Journal articles: 'Cardiac stiffness'

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Heller, Lois Jane, David E. Mohrman, and 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, no. 6 (June 1, 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., and Ryan C. Dean. "Stiffness Analysis of Cardiac Electrophysiological Models." Annals of Biomedical Engineering 38, no. 12 (June 26, 2010): 3592–604. http://dx.doi.org/10.1007/s10439-010-0100-9.

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Childers, Rachel C., Pamela A. Lucchesi, and Keith J. Gooch. "Decreased Substrate Stiffness Promotes a Hypofibrotic Phenotype in Cardiac Fibroblasts." International Journal of Molecular Sciences 22, no. 12 (June 9, 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, and Tamás Radovits. "Increased Expression of N2BA Titin Corresponds to More Compliant Myofibrils in Athlete’s Heart." International Journal of Molecular Sciences 22, no. 20 (October 15, 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, and R. Ventura-Clapier. "Energy-linked functional alterations in experimental cardiomyopathies." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 4 (October 1, 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, and R. Ventura-Clapier. "Energy-linked functional alterations in experimental cardiomyopathies." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 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, and Richard Lueker. "Improvement in arterial stiffness following cardiac rehabilitation." International Journal of Cardiology 167, no. 6 (September 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, and Pierre Boutouyrie. "Arterial Stiffness in the Heart Disease of CKD." Journal of the American Society of Nephrology 30, no. 6 (April 30, 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., and S. P. Farnsworth. "Cardiac myocyte stiffness following extraction with detergent and high salt solutions." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 6 (June 1, 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., and A. J. Brady. "Stiffness and shortening changes in myofilament-extracted rat cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (February 1, 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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Liatis, S., K. Alexiadou, A. Tsiakou, K. Makrilakis, N. Katsilambros, and N. Tentolouris. "Cardiac Autonomic Function Correlates with Arterial Stiffness in the Early Stage of Type 1 Diabetes." Experimental Diabetes Research 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/957901.

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Arterial stiffness is increased in type 1 diabetes (T1D), before any clinical complications of the disease are evident. The aim of the present paper was to investigate the association between cardiac autonomic function and arterial stiffness in a cohort of young T1D patients, without history of hypertension and any evidence of macrovascular and/or renal disease. Large artery stiffness was assessed by measurement of carotid-femoral pulse wave velocity (PWV). Cardiac autonomic function was assessed by the cardiovascular tests proposed by Ewing and Clarke. Patients with a high cardiac autonomic neuropathy score (4) had significantly higher PWV than those with a low score (0-1). A negative, heart rate-independent, correlation between PWV and heart rate variation during respiration was observed (). In multivariable analysis, index was the strongest correlate of PWV (β-coefficient = −0.326, ). Cardiac parasympathetic function is a strong predictor of large arterial stiffness, in young T1D patients free of macrovascular and renal complications.

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Zhu, Tong, Jingjing Song, Bin Gao, Junjie Zhang, Yabei Li, Zhaoyang Ye, Yuxiang Zhao, Xiaogang Guo, Feng Xu, and Fei Li. "Effect of Extracellular Matrix Stiffness on Candesartan Efficacy in Anti-Fibrosis and Antioxidation." Antioxidants 12, no. 3 (March 9, 2023): 679. http://dx.doi.org/10.3390/antiox12030679.

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Myocardial fibrosis progression and imbalanced redox state are closely associated with increased extracellular matrix (ECM) stiffness. Candesartan (CAN), an angiotensin II (Ang II) receptor inhibitor, has shown promising anti-fibrosis and antioxidant efficacy in previous cardiovascular disease studies. However, the effect of ECM stiffness on CAN efficacy remains elusive. In this study, we constructed rat models with three different degrees of myocardial fibrosis and treated them with CAN, and then characterized the stiffness, cardiac function, and NADPH oxidase-2 (NOX2) expression of the myocardial tissues. Based on the obtained stiffness of myocardial tissues, we used polyacrylamide (PA) gels with three different stiffness to mimic the ECM stiffness of cardiac fibroblasts (CFs) at the early, middle, and late stages of myocardial fibrosis as the cell culture substrates and then constructed CFs mechanical microenvironment models. We studied the effects of PA gel stiffness on the migration, proliferation, and activation of CFs without and with CAN treatment, and characterized the reactive oxygen species (ROS) and glutathione (GSH) levels of CFs using fluorometry and scanning electrochemical microscopy (SECM). We found that CAN has the best amelioration efficacy in the cardiac function and NOX2 levels in rats with medium-stiffness myocardial tissue, and the most obvious anti-fibrosis and antioxidant efficacy in CFs on the medium-stiffness PA gels. Our work proves the effect of ECM stiffness on CAN efficacy in myocardial anti-fibrosis and antioxidants for the first time, and the results demonstrate that the effect of ECM stiffness on drug efficacy should also be considered in the treatment of cardiovascular diseases.

