTF-A and YAP. ACF CFs appear to have a mechanical memory of a softer environment, supported by a hypofibrotic phenotype overall compared to sham with less YAP detected in the nucleus, and less CTGF and transgelin on all stiffnesses.
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Kellermayer, Dalma, Bálint Kiss, Hedvig Tordai, Attila Oláh, Henk L. Granzier, Béla Merkely, Miklós Kellermayer i Tamás Radovits. "Increased Expression of N2BA Titin Corresponds to More Compliant Myofibrils in Athlete’s Heart". International Journal of Molecular Sciences 22, nr 20 (15.10.2021): 11110. http://dx.doi.org/10.3390/ijms222011110.

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Long-term exercise induces physiological cardiac adaptation, a condition referred to as athlete’s heart. Exercise tolerance is known to be associated with decreased cardiac passive stiffness. Passive stiffness of the heart muscle is determined by the giant elastic protein titin. The adult cardiac muscle contains two titin isoforms: the more compliant N2BA and the stiffer N2B. Titin-based passive stiffness may be controlled by altering the expression of the different isoforms or via post-translational modifications such as phosphorylation. Currently, there is very limited knowledge about titin’s role in cardiac adaptation during long-term exercise. Our aim was to determine the N2BA/N2B ratio and post-translational phosphorylation of titin in the left ventricle and to correlate the changes with the structure and transverse stiffness of cardiac sarcomeres in a rat model of an athlete’s heart. The athlete’s heart was induced by a 12-week-long swim-based training. In the exercised myocardium the N2BA/N2B ratio was significantly increased, Ser11878 of the PEVK domain was hypophosphorlyated, and the sarcomeric transverse elastic modulus was reduced. Thus, the reduced passive stiffness in the athlete’s heart is likely caused by a shift towards the expression of the longer cardiac titin isoform and a phosphorylation-induced softening of the PEVK domain which is manifested in a mechanical rearrangement locally, within the cardiac sarcomere.
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Kapelko, V. I., V. I. Veksler, M. I. Popovich i R. Ventura-Clapier. "Energy-linked functional alterations in experimental cardiomyopathies". American Journal of Physiology-Lung Cellular and Molecular Physiology 261, nr 4 (1.10.1991): L39—L44. http://dx.doi.org/10.1152/ajplung.1991.261.4.l39.

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Changes in high-energy phosphate content and cardiac contractile function of isolated rat hearts as well as changes in Ca2+ sensitivity and mitochondrial respiration of myocardial skinned fibers were assessed in hereditary cardiomyopathies and in cardiomyopathies induced by chronic treatment with adriamycin or norepinephrine, by autoimmunization, by diabetes, or by creatine deficiency. The sum of ATP and phosphocreatine contents as well as cardiac output at standard load conditions was substantially lower in almost all groups. The common features of cardiac pump failure were mild bradycardia, elevated left ventricular (LV) diastolic pressure, and stiffness that limited cardiac contractile adaptation to volume or resistance loads. The LV diastolic stiffness at maximal functional load was inversely correlated with high-energy phosphate content. Increased myofibrillar sensitivity to Ca2+ and defective function of mitochondrial creatine kinase were found in skinned myocardial fibers. These results suggested that both increased myofibrillar Ca2+ sensitivity and energy deficiency within myofibrils may contribute to increased myocardial stiffness. Increased stiffness limits LV filling but facilitates pressure development, which partly compensates for decreased contractility of cardiomyopathic hearts. cardiac contractile function; high-energy phosphates; isolated heart; myocardial stiffness
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Kapelko, V. I., V. I. Veksler, M. I. Popovich i R. Ventura-Clapier. "Energy-linked functional alterations in experimental cardiomyopathies". American Journal of Physiology-Heart and Circulatory Physiology 261, nr 4 (1.10.1991): 39–44. http://dx.doi.org/10.1152/ajpheart.1991.261.4.39.

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Changes in high-energy phosphate content and cardiac contractile function of isolated rat hearts as well as changes in Ca2+ sensitivity and mitochondrial respiration of myocardial skinned fibers were assessed in hereditary cardiomyopathies and in cardiomyopathies induced by chronic treatment with adriamycin or norepinephrine, by autoimmunization, by diabetes, or by creatine deficiency. The sum of ATP and phosphocreatine contents as well as cardiac output at standard load conditions was substantially lower in almost all groups. The common features of cardiac pump failure were mild bradycardia, elevated left ventricular (LV) diastolic pressure, and stiffness that limited cardiac contractile adaptation to volume or resistance loads. The LV diastolic stiffness at maximal functional load was inversely correlated with high-energy phosphate content. Increased myofibrillar sensitivity to Ca2+ and defective function of mitochondrial creatine kinase were found in skinned myocardial fibers. These results suggested that both increased myofibrillar Ca2+ sensitivity and energy deficiency within myofibrils may contribute to increased myocardial stiffness. Increased stiffness limits LV filling but facilitates pressure development, which partly compensates for decreased contractility of cardiomyopathic hearts. cardiac contractile function; high-energy phosphates; isolated heart; myocardial stiffness
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Laskey, Warren, Saadi Siddiqi, Cheri Wells i Richard Lueker. "Improvement in arterial stiffness following cardiac rehabilitation". International Journal of Cardiology 167, nr 6 (wrzesień 2013): 2734–38. http://dx.doi.org/10.1016/j.ijcard.2012.06.104.