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Lartaud-Idjouadiene, I., N. Niederhoffer, J. J. Debets, H. A. Struyker-Boudier, J. Atkinson, and J. F. Smits. "Cardiac function in a rat model of chronic aortic stiffness." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 5 (May 1, 1997): H2211—H2218. http://dx.doi.org/10.1152/ajpheart.1997.272.5.h2211.

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Cardiac function was investigated in conscious normotensive rats in which increased aortic stiffness was produced as a result of vascular calcium overload after treatment with vitamin D3 plus nicotine (VDN rats, n = 16; controls, n = 17). Baseline stroke volume, cardiac output, and cardiac response to a venous volume overload were unchanged after 1 mo of exposure to increased aortic stiffness, as were baseline venous return and total vascular capacitance. The latter was estimated from the change in mean circulatory filling pressure after modification of circulatory volume. Cardiovascular reflexes were modified in VDN rats. Bradycardia evoked by an increase in arterial PCO2 (PaCO2) or hypotensive hemorrhage was more pronounced. The PaCO2-induced bradycardia was accompanied by a fall in cardiac output in VDN rats but not in controls. In VDN rats, the attenuation of sympathetic reflexes may explain the slower recovery of blood pressure after hypotensive hemorrhage. In conclusion, a chronic increase in aortic stiffness does not compromise cardiac performance, but cardiovascular reflexes are impaired in VDN rats. Whether this is because of the increase in aortic stiffness or the effect of VDN treatment on the baroreceptors or other components of the reflex arc remains to be elucidated.

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EVESON, David J., Thompson G. ROBINSON, Nainal S. SHAH, Ronney B. PANERAI, Sanjoy K. PAUL, and John F. POTTER. "Abnormalities in cardiac baroreceptor sensitivity in acute ischaemic stroke patients are related to aortic stiffness." Clinical Science 108, no. 5 (April 22, 2005): 441–47. http://dx.doi.org/10.1042/cs20040264.

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Cardiac BRS (baroreceptor reflex sensitivity) is impaired following ischaemic stroke and predicts the risk of subsequent long-term death and disability. Impaired cardiac BRS may be due to impaired central processing of baroreceptor information following stroke or reduced baroreceptor activity due to increased large artery stiffness. We evaluated the relationship between large (aortic) artery stiffness and cardiac BRS during the acute phase of ischaemic stroke and in comparison with a group of stroke-free control subjects. Thirty-one ischaemic stroke patients were studied within 48 h of onset and again on day 14, along with 26 control subjects free of cerebrovascular disease. Cardiac BRS (determined by spectral analyses) and arterial stiffness estimated by PWVcf (carotid–femoral pulse wave velocity) using applanation tonometry were obtained. At baseline, cardiac BRS was lower in the stroke compared with the control group (4.3±2.3 compared with 6.5±4.2 ms/mmHg; P<0.05). Cardiac BRS values were correlated with PWVcf at <48 h (r=−0.51, P<0.01) and on day 14 (r=−0.54, P<0.01), but not in the control group (r=−0.27, P=not significant). In quantile regression models, taking into account the effect of all cardiovascular variables, cardiac BRS was independently related to PWVcf at baseline and on day 14 in the stroke patients, but stroke was not related to cardiac BRS level when other cardiovascular variables were considered. Wall stiffness of the arterial vessels involved in the baroreflex arc may account for, at least in part, the reduced cardiac BRS observed in acute stroke patients.

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Caenen, Annette, Mathieu Pernot, Kathryn R. Nightingale, Jens-Uwe Voigt, Hendrik J. Vos, Patrick Segers, and Jan D’hooge. "Assessing cardiac stiffness using ultrasound shear wave elastography." Physics in Medicine & Biology 67, no. 2 (January 17, 2022): 02TR01. http://dx.doi.org/10.1088/1361-6560/ac404d.

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Abstract Shear wave elastography offers a new dimension to echocardiography: it measures myocardial stiffness. Therefore, it could provide additional insights into the pathophysiology of cardiac diseases affecting myocardial stiffness and potentially improve diagnosis or guide patient treatment. The technique detects fast mechanical waves on the heart wall with high frame rate echography, and converts their propagation speed into a stiffness value. A proper interpretation of shear wave data is required as the shear wave interacts with the intrinsic, yet dynamically changing geometrical and material characteristics of the heart under pressure. This dramatically alters the wave physics of the propagating wave, demanding adapted processing methods compared to other shear wave elastography applications as breast tumor and liver stiffness staging. Furthermore, several advanced analysis methods have been proposed to extract supplementary material features such as viscosity and anisotropy, potentially offering additional diagnostic value. This review explains the general mechanical concepts underlying cardiac shear wave elastography and provides an overview of the preclinical and clinical studies within the field. We also identify the mechanical and technical challenges ahead to make shear wave elastography a valuable tool for clinical practice.