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Zanoli, Luca, Paolo Lentini, Marie Briet, Pietro Castellino, Andrew A. House, Gerard M. London, Lorenzo Malatino, Peter A. McCullough, Dimitri P. Mikhailidis i Pierre Boutouyrie. "Arterial Stiffness in the Heart Disease of CKD". Journal of the American Society of Nephrology 30, nr 6 (30.04.2019): 918–28. http://dx.doi.org/10.1681/asn.2019020117.

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CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
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Brady, A. J., i S. P. Farnsworth. "Cardiac myocyte stiffness following extraction with detergent and high salt solutions". American Journal of Physiology-Heart and Circulatory Physiology 250, nr 6 (1.06.1986): H932—H943. http://dx.doi.org/10.1152/ajpheart.1986.250.6.h932.

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Myocytes were prepared from enzymatically digested adult rat hearts and attached to concentric double-barreled suction micropipettes. Myocyte stiffness was calculated as the ratio of the oscillatory tension-to-strain amplitude, where the strain was produced by an applied 5-Hz perturbation. Stiffness, as a function of cell length, was measured in relaxing solution (pCa = 9) as the control solution, 0.5% Triton X-100 detergent, 0.47 M KCl, and 0.6 M KI. Ultrastructure of unattached cells in each solution is illustrated with electron micrographs. The dependence of cell stiffness on cell length was described by an exponential relation with a length constant that increased slightly in detergent, whereas the stiffness at control length appeared to fall. The major fall in absolute stiffness occurred with myosin extraction in KCl. Both the stiffness at control length and the slope of the ln stiffness-to-length relation declined with the disappearance of the A band. A further, but smaller, decline of stiffness occurred with KI extraction of the thin filaments. A highly compliant "ghost" remained after KI extraction but the stiffness-to-length relation was still measurable. The fall in stiffness with myosin extraction is discussed in relation to cytoskeletal filaments (titin, nebulin, and intermediate filaments.
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Roos, K. P., i A. J. Brady. "Stiffness and shortening changes in myofilament-extracted rat cardiac myocytes". American Journal of Physiology-Heart and Circulatory Physiology 256, nr 2 (1.02.1989): H539—H551. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h539.

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Sarcomere lengths, cell widths, volumes, stiffness, and regional striation uniformity were determined from isolated adult cardiac myocytes. Single cells were examined in the control saline solution followed by a sequence of relaxing, membrane skinning, and myofilament extraction solutions. Cell size and shape parameters were determined from freely dispersed myocytes, whereas stiffness was measured from myocytes attached to a perturbator and tension transducer with micropipettes. There were small changes in cell appearance, size, shape, and stiffness in the relaxing and skinning solutions. However, in 0.17-0.56 M KCl myosin extraction media, cell length declined significantly to 1.19 microns, and stiffness fell to 5-10% of control. The rate of cell shortening and stiffness decline was dependent on KCl concentration and pH. Subsequent exposure to higher ionic strength 0.60 M KI thin filament extraction media elicited additional decreases in stiffness (less than 5% of control) and cell length (0.98 micron). Cell shortening and stiffness decline have similar time courses under the same conditions, and they appear to coincide with A-band disassembly as indicated by electron micrographs. These data suggest that cardiac myocyte stiffness, size, and shape are determined in part by a stressed cytoskeleton that is associated with the myofilament apparatus.
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Rozprawy doktorskie na temat "Cardiac stiffness"

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Chaturvedi, Rajiv Ranjan. "Passive stiffness of human cardiac muscle". Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429158.

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Slater, Rebecca E., i Rebecca E. Slater. "Modulation of Cardiac Titin Stiffness in Physiological and Pathophysiological States". Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/623160.

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The giant sarcomeric protein titin spans the length of the half sarcomere and contains an I-band spanning region that functions as a molecular spring that develops passive force during diastole. Titin stiffness is modulated both by isoform switching and post-translational modifications including phosphorylation. Modulation of titin stiffness occurs in physiological and pathophysiological states including Heart Failure with Preserved Ejection Fraction (HFpEF) which is marked by increased diastolic stiffness. Here, I investigated the effects of titin phosphorylation by two kinases, ERK2 and CaMKIIδ, at the level of the protein and the myocardium. Additionally, I used mouse models of HFpEF to test if modulating titin stiffness could ameliorate increased diastolic stiffness. Specifically, I used the TAC/DOCA model (surgical) and the N2B KO model (genetic) of HFpEF to test the effects of metformin on titin stiffness and diastolic function. HFpEF mice treated with metformin had improved diastolic function, reduced passive stiffness, and increased PKA phosphorylation compared to non-treated HFpEF animals. Interestingly, these results were only found in animals with an intact N2B-element indicating an underlying mechanism that arises from the N2B element and that includes an increase in PKA-phosphorylation. Additionally, I used the TtnΔIAjxn mouse model, as a mechanical analog of the increased diastolic stiffness in HFpEF, to test the therapeutic effects of exercise and heart rate reduction. Exercise induced hypo-phosphorylation of the PEVK element of titin consistent with reduced passive tension while heart-rate reduction had no effect on passive stiffness. These studies build on the increasing understanding of how titin's stiffness can be modulated and the ways to take advantage of titin in a beneficial manner for diastolic function.
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Filipe, Daniel V. "Modifying and Measuring the Stiffness of a Regenerative Cardiac Scaffold In Vitro". Digital WPI, 2010. https://digitalcommons.wpi.edu/etd-theses/1098.

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"The stiffness of scaffolds used in surgical ventricular restoration may play an important role in the degree to which they facilitate regeneration of functional cardiac tissue. The stiffness of the scaffold influences the phenotype of cells which are present in it as well as their ability to deform the scaffold. The goal of this study was to evaluate in vitro methods to characterize and alter the stiffness of new scaffold materials. Membrane inflation testing, an in vitro mechanical testing method, was evaluated in this study because of its ease of use and the similar mode of loading which it shares with scaffolds implanted in vivo. The structural stiffness of two scaffold materials, urinary bladder matrix and Dacron, were determined in vivo and using membrane inflation testing. Despite higher tensions and lower area stretch ratios for scaffolds tested using membrane testing, similar changes in structural stiffness between the two materials were found for both methods (5.6 ± 3.3 fold in vivo, 5.0 ± 1.0 in vitro). This finding demonstrated that membrane inflation testing is a useful in vitro method for measuring changes in structural stiffness between scaffold materials with a level of sensitivity similar to that which is measured in vivo. Membrane inflation testing was used to assess the effectiveness of altering scaffold stiffness through exposure to various cell culture conditions. Incubation of a biological membrane in cell culture media resulted in a drastic decrease in the elastic modulus from its initial value (3.55 ± 0.52 MPa) after 2 weeks (1.79 ± 0.30 MPa), 4 weeks (1.04 ± 0.09 MPa), and 10 weeks (0.014 ± 0.01 MPa). When fibroblasts were cultured on the scaffolds for 10 weeks an increase in elastic modulus (0.134 ± 0.05 MPa) over scaffolds incubated in culture media for the same amount of time was observed. The increase in elastic modulus due to the presence of fibroblasts was accompanied by an increase in the percentage of collagen in the samples (54.1 ± 5.1 % without fibroblasts, 83.2 ± 5.1 % with fibroblasts). Contrary to expectation, addition of ascorbic acid to the media to increase production of collagen by the fibroblasts resulted in a decrease in elastic modulus (0.030 ± 0.01 MPa) compared to scaffolds cultured with fibroblasts in standard media and a decrease in the amount of enzymatically degraded collagen (40.8 ± 4.7 % without ascorbic acid, 21.1 ± 3.3 % with ascorbic acid). Regeneration of cardiac tissue after a myocardial infarction is a complicated process which is influenced by a myriad of different factors. Future studies investigating the exact role which substrate stiffness has on regeneration will be essential to the development of improved cardiac scaffolds. Characterization of the stiffness of these scaffolds by membrane inflation and manipulation through exposure to cell culture conditions are powerful approaches to facilitate future studies."
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Müller, Anna-Eliane [Verfasser]. "Modulation of cardiac titin stiffness in diabetic and exercised hearts / Anna-Eliane Müller". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2015. http://d-nb.info/1066359237/34.

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Krishnamoorthy, Suresh. "Arterial stiffness, macro-vascular, micro-vascular endothelial function and cardiac remodelling in arterial fibrillation". Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5957/.

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In patients with atrial fibrillation (AF) there appears a close link between arterial stiffness, endothelial function and cardiac remodelling thereby contributing to the development and progression of AF as well as to its complications. However this complex interaction(s) is not well understood. In the cross-sectional study with PAF patients, higher arterial stiffness (PP, Pr) is strongly associated with endothelial-dependent macro-vascular dysfunction (Δ%AIx Salbutamol). Similarly a strong relationship observed between arterial stiffness (PP, PWV cf, Pr) and abnormal LA remodelling (LAV and LAD) in PAF patients. Higher levels of vWf and soluble E-Selectin at baseline are independently associated with increased risk of adverse clinical events (including AMI and ischaemic stroke) in ‘real world’ AF patients, and may aid clinical risk stratification towards identifying patients at higher risk. In the longitudinal study of dual chamber pacemaker patients there was a close relationship observed between arterial stiffness (PP, PWV cf, Pr), macro-vascular (Δ%AIx Sal) / micro-vascular (∆%LDF Ach) endothelial function and cardiac remodelling (EF, E/A ratio, E_M, A_M). These findings support the close interaction between ventricular contraction, arterial system and endothelial function towards the development of AF in pacemaker patients, beyond the adverse effects of pacing per se.
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Patel, Kunal. "Stiffness Gradient Scaffolds as an In Vitro Model for Stem Cell Based Cardiac Cell Therapy". University of Akron / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=akron1386725736.

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Querceto, Silvia. "Biomimetic materials for novel cardiac regeneration approaches". Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1211514.

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The quest for novel biomaterials to promote cell structural and functional maturation for cardiac tissue regeneration has emphasized a need to create microenvironments with physiological features. Substrate stiffness constitutes a structural property of crucial importance in the field of tissue engineering and many studies have shown how cardiac cells sense the rigidity of the substrate on which they grow. In this work, we focused on the relevance of substrates mimicking cardiac extracellular matrix (cECM) rigidity for the understanding of the complex interplay between the extracellular and intracellular compartments. Among the most promising biomaterials, Liquid Crystalline Elastomers (LCEs) represent a novel class of polymers previously investigated both as artificial muscles for biomedical purposes and dynamic cell scaffolds. The development of new smart materials which can provide bioactive cues to control and regulate cell fate has been recently encouraged. Indeed, mechanical cues play a significant role in maintaining cell and tissues/organs functions and, in this respect, cell models and substrate stiffness appear as intriguing tools for the investigation of cECM-cell interactions both in physiological and pathological conditions. From the perspective of materials, we have explored the fabrication of biomimetic patterned substrates to direct human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM) growth and evaluate their effect on cell functional properties. In the field of regenerative medicine, the advent of hiPSC-CMs has paved the way for a patient-specific therapy but the development of more mature hiPSC-CMs is still needed. Promising approaches that have begun to be investigated include long-term culture, mechanical loading, 3-dimensional tissue engineering and, above all, the use of dynamic scaffolds to boost cell maturation by giving a mechanical stimulus. Finally, with the aim of creating an effective dynamic cell substrate, we have introduced the design of the first prototype of LCE-based biomimetic contractile unit by optimizing a miniaturization of the mechanical device. The functional properties of the contractile apparatus have been investigated and then modulated to closely reproduce the features of native myocardium. Overall, in this work we have provided an overview of some functional aspects of biomaterials which are considered of key relevance in different biomedical fields to elucidate how recent advances may impact future tissue engineering applications.
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Gordon-Walker, Timothy Thomas. "Effect of matrix stiffness on the behaviour of liver resident cell populations in chronic liver disease and hepatocarcinogenesis". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9537.