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Serhiyenko, Victoria A., Ludmila M. Serhiyenko, Volodymyr B. Sehin, and Alexandr A. Serhiyenko. "Pathophysiological and clinical aspects of the circadian rhythm of arterial stiffness in diabetes mellitus: A minireview." Endocrine Regulations 56, no. 4 (October 1, 2022): 284–94. http://dx.doi.org/10.2478/enr-2022-0031.

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Abstract Several cross-sectional trials have revealed increased arterial stiffness connected with the cardiac autonomic neuropathy in types 2 and 1 diabetic patients. The pathophysiological relationship between arterial stiffness and autonomic dysfunction in diabetes mellitus is still underinvestigated and the question whether the presence of cardiac autonomic neuropathy leads to arterial stiffening or increased arterial stiffness induced autonomic nervous system impairment is still open. Both arterial stiffness and dysfunction of the autonomic nervous system have common pathogenetic pathways, counting state of the chronic hyperinsulinemia and hyperglycemia, increased formation of advanced glycation end products, activation of protein kinase C, development of endothelial dysfunction, and chronic low-grade inflammation. Baroreceptor dysfunction is thought to be one of the possible reasons for the arterial wall stiffening development and progression. On the contrary, violated autonomic nervous system function can affect the vascular tone and by this way alter the large arteries walls elastic properties. Another possible mechanism of attachment and/or development of arterial stiffness is the increased heart rate and autonomic dysfunction corresponding progression. This minireview analyzes the current state of the relationship between the diabetes mellitus and the arterial stiffness. Particular attention is paid to the analysis, interpretation, and application of the results obtained in patients with type 2 diabetes mellitus and diabetic cardiac autonomic neuropathy.

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GORGULU, Sevket, Nevzat USLU, Mehmet EREN, Seden CELIK, Aydın YILDIRIM, Bahadır DAGDEVIREN, and Tuna TEZEL. "Aortic stiffness in patients with cardiac syndrome X." Acta Cardiologica 58, no. 6 (December 1, 2003): 507–11. http://dx.doi.org/10.2143/ac.58.6.2005314.

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Hamdani, Nazha, and Wolfgang A. Linke. "Myocardial Titin: An Important Modifier of Cardiac Stiffness." Biophysical Journal 106, no. 2 (January 2014): 346a. http://dx.doi.org/10.1016/j.bpj.2013.11.1972.

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Spiteri, Raymond J., and Ryan C. Dean. "Erratum to: Stiffness Analysis of Cardiac Electrophysiological Models." Annals of Biomedical Engineering 40, no. 7 (May 8, 2012): 1622–25. http://dx.doi.org/10.1007/s10439-011-0488-x.

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Nemes, Attila, Dóra Földeák, Péter Domsik, Anita Kalapos, Árpád Kormányos, Zita Borbényi, and Tamás Forster. "Cardiac amyloidosis is associated with increased aortic stiffness." Journal of Clinical Ultrasound 46, no. 3 (October 24, 2017): 183–87. http://dx.doi.org/10.1002/jcu.22547.

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Gao, Likun, Yanlin He, Hangwei Zhu, Guangkai Sun, and Lianqing Zhu. "Stiffness Modelling and Performance Evaluation of a Soft Cardiac Fixator Flexible Arm with Granular Jamming." Machines 9, no. 12 (November 23, 2021): 303. http://dx.doi.org/10.3390/machines9120303.

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To meet the practical application requirements of cardiac fixation during off-pump coronary artery bypass surgery, a soft cardiac fixator with a flexible arm was previously designed. To enable the soft cardiac fixator to adapt to uncertain external forces, this study evaluates the variable-stiffness performance of the flexible arm. First, the flexible arm was simplified as a soft silicone manipulator measuring 60 mm × 90 mm × 120 mm, which can actuate, soften, or stiffen independently along the length of the arm by combining granular jamming with input pressure. Then, the soft manipulator was modelled as a cantilever beam to analyse its variable-stiffness performance with granular jamming. Next, based on theoretical analysis and calculations, many experiments were conducted to evaluate the variable-stiffness performance of the soft manipulator. The experimental results demonstrated that the variable-stiffness performance is influenced by the flexible arm length, the size of the granules, and the input pressure.