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Introduction: The development of liver fibrosis is characterised by dramatic changes in the biomechanical composition and mechanical properties of the extracellular matrix (ECM). Increases in matrix stiffness associated with inflammation and fibrosis are implicated in promoting cancer development. Clinical studies have demonstrated a close association between increases in liver stiffness and the incidence of hepatocellular carcinoma (HCC). The effect of changes in matrix stiffness on tissue-resident hepatic progenitor cells (HPC) is unknown. Aberrant HPC proliferation has been implicated in the pathogenesis of HCC. It was hypothesised that changes in the stiffness of the cellular microenvironment are important in regulating the behaviour of liver-resident cell populations and may promote the development of HCC. Aims: i) to determine how changes in the stiffness of the cancer cell niche might regulate proliferation, differentiation and chemotherapeutic resistance in HCC; ii) to determine the relationship between changes in liver stiffness and hepatic progenitor cell (HPC) response in rodent models of chronic liver disease; and iii) to determine whether changes in the stiffness of the HPC niche regulate proliferation and differentiation in these cells. A secondary aim of the thesis was to characterise the pattern of histological changes observed in rodent models of chronic hepatic congestion and whether this might provide insight into the effect of oedema and congestion on the development of liver fibrosis. Methods: Cell culture experiments in HCC (Huh7/ HepG2) and HPC cell lines were performed using a system of ligand-coated polyacrylamide (PA) gel supports of variable stiffness. The stiffness of the PA supports (expressed as shear modulus) was altered across a physiological change (1-12kPa) corresponding to values encountered in normal and fibrotic livers. Thiacetamide and carbon tetrachloride (CCl4) models of liver fibrosis were used to investigate the relationship between increasing liver fibrosis, changes in matrix stiffness and HPC response. The pattern of histological changes in the liver in response to hepatic congestion was assessed in two unrelated murine models of dilated cardiomyopathy; the python and CREB S133A mice. Results: Increases in matrix stiffness, as would be encountered in liver fibrosis, promote HCC cell proliferation. Increasing matrix stiffness is associated with enhanced basal and hepatocyte growth factor-mediated signalling though ERK, PKB/ Akt and STAT3. Stiffness-dependent HCC cell proliferation is modulated by β1-integrin and focal adhesion kinase. Increasing matrix stiffness is associated with a reduction in chemotherapy-induced apoptosis in HCC cells. However, following chemotherapy there was an increase in the frequency of clone-initiating cells for cells maintained in a low stiffness environment. Flow cytometry in HepG2 cells demonstrated that culture in a low stiffness environment was associated with an increase in the frequency of the stem cell markers CD44, CD133 and CXCR-4. This effect was further enhanced in the presence of chemotherapy. There is a close association between HPC numbers and liver stiffness measurements in a rat CCl4 model of chronic liver fibrosis. The major expansion in HPC numbers in this model coincides with a similarly large increase in fibrous tissue deposition. In vitro experiments using PA supports demonstrate that increasing matrix stiffness promotes the proliferation of both primary murine HPCs and an immortalised HPC line (BMOL). Changes in matrix stiffness regulate the expression of hepatocyte and biliary markers in BMOL cells. Histological studies in both the Python and CREB S133A models reveal findings consistent with acute on chronic cardiac hepatopathy (ischaemic hepatitis). Features of chronic passive congestion and centrilobular necrosis are present concurrently and develop rapidly. Bridging fibrosis and cirrhosis are not present. Conclusions: Physiologically-relevant changes in matrix stiffness regulate proliferation, differentiation, chemotherapeutic-resistance and stem cell marker expression in HCC cells. Similarly, increases in matrix stiffness are closely correlated to HPC response in vivo and regulate HPC proliferation and differentiation in vitro.
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Nilsson, Ulf. "Cardiovascular aspects on chronic obstructive pulmonary disease : with focus on ischemic ECG abnormalities, QT prolongation and arterial stiffness". Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-138787.

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Background Chronic Obstructive Pulmonary disease (COPD) is an under-diagnosed disease with a prevalence of approximately 10%, highly dependent on age and smoking habits. Comorbidities are common in COPD and of these, cardiovascular diseases (CVD) are the most common. COPD is the fourth leading cause of death globally, and CVD probably contribute to the high mortality. Within CVD, Ischemic Heart Disease (IHD) is the most common. It is highly clinically relevant to identify signs of ischemic heart disease, other cardiac conditions, and risk factors for CVD in COPD. Electrocardiogram (ECG) is a simple but still major diagnostic tool in clinical cardiology, including disturbances in the electric conduction system and ischemia. Due to the under-diagnosis of COPD, there is limited knowledge regarding the prevalence and prognostic impact of ECG abnormalities in COPD. Arterial stiffness is a risk factor for CVD, which has raised an increased interest, however not evaluated in population based studies of COPD. Aim The overall aim was to describe cardiovascular aspects on COPD, with a specific focus on arterial stiffness, prevalence and prognostic impact of ischemic ECG abnormalities and prolonged QT interval, by comparing subjects with and without obstructive lung function impairment in a population-based cohort. Methods The thesis is based on the Obstructive Lung Disease in Northern Sweden (OLIN) COPD study; a population-based longitudinal cohort study. During the years 2002-2004, all participants in clinical examinations from previously recruited large population-based cohorts were invited to re-examination including spirometry and a structured interview. All subjects with obstructive lung function impairment (n=993) were identified, together with 993 age and sex-matched referents without airway obstruction. The study population (n=1986) has been invited to annual examinations since 2005 including spirometry and structured interview. Papers I-III are based on data from 2005 when electrocardiogram (ECG) was recorded in addition to the basic program. All ECGs were Minnesota coded and QT-time was measured. Paper IV is based data from 2010 when non-invasive measurements of arterial stiffness, assessed as pulse wave velocity (PWV), was added to the program. Spirometric data were classified as normal lung function (NLF), restrictive spirometric pattern (RSP) and airway obstruction (COPD). The following spirometric criteria for COPD were used: post-bronchodilator FEV1/VC<0.70 (papers I-IV, in paper III labelled GOLD-COPD) and lower limit of normal, LLN (LLN-COPD) (paper III). Spirometric classification of COPD severity was based on FEV1 % predicted as a continuous variable or according to the Global Initiative for Obstructive Lung Disease (GOLD), divided into GOLD 1-4. Results The prevalence of ischemic heart disease (IHD), both self-reported and assessed as probable and possible ischemic ECG abnormalities (I-ECG) according to the Whitehall criteria, was similar among subjects with NLF and COPD. The prevalence of both self-reported and probable (I-ECG) according to Whitehall increased by GOLD grade.  Among those with COPD, self-reported IHD was associated with disease severity, assessed as FEV1 % predicted also after adjustment for age and sex (paper I). In both COPD and NLF, those with I-ECG had a higher cumulative mortality over 5 years than those without I-ECG (29.6 vs. 10.6%, p<0.001 and 17.1 vs. 6.3 %, p=0.001). When analysed in a multivariate model, the Mortality Risk Ratio (MRR, 95%CI) was increased for subjects with COPD and I-ECG (2.4, 1.5-3.9), and non-significantly so for NLF with I-ECG (1.65, 0.94-2.90), when compared to NLF without I-ECG.  When analyzed separately among subjects with COPD, the increased risk for death associated with I-ECG persisted independent of age, sex, BMI-class, smoking habits and disease severity assessed as FEV1 % predicted (1.89, 1.20-2.99). The proportion without reported IHD was high among those with I-ECG; 72.4% in NLF and 67.3% in COPD. The pattern was similar also among them; I-ECG was associated with an increased risk for death in COPD and non-significantly so in NLF (paper II). Mean corrected QT-time (QTc) and prevalence of QTc prolongation was higher in RSP than NLF but similar in NLF and GOLD-COPD. The prevalence of borderline as well as prolonged QTc increased by GOLD grade (test for trend p=0.012 for both groups). Of those with GOLD-COPD, 52% fulfilled the LLN-criterion (LLN-COPD). When comparing LLN-COPD and NLF, the pattern was similar as when comparing NLF and GOLD-COPD. The cumulative mortality over 5 years was higher among subjects with borderline and prolonged QTc than those with normal QTc in subjects with GOLD-COPD and LLN-COPD but not in NLF and RSP (paper III). Arterial stiffness, assessed as PWV, was higher in GOLD 3-4 compared to non-COPD (10.52 vs. 9.13 m/s, p=0.042). Reported CVD and age >60 were both associated with significantly higher PWV in COPD as well as in non-COPD. In a multivariate model, GOLD 3-4 remained associated with higher PWV when compared with non-COPD, also when adjusted for sex, age group, smoking habits, blood pressure, reported CVD and pulse rate (paper IV). Conclusion In this population-based study, the prevalence of ischemic ECG abnormalities was similar among subjects with normal lung function and COPD, but increased by disease severity among subjects with COPD. Ischemic ECG abnormalities were associated with an increased mortality among subjects with COPD, independent of common confounders and disease severity, also among those without known heart disease. Whilst the prevalence of QTc prolongation was similar in NLF, COPD and LLN-COPD, it was associated with an increased mortality only in the COPD-groups. ECG is a simple non-invasive method and seems to identify findings of prognostic importance among subjects with COPD. Central arterial stiffness, a known risk factor for cardiovascular disease, was increased among subjects with severe and very severe COPD when compared to subjects without COPD independent of common confounders.
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Maksuti, Elira. "Imaging and modeling the cardiovascular system". Doctoral thesis, KTH, Medicinsk bildteknik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-196538.

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Understanding cardiac pumping function is crucial to guiding diagnosis, predicting outcomes of interventions, and designing medical devices that interact with the cardiovascular system.  Computer simulations of hemodynamics can show how the complex cardiovascular system is influenced by changes in single or multiple parameters and can be used to test clinical hypotheses. In addition, methods for the quantification of important markers such as elevated arterial stiffness would help reduce the morbidity and mortality related to cardiovascular disease. The general aim of this thesis work was to improve understanding of cardiovascular physiology and develop new methods for assisting clinicians during diagnosis and follow-up of treatment in cardiovascular disease. Both computer simulations and medical imaging were used to reach this goal. In the first study, a cardiac model based on piston-like motions of the atrioventricular plane was developed. In the second study, the presence of the anatomical basis needed to generate hydraulic forces during diastole was assessed in heathy volunteers. In the third study, a previously validated lumped-parameter model was used to quantify the contribution of arterial and cardiac changes to blood pressure during aging. In the fourth study, in-house software that measures arterial stiffness by ultrasound shear wave elastography (SWE) was developed and validated against mechanical testing. The studies showed that longitudinal movements of the atrioventricular plane can well explain cardiac pumping and that the macroscopic geometry of the heart enables the generation of hydraulic forces that aid ventricular filling. Additionally, simulations showed that structural changes in both the heart and the arterial system contribute to the progression of blood pressure with age. Finally, the SWE technique was validated to accurately measure stiffness in arterial phantoms.