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Li, Jieli, Michael A. Mkrtschjan, Ying-Hsi Lin, and Brenda Russell. "Variation in stiffness regulates cardiac myocyte hypertrophy via signaling pathways." Canadian Journal of Physiology and Pharmacology 94, no. 11 (November 2016): 1178–86. http://dx.doi.org/10.1139/cjpp-2015-0578.

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Much diseased human myocardial tissue is fibrotic and stiff, which increases the work that the ventricular myocytes must perform to maintain cardiac output. The hypothesis tested is that the increased load due to greater stiffness of the substrata drives sarcomere assembly of cells, thus strengthening them. Neonatal rat ventricular myocytes (NRVM) were cultured on polyacrylamide or polydimethylsiloxane substrates with stiffness of 10 kPa, 100 kPa, or 400 kPa, or glass with stiffness of 61.9 GPa. Cell size increased with stiffness. Two signaling pathways were explored, phosphorylation of focal adhesion kinase (p-FAK) and lipids by phosphatidylinositol 4,5-bisphosphate (PIP2). Subcellular distributions of both were determined in the sarcomeric fraction by antibody localization, and total amounts were measured by Western or dot blotting, respectively. More p-FAK and PIP2 distributed to the sarcomeres of NRVM grown on stiffer substrates. Actin assembly involves the actin capping protein Z (CapZ). Both actin and CapZ dynamic exchange were significantly increased on stiffer substrates when assessed by fluorescence recovery after photobleaching (FRAP) of green fluorescent protein tags. Blunting of actin FRAP by FAK inhibition implicates linkage from mechano-signalling pathways to cell growth. Thus, increased stiffness of cardiac disease can be modeled with polymeric materials to understand how the microenvironment regulates cardiac hypertrophy.

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Brady, A. J. "Length dependence of passive stiffness in single cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (April 1, 1991): H1062—H1071. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1062.

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Passive elastic properties have been studied in detergent-skinned isolated single cardiac myocytes of rat, guinea pig, and rabbit in an attempt to determine whether a measurable difference exists in passive cellular elastic characteristics of these mammalian species. Although the cross-sectional area of isolated cardiac myocytes is complex, a small but statistical difference appears to exist in the elastic modulus of detergent-skinned mammalian cardiac myocytes at 2.2 microns sarcomere length (SL) in the order rat is greater than rabbit, which is greater than guinea pig. The stiffness of rat cells increases least rapidly with increases in SL, and that of the rabbit cells increases most rapidly. In comparison with intact cardiac tissue in the literature, the proportion of stress contributed by skinned myocytes may be as much as half that of the trabeculae at 2.2 microns SL and approximately 10% of that of papillary muscles. Below 2.2 microns SL, the relative cellular proportion increases such that cellular elements may be a major contributor at 1.9 microns SL. Above 2.2 microns SL, the relative cellular contribution declines such that by 2.4 microns SL the cellular contribution is insignificant. It is concluded that at functional SLs intracellular elastic elements may contribute measurably to total cardiac passive elasticity, but at extended lengths the extracellular structures constitute the major limitation to extension.

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Ostroumova, O. D., and A. I. Kochetkov. "Myocardial Strain and Stiffness Parameters as a Novel Target of Antihypertensive Treatment." Kardiologiia 58, no. 11 (November 24, 2018): 72–81. http://dx.doi.org/10.18087/cardio.2018.11.10203.

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In the review, the clinical significance of increased myocardial stiffness and strain impairment in the settings of arterial hypertension is considered. The mechanisms of increasing myocardial stiffness as a part of hypertensive heart disease are presented. Particular attention is paid to the role of the sympathetic nervous system activation as one of the triggers that induce the connective tissue alteration of cardiac interstitium. The possibilities of echocardiography in the early noninvasive detection of myocardial strain abnormalities are discussed. New ultrasound parameters for describing stiffness properties of the heart are presented. From the evidence-based medicine point of view, the prognostic significance of increasing myocardial stiffness as a risk factor of the adverse cardiovascular events, as well as the possibility of its management with different antihypertensive drugs, is considered. Finally, there are presented clinical trials data, indicating high potential of the highly selective ^1-adrenoblocker bisoprolol for of correction myocardial stiffness and strain impairment.

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Ihne-Schubert, Sandra Michaela, Oliver Goetze, Felix Gerstendörfer, Floran Sahiti, Ina Schade, Aikaterini Papagianni, Caroline Morbach, et al. "Cardio-Hepatic Interaction in Cardiac Amyloidosis." Journal of Clinical Medicine 13, no. 5 (March 1, 2024): 1440. http://dx.doi.org/10.3390/jcm13051440.