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Książki na temat "Cardiac stiffness"

1

Zumbro, Emiko. Active variable stiffness catheter for cardiac surgery. 2013, 2013.

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Townend, Jonathan N., i Charles J. Ferro. Vascular stiffness in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0111.

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Increased arterial stiffness is a hallmark of chronic kidney disease and is associated with adverse alterations in cardiac structure and function that predispose to an increased risk of cardiovascular death. These changes are already apparent in early kidney disease, which is common in the ageing population in the developed world. The mechanisms underlying increased arterial stiffness in chronic kidney disease are complex, but some are alterable by therapies, for instance those that affect the endothelium or renin-angiotensin system. This may contribute to lowering cardiovascular risk in chronic kidney disease.
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Elliott, Perry, Kristina H. Haugaa, Pio Caso i Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.
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Montgomery, Hugh, i Rónan Astin. Normal physiology of the cardiovascular system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0128.

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Preload modulates contractile performance, and is determined by end-diastolic volume (EDV) and ventricular compliance. Compliance falls with increasing preload, muscle stiffness or ventricular hypertrophy, making central venous pressure (CVP) a poor surrogate for EDV. Responsiveness to fluid loading can be identified by seeking a change in stroke volume (SV) with changes in cardiac loading. Afterload, the force to be overcome before cardiac muscle can shorten to eject blood, rises with transmural pressure and end-diastolic radius, and inversely with wall thickness. Afterload, being the tension across the ventricular wall, is influenced by pleural pressure. Reductions in afterload increase SV for any cardiac work, as do reductions in vascular resistance. Resistance is modified by changes in arteriolar cross-sectional area. A rise in resistance increases blood pressure and microvascular flow velocity. Increased resistance may reduce CO if cardiac work cannot be augmented sufficiently. Flow autoregulationis the ability of vascular beds to maintain constant flow across varied pressures by adjusting local resistance.
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Saeed, Sahrai, i Eva Gerdts. Echocardiography. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0010.

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Current guidelines recommend extensive cardiovascular imaging in patients who experience ischaemic stroke or a transient ischaemic attack to prevent recurrent stroke. High-quality echocardiography is crucial for detection of the wide range of cardiac and proximal aortic conditions that can predispose to cerebral embolism. These conditions may be classified as major, minor, or uncertain risk sources of embolism. Although both transthoracic (TTE) and transoesophageal echocardiography (TOE) have substantial clinical utility in patients with cryptogenic stroke, these methods offer complementary information. TOE is typically used for assessment of defects in the atrial septum or detection of thrombus in the left atrial appendage. In contrast, TTE is the recommended method for assessment of cardiac chamber structure and function, and valvular disease. Furthermore, assessment of aortic stiffness and electrocardiography may offer additional insight to cardiac function. This chapter gives an overview of the use of echocardiography in ischaemic stroke patients.
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Dhaun, Neeraj, i David J. Webb. Endothelins and their antagonists in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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Części książek na temat "Cardiac stiffness"

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Krüger, Martina. "Posttranslational Modification of the Titin Springs: Dynamic Adaptation of Passive Sarcomere Stiffness". W Cardiac Cytoarchitecture, 109–24. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15263-9_6.

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Serizawa, Takashi, Osami Kohmoto, Masahiko Iizuka, Tetsuo Ohya, Shin-ich Momomura i Tsuneaki Sugimoto. "Discrepancy Between Slow Relaxation and Increased Myocardial Stiffness". W Cardiac Mechanics and Function in the Normal and Diseased Heart, 131–35. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-67957-8_13.

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Roman, Mary J., i Richard B. Devereux. "Arterial Stiffness, Central Blood Pressure and Cardiac Remodelling: From Cardiac Hypertrophy to Heart Failure". W Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases, 297–306. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-5198-2_24.

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Huntsman, Lee L., i Donald A. Martyn. "Segment length mechanics of cardiac muscle; force, velocity and stiffness in cardiac muscle vary with length and calcium". W Developments in Cardiovascular Medicine, 107–11. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3311-8_9.

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Mirsky, Israel. "The Concept of Systolic Myocardial Stiffness with Applications to the Assessment of Myocardial Contractility in Health and Disease". W Cardiac Mechanics and Function in the Normal and Diseased Heart, 91–101. Tokyo: Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-67957-8_10.

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Linke, Wolfgang A., i Julio M. Fernandez. "Cardiac titin: molecular basis of elasticity and cellular contribution to elastic and viscous stiffness components in myocardium". W Mechanics of Elastic Biomolecules, 483–97. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0147-2_9.

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Huang, Stephen. "Cardiac mechanics". W Oxford Textbook of Advanced Critical Care Echocardiography, redaktorzy Anthony McLean, Stephen Huang i Andrew Hilton, 53–72. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749288.003.0004.