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Background: Congestion is associated with poor prognosis in cardiac amyloidosis (CA). The cardio-hepatic interaction and the prognostic impact of secondary liver affection by cardiac congestion in CA are poorly understood and require further characterisation. Methods: Participants of the amyloidosis cohort study AmyKoS at the Interdisciplinary Amyloidosis Centre of Northern Bavaria with proven transthyretin (ATTR-CA) and light chain CA (AL-CA) underwent serial work-up including laboratory tests, echocardiography, and in-depth hepatic assessment by vibration-controlled transient elastography (VCTE) and 13C-methacetin breath test. Results: In total, 74 patients with AL-CA (n = 17), ATTR-CA (n = 26) and the controls (n = 31) were analysed. ATTR-CA patients showed decreased microsomal liver function expressed by maximal percentage of dose rate (PDRpeak) related to hepatic congestion. Reduced PDRpeak in AL-CA could result from altered pharmacokinetics due to changed hepatic blood flow. Liver stiffness as a combined surrogate of chronic liver damage and congestion was identified as a predictor of all-cause mortality. Statistical modelling of the cardio-hepatic interaction revealed septum thickness, NT-proBNP and PDRpeak as predictors of liver stiffness in both CA subtypes; dilatation of liver veins and the fibrosis score FIB-4 were only significant for ATTR-CA. Conclusions: Non-invasive methods allow us to characterise CA-associated hepatic pathophysiology. Liver stiffness might be promising for risk stratification in CA.

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Arani, Arvin, Shivaram P. Arunachalam, Ian C. Y. Chang, Francis Baffour, Phillip J. Rossman, Kevin J. Glaser, Joshua D. Trzasko, et al. "Cardiac MR elastography for quantitative assessment of elevated myocardial stiffness in cardiac amyloidosis." Journal of Magnetic Resonance Imaging 46, no. 5 (February 25, 2017): 1361–67. http://dx.doi.org/10.1002/jmri.25678.

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Yong, Kar Wey, YuHui Li, GuoYou Huang, Tian Jian Lu, Wan Kamarul Zaman Wan Safwani, Belinda Pingguan-Murphy, and Feng Xu. "Mechanoregulation of cardiac myofibroblast differentiation: implications for cardiac fibrosis and therapy." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 4 (August 15, 2015): H532—H542. http://dx.doi.org/10.1152/ajpheart.00299.2015.

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Cardiac myofibroblast differentiation, as one of the most important cellular responses to heart injury, plays a critical role in cardiac remodeling and failure. While biochemical cues for this have been extensively investigated, the role of mechanical cues, e.g., extracellular matrix stiffness and mechanical strain, has also been found to mediate cardiac myofibroblast differentiation. Cardiac fibroblasts in vivo are typically subjected to a specific spatiotemporally changed mechanical microenvironment. When exposed to abnormal mechanical conditions (e.g., increased extracellular matrix stiffness or strain), cardiac fibroblasts can undergo myofibroblast differentiation. To date, the impact of mechanical cues on cardiac myofibroblast differentiation has been studied both in vitro and in vivo. Most of the related in vitro research into this has been mainly undertaken in two-dimensional cell culture systems, although a few three-dimensional studies that exist revealed an important role of dimensionality. However, despite remarkable advances, the comprehensive mechanisms for mechanoregulation of cardiac myofibroblast differentiation remain elusive. In this review, we introduce important parameters for evaluating cardiac myofibroblast differentiation and then discuss the development of both in vitro (two and three dimensional) and in vivo studies on mechanoregulation of cardiac myofibroblast differentiation. An understanding of the development of cardiac myofibroblast differentiation in response to changing mechanical microenvironment will underlie potential targets for future therapy of cardiac fibrosis and failure.

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Brozic, Anka P., Susan Marzolini, and Jack M. Goodman. "Effects of an adapted cardiac rehabilitation programme on arterial stiffness in patients with type 2 diabetes without cardiac disease diagnosis." Diabetes and Vascular Disease Research 14, no. 2 (January 17, 2017): 104–12. http://dx.doi.org/10.1177/1479164116679078.

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Purpose: To determine the effects of a 12-week cardiac rehabilitation programme of aerobic and resistance exercise training on arterial stiffness, peak calf vasodilatory reserve, and haemostatic markers in patients with type 2 diabetes. Methods: Observational cohort study examining effects of 12 weeks of exercise training in 23 subjects (13 men, 10 women; mean age of 56.1 ± 10.1 years) with type 2 diabetes mellitus. Subjects performed exercise training for 12 weeks [aerobic training 5 days/week, 70%–75% peak cardiovascular fitness (VO2peak) and resistance training 2–3 days/week, 60% of one repetition maximum]. Vascular stiffness (pulse-wave velocity), augmentation index, peak calf vasodilatory reserve, and VO2peak were measured pre- and post-exercise training. Secondary outcomes included heart rate variability and haemostatic measures. Results: VO2peak increased by 16% (20.1 ± 5.5 vs 23.2 ± 8.8 mL/kg/min, p = 0.002) and abdominal circumference was reduced (101.9 ± 13.3 vs 97.9 ± 12.7 cm, p < 0.03). Vascular function was improved including central arterial stiffness (central pulse-wave velocity: 8.44 ± 1.75 vs 8.02 ± 1.60 m/s, p = 0.026) and the aortic augmentation index (21.7 ± 10.6% vs 18.3 ± 12.6%, p = 0.005); peak calf vasodilatory reserve increased from 30.3 ± 10.6 mL/100 mL/min to 38.0 ± 15.3 mL/100 mL/min ( p = 0.04). No changes were seen in heart rate variability, blood lipids, glycated haemoglobin and C-reactive protein. Conclusion: A 12-week cardiac rehabilitation programme of aerobic and resistance training significantly reduces arterial stiffness and improves aerobic fitness in individuals with type 2 diabetes mellitus.

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Woodiwiss, A. J., and G. R. Norton. "Exercise-induced cardiac hypertrophy is associated with an increased myocardial compliance." Journal of Applied Physiology 78, no. 4 (April 1, 1995): 1303–11. http://dx.doi.org/10.1152/jappl.1995.78.4.1303.

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Left ventricular (LV) chamber and myocardial wall compliance were investigated in rats with exercise-induced cardiac hypertrophy. Voluntary exercise training was performed on running wheels. After 16 wk of exercise training, cardiac performance was measured in anesthetized open-chest ventilated rats. LV end-diastolic performance was calculated from both short-axis external diameter and long-axis segmental length measurements. Exercise-trained rats developed significant LV hypertrophy (1.03 +/- 0.02 g) compared with control rats (0.91 +/- 0.03 g; P < 0.01). The physiological hypertrophy was associated with an increased LV wall thickness-to-internal radius ratio consistent with a concentric geometry. LV end-diastolic stiffness (slope of the linearized LV end-diastolic pressure-strain relationship) was decreased in both the short (P < 0.02) and long (P < 0.02) axis of LV as a result of exercise training. The LV end-diastolic chamber stiffness (slope of the linearized LV end-diastolic pressure-volume relationship) was also decreased in the exercised group (P < 0.05). The decreased chamber stiffness occurred as a consequence of a decrease in the regional myocardial wall elastic stiffness (slope of the linearized LV end-diastolic stress-strain relationship; P < 0.05). Thus an increased LV wall thickness as a result of exercise-induced LV hypertrophy is associated with an enhanced ventricular chamber compliance, which in turn is attributed to a decrease in the diastolic stiffness of the myocardial wall.

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Krishnamurthy, Gaurav, Akinobu Itoh, Julia C. Swanson, D. Craig Miller, and Neil B. Ingels. "Transient stiffening of mitral valve leaflets in the beating heart." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 6 (June 2010): H2221—H2225. http://dx.doi.org/10.1152/ajpheart.00215.2010.

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Anterior mitral leaflet stiffness during isovolumic contraction (IVC) is much greater than that during isovolumic relaxation (IVR). We have hypothesized that this stiffening is due to transient early systolic force development in the slip of cardiac myocytes in the annular third of the anterior leaflet. Because the atrium is excited before IVC and leaflet myocytes contract for ≤250 ms, this hypothesis predicts that IVC leaflet stiffness will drop to near-IVR values in the latter half of ventricular systole. We tested this prediction using radiopaque markers and inverse finite element analysis of 30 beats in 10 ovine hearts. For each beat, circumferential ( Ec) and radial ( Er) stiffness was determined during IVC (Δ t1), end IVC to midsystole (Δ t2), midsystole to IVR onset (Δ t3), and IVR (Δ t4). Group mean stiffness ( Ec ± SD; Er ± SD; in N/mm2) during Δ t1 (44 ± 16; 15 ± 4) was 1.6–1.7 times that during Δ t4 (28 ± 11; 9 ± 3); Δ t2 stiffness (39 ± 15; 14 ± 4) was 1.3–1.5 times that of Δ t4, but Δ t3 stiffness (32 ± 12; 11 ± 3) was only 1.1–1.2 times that of Δ t4. The stiffness drop during Δ t3 supports the hypothesis that anterior leaflet stiffening during IVC arises primarily from transient force development in leaflet cardiac myocytes, with stiffness reduced as this leaflet muscle relaxes in the latter half of ventricular systole.

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Morgan, Eric E., Michael P. Morran, Nicholas G. Horen, David A. Weaver, and Andrea L. Nestor-Kalinoski. "RNO3 QTL regulates vascular structure and arterial stiffness in the spontaneously hypertensive rat." Physiological Genomics 53, no. 12 (December 1, 2021): 534–45. http://dx.doi.org/10.1152/physiolgenomics.00038.2021.