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Cardiac mechanics involves the study of the mechanical properties of the heart (ventricles) as a pump, and the physical factors that alter these properties. Neurohumoral factors aside, the function of the heart is determined by its intrinsic physical properties as well as extrinsic physical factors. The intrinsic properties include ventricular wall stress, elastance (stiffness) of the ventricle, contractility, and heart rate. The main extrinsic physical factors are blood volume, vessels properties, and extracardiac pressures. This chapter will review these intrinsic properties and how they interact with extrinsic factors to alter the cardiac (pump) function. Neurohumoral factors are excluded in this consideration. LaPlace’s law will be introduced to explain the idea of ventricular wall stress, hence the concepts of preload and afterload. The left ventricular pressure–volume relationship will be reviewed to explain how preload, afterload, and ventricular contractility interact and affect stroke volume. Finally, for completeness, the Frank–Starling relationship and Guyton’s venous return graph will be covered to explain steady state cardiac output.
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Lourenço, André P., Thierry C. Gillebert i Adelino F. Leite-Moreira. "Myocardial function: from myofilaments to cardiac pump". W Textbook of Arterial Stiffness and Pulsatile Hemodynamics in Health and Disease, 211–25. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91391-1.00013-3.

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Gielen, Stephan, M. Harold Laughlin i Dirk J. Duncker. "Vascular remodelling". W The ESC Textbook of Sports Cardiology, redaktorzy Antonio Pelliccia, Hein Heidbuchel, Domenico Corrado, Mats Börjesson i Sanjay Sharma, 41–48. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779742.003.0005.

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Vascular remodelling plays an important role in the adaptation of the athlete to increased exercise duration and intensity. Endurance exercise improves endothelium-dependent flow-mediated vasodilation and leads to increases in conduit artery lumen diameter after regular exercise, typically in the trained limb. These changes result in a reduced vascular stiffnes. On the contrary strength training (e.g. for weight-lifting) produces increased vascular stiffness and enlarged central vessels (e.g. aortic root diameters), while the diameters of peripheral vessels are unchanged. In the skeletal muscle, endurance training increases capillary density and improves oxygen exchange, thus adding further functional reserves to the aerobic exercise capacity. Aerobic exercise leads to a large increase in cardiac functional reserves, hence myocardial perfusion is increased in line with metabolic demands. In addition to improved endothelium-dependent vasodilation, coronary arterioles also exhibit an increased myogenic tone.
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Evers, Stefan, Michael Barenbrock i Ingo W. Husstedt. "Arterial distensibility in ergotamine and sumatriptan abuse". W The Triptans: Novel Drugs for Migraine, 173–77. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192632142.003.0024.

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Abstract Arterial compliance plays an important role in cardioand cerebrovascular haemodynamics by damping down the Fluctuation in arterial pressure and blood low generated by the intermittent cardiac output. Stiffness of large arteries impairs the buffering function of the arterial system leading to a disproportionate increase in systolic pressure and increase in pulse pressure at any given value of mean arterial pressure. Furthermore, the impaired buffering function contributes to the afterload imposed on the heart leading to left ventricular hypertrophy.
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Streszczenia konferencji na temat "Cardiac stiffness"

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Yan, Karen Chang, Mary Kate McDonough, James J. Pilla i Chun Xu. "Stiffness Characterization Using a Dynamic Heart Phantom and Magnetic Resonance Imaging". W ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-65222.

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Heart disease is the number one cause of death in the United States [1]. Cardiac Magnetic Resonance Imaging (MRI) technology can be used to diagnose and evaluate a number of diseases and conditions such as coronary artery disease, damage caused by a heart attack, heart failure, and heart valve problems etc. Given the inherent difficulty in imaging the heart in motion, many efforts have been made to improve cardiac motion tracking and eliminate motion related artifacts. A dynamic heart phantom (DHP) capable of simulating true physiological motions is a valuable research tool for improving quality of MR images and determining critical diagnostic information. For instance, MR images have been used to quantify myocardial strain and estimate soft tissue material parameters and in turn to learn about cardiac structure and function [2–4]. In these studies, heart phantoms made of rubber like materials with known material properties are often used as a mean of validation.
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Young, Jennifer L., Kyle Kretchmer i Adam J. Engler. "Temporally-Stiffening Hydrogel Regulates Cardiac Differentiation via Mechanosensitive Signaling". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14674.

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Stiffness of the extracellular matrix (ECM) surrounding cells plays an integral role in affecting how a cell spreads, migrates, and differentiates, in the case of stem cells. For mature cardiomyocytes, stiffness regulates myofibril striation, beating rate, and fiber alignment, but does not induce de-differentiation [1,2]. Despite improved myocyte function on materials which mimic the ∼10 kPa heart stiffness, the heart does not begin as a contractile ∼10 kPa material, but instead undergoes ∼10-fold myocardial stiffening during development [3]. Thiolated hyaluronic acid (HA) hydrogels have been used to mimic these stiffening dynamics by varying hydrogel functionality and component parameters. Recently, we have shown that pre-cardiac mesodermal cells plated on top of these stiffening HA hydrogels improves cardiomyocyte maturation compared to static, compliant polyacrylamide (PA) hydrogels [3]. While active mechanosensing causes maturation, the specific mechanisms responsible for responding to time-dependent stiffness remain unknown. Here we examined protein kinase signaling and mechanics in response to dynamic vs. static stiffness during the commitment process from embryonic stem cells (ESCs) through cardiomyocytes to better understand how developmentally-appropriate temporal changes in stiffness regulate cell commitment.
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Fleury, Joao, Matheus Carvalho Barbosa Costa, Saulo Gonçalves, Mário Silva i Rudolf Huebner. "influence of tissue stiffness on leaflet oscillation dynamics during a cardiac cycle." W 27th Brazilian Congress of Thermal Sciences and Engineering. ABCM, 2023. http://dx.doi.org/10.26678/abcm.cobem2023.cob2023-0375.