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Increased arterial stiffness is an independent risk factor for hypertension, stroke, and cardiovascular morbidity. Thus, understanding the factors contributing to vascular stiffness is of critical importance. Here, we used a rat model containing a known quantitative trait locus (QTL) on chromosome 3 (RNO3) for vasoreactivity to assess potential genetic elements contributing to blood pressure, arterial stiffness, and their downstream effects on cardiac structure and function. Although no differences were found in blood pressure at any time point between parental spontaneously hypertensive rats (SHRs) and congenic SHR.BN3 rats, the SHRs showed a significant increase in arterial stiffness measured by pulse wave velocity. The degree of arterial stiffness increased with age in the SHRs and was associated with compensatory cardiac changes at 16 wk of age, and decompensatory changes at 32 wk, with no change in cardiac structure or function in the SHR.BN3 hearts at these time points. To evaluate the arterial wall structure, we used multiphoton microscopy to quantify cells and collagen content within the adventitia and media of SHR and SHR.BN3 arteries. No difference in cell numbers or proliferation rates was found, although phenotypic diversity was characterized in vascular smooth muscle cells. Herein, significant anatomical and physiological differences related to arterial structure and cardiovascular tone including collagen, pulse wave velocity (PWV), left ventricular (LV) geometry and function, and vascular smooth muscle cell (VSMC) contractile apparatus proteins were associated with the RNO3 QTL, thus providing a novel platform for studying arterial stiffness. Future studies delimiting the RNO3 QTL could aid in identifying genetic elements responsible for arterial structure and function.

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Leite-Moreira, Adelino F., Silvia-Marta Oliveira, and Paolo Marino. "Left atrial stiffness and its implications for cardiac function." Future Cardiology 3, no. 2 (March 2007): 175–83. http://dx.doi.org/10.2217/14796678.3.2.175.

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Hashimoto, Yuto, and Takanobu Okamoto. "Relationship Between Arterial Stiffness And Cardiac Function In Athletes." Medicine & Science in Sports & Exercise 51, Supplement (June 2019): 670. http://dx.doi.org/10.1249/01.mss.0000562506.99507.e1.

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Milazzo, Valeria, Simona Maule, Cristina Di Stefano, Francesco Tosello, Silvia Totaro, Franco Veglio, and Alberto Milan. "Cardiac Organ Damage and Arterial Stiffness in Autonomic Failure." Hypertension 66, no. 6 (December 2015): 1168–75. http://dx.doi.org/10.1161/hypertensionaha.115.05913.

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Jia, Guanghong, Annayya R. Aroor, and James R. Sowers. "Arterial Stiffness: A Nexus between Cardiac and Renal Disease." Cardiorenal Medicine 4, no. 1 (2014): 60–71. http://dx.doi.org/10.1159/000360867.

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Christensen, Tova, Kristi Anseth, and Leslie Leinwand. "Matrix Stiffness Contributes to Pathological Activation of Cardiac Fibroblasts." Biophysical Journal 114, no. 3 (February 2018): 110a. http://dx.doi.org/10.1016/j.bpj.2017.11.635.

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KHOZYAINOVA, N. "The arterial stiffness and cardiac remodeling in hypertensive patients." American Journal of Hypertension 17, no. 5 (May 2004): S166. http://dx.doi.org/10.1016/j.amjhyper.2004.03.436.

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Holewijn, Suzanne, Erik Groot Jebbink, Wim Aengevaeren, Jasper Martens, Marcel Hovens, and Michel Reijnen. "8.1 ARTERIAL STIFFNESS, BLOOD PRESSURE AND CARDIAC OUTPUT STUDY." Artery Research 16, no. C (2016): 65. http://dx.doi.org/10.1016/j.artres.2016.10.057.

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Wesley, Callan D., Annarita Sansonetti, Cedric H. G. Neutel, Dustin N. Krüger, Guido R. Y. De Meyer, Wim Martinet, and Pieter-Jan Guns. "Short-Term Proteasome Inhibition: Assessment of the Effects of Carfilzomib and Bortezomib on Cardiac Function, Arterial Stiffness, and Vascular Reactivity." Biology 13, no. 10 (October 21, 2024): 844. http://dx.doi.org/10.3390/biology13100844.