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Walsh, Peter W., Craig McLachlan, Leigh Ladd i R. Mark Gillies. "Novel Extra Aortic Counterpulsation Device for Enhancing Cardiac Performance". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53699.

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Heart failure is the fastest growing cardiovascular disorder. Incidence is rising at a rate of approximately 2% to 5% in people over 65 years of age, and 10% in people over 75 years of age [1]. Over 13 Million people suffer from heart failure in the USA, Europe, Canada and Australia, and heart failure is a leading cause of hospital admissions and re-admissions in Americans older than 65 years of age [2]. The secondary heart pump system is the expansion and recoil of the aorta which reduces heart load and drives left coronary artery blood flow. Increases in aortic stiffness are a result of elastin degradation due to ageing and/or cardiovascular diseases such as atherosclerosis [3–5], which increase heart load and pulse pressure [6–10]. Significantly higher aortic stiffness is found in hypertensive and heart failure suffers [6,7,9–11]. Specifically, healthy aged subjects have been found to have aortic stiffness 50% higher relative to subjects in a young and healthy group, while symptomatic hypertensive patients in heart failure have aortic stiffness further increased by approx. 77% relative to the age matched healthy cohort (i.e. by ∼88% relative to the young and healthy group) [11].
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Vejdani-Jahromi, Maryam, Yang Jiang, Gregg E. Trahey i Patrick D. Wolf. "M-mode ARFI imaging demonstrates the effect of coronary perfusion on cardiac stiffness". W 2014 IEEE International Ultrasonics Symposium (IUS). IEEE, 2014. http://dx.doi.org/10.1109/ultsym.2014.0029.

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Fan, Zhaopeng, Gong Zhang i Simon Liao. "Clinical analysis for cardiovascular disease by calculating Stiffness Index, Cardiac Output from pulse wave". W 2009 Canadian Conference on Electrical and Computer Engineering (CCECE). IEEE, 2009. http://dx.doi.org/10.1109/ccece.2009.5090180.

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Baicu, Catalin F., i Michael R. Zile. "Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells". W ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23158.

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Abstract Pathological processes which cause diastolic congestive heart failure (CHF), such as pressure overload hypertrophy (POH), produce abnormalities in the material properties of cardiac muscle cells (cardiomyocytes) and may selectively alter its elastic stiffness, viscosity, or both. Previous methods used to characterize these cardiomyocyte viscoelastic properties were constrained by specific biological and engineering limitations, which prevented testing in conditions that mimic normal physiology. The current study proposes an uniaxial variable-rate stretching method, in which isolated cardiomyocytes embedded in a three-dimensional gel matrix were subjected to stretch. Physiological Ca++ (2.5 mM) and rapid stretch rates up to 100 μm/sec provided experimental conditions parallel to in vivo physiology. The proposed method identified and individually quantified both cellular stiffness and viscosity, and showed that POH increased both elastic and viscous cardiomyocyte diastolic properties.
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Mattson, Alexander R., Michael D. Eggen, Vladimir Grubac i Paul A. Iaizzo. "Assessing the Relationship Between Right Atrial Stiffness and Chamber Pressure to Quantitatively Define Myocardial Tensile Properties". W 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3491.

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Developing a successful cardiac device requires detailed knowledge of cardiac mechanical properties. For example, tissue failure characteristics and compliance feed into design criteria for many pacemaker leads (Zhao et al., 2011). In the right atrium, tensile forces are exerted on the right atrial appendage in multiple clinical procedures. In a traditional lead implant, mechanical manipulations with a stylet aid a clinician in assessing lead fixation, with a seldom used “tug” test providing additional input. Atrial lead dislodgement remains one of the top complications for bradycardia pacing leads (Chahuan et al., 1994), in part because there is no standard mechanical assessment at implant to verify fixation. Thus, a deeper understanding of forces exerted on the atrium during implant, is fundamental to understanding the problem. Further characterization of the biomechanics relevant to atrial device implants will provide valuable design input for fixation tests and help drive research toward new atrial fixation mechanisms. This study aims to better define the relationships between right atrial stiffness and the chamber pressures within the right atrium, so to characterize the link between tensile displacement within the right atrium, and the force exerted on an implanted device in a functional heart. These experiments quantitatively define the fixation force of a fixed cardiac device with a given pulled displacement; i.e. displacing the device a given distance will effectively ensure the experimentally derived fixation force.
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Bayoumy, Ahmed A., Natalia J. Braams, Sophia A. Mouratoglou, Onno A. Spruijt, Frances S. De Man, Anton Vonk-Noordegraaf, Samara M. A. Jansen i in. "Determinants of right ventricular diastolic stiffness in precapillary pulmonary hypertension: a cardiac magnetic resonance study". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4046.

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Tang, Xin, Piyush Bajaj, Rashid Bashir i Taher Saif. "Mechanical Communication Between Cardiac Cell Leads to Synchrony in Beating". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80937.

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It is generally understood that cardiac cells synchronize their beating through electro-chemical signalling. Here we show, theoretically and experimentally, that isolated cardiac cells can communicate with each other through an intervening deformable media. Such communication leads to coupled dynamics and emergence of synchronous beating. The interaction between the cells depends inversely with the elastic modulus of the media, and the distance between them. This finding may explain asynchronous beating of the atrium in patients with atrial fibrillation where the stiffness of the atrial wall becomes significantly harder due to fibrosis [1].
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