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Proteasome inhibitors such as bortezomib and carfilzomib induce apoptosis and are a cornerstone in the treatment of relapsed or refractory multiple myeloma. However, concerns have emerged concerning their link to cancer therapy-related cardiovascular dysfunction (CTRCD). Bortezomib, a reversible first-generation inhibitor, and carfilzomib, a second-generation irreversible inhibitor, are associated with hypertension, heart failure, and cardiac arrhythmias. The current study investigated the effects of bortezomib and carfilzomib on cardiac (left ventricular ejection fraction, LVEF) and vascular (arterial stiffness, vascular reactivity) function. Cardiac function assessment aimed to build upon existing evidence of proteasome inhibitors CTRCD, while arterial stiffness served as an early indicator of potential vascular remodeling. Groups of 12-week-old C57BL/6J male mice (n = 8 per group) were randomly assigned to receive vehicle, carfilzomib (8 mg/kg I.P.), or bortezomib (0.5 mg/kg I.P.). Additionally, proteasome inhibition was assessed in mice treated with L-NAME (0.5 mg/kg) to induce hypertension. Cardiac and vascular parameters were evaluated via echocardiography on days 0 and 3. On day 6, mice were sacrificed for ex vivo analysis of arterial stiffness and vascular reactivity. Overall, no changes in arterial stiffness were detected either in vivo or ex vivo at basal pressures. However, a steeper pressure–stiffness curve was observed for carfilzomib in normotensive (p < 0.01) and hypertensive (p < 0.0001) mice ex vivo. Additionally, in hypertensive mice, carfilzomib decreased LVEF (p = 0.06), with bortezomib exhibiting similar trends. Vascular reactivity remained largely unchanged, but proteasome inhibition tended to enhance endothelial-independent relaxations in both control and hypertensive mice. In conclusion, short-term treatment with carfilzomib and bortezomib is considered relatively safe for the protocols assessed in the study.

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Emre, Ender, Gulay Uzun, Ahmet Özderya, Mustafa Çetin, Muhammet Raşit Sayın, and Ezgi Kalaycıoğlu. "Exercise-Based Cardiac Rehabilitation Reduced Arterial Stiffness in Patients with Coronary Artery Disease, determined by CAVI method “Cardiac Rehabilitation Reduced Arterial Stiffness”." Kocaeli Medical Journal 12, no. 1 (2023): 158–65. http://dx.doi.org/10.5505/ktd.2023.81593.

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Herrmann, Keith L., Andrew D. McCulloch, and Jeffrey H. Omens. "Glycated collagen cross-linking alters cardiac mechanics in volume-overload hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 4 (April 1, 2003): H1277—H1284. http://dx.doi.org/10.1152/ajpheart.00168.2002.

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Alteration of hemodynamic loading induces remodeling that includes changes in myocardial properties and extracellular matrix structure. We investigated the hypothesis that cardiac hypertrophy due to volume overload produces changes in myocardial diastolic mechanics and stiffness that are in part due to alterations in advanced glycation end-product (AGE) collagen cross-linking. Rats developed volume overload induced by arteriovenous fistula (AVF). To assess the dependence of AGE cross-linking on mechanics, we prevented AGE formation by administering the drug aminoguanidine (AG) to one group of AVF rats (AG+AVF). Volume overload did not modify collagen concentration. Right ventricular AGE cross-links were modestly elevated in AVF hearts but were significantly reduced by AG. AVF rats exhibited significantly increased septal AGE cross-links that were inhibited in the AG+AVF group. AVF-induced increases in left ventricular longitudinal stiffness and septal circumferential stiffness were prevented in AG+AVF hearts. Volume overload appears to regionally modify AGE collagen cross-linking and stiffness, and AG treatment prevented these increases, demonstrating that AGE cross-linking plays a role in mediating diastolic compliance in volume-overload hypertrophy.

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Allijn, Iris, Marcelo Ribeiro, André Poot, Robert Passier, and Dimitrios Stamatialis. "Membranes for Modelling Cardiac Tissue Stiffness In Vitro Based on Poly(trimethylene carbonate) and Poly(ethylene glycol) Polymers." Membranes 10, no. 10 (October 3, 2020): 274. http://dx.doi.org/10.3390/membranes10100274.

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Despite the increased expenditure of the pharmaceutical industry on research and development, the number of drugs for cardiovascular diseases that reaches the market is decreasing. A major issue is the limited ability of the current in vitro and experimental animal models to accurately mimic human heart disease, which hampers testing of the efficacy of potential cardiac drugs. Moreover, many non-heart-related drugs have severe adverse cardiac effects, which is a major cause of drugs’ retraction after approval. A main hurdle of current in vitro models is their inability to mimic the stiffness of in vivo cardiac tissue. For instance, poly(styrene) petri dishes, which are often used in these models, have a Young’s modulus in the order of GPa, while the stiffness of healthy human heart tissue is <50 kPa. In pathological conditions, such as scarring and fibrosis, the stiffness of heart tissue is in the >100 kPa range. In this study, we focus on developing new membranes, with a set of properties for mimicry of cardiac tissue stiffness in vitro, based on methacrylate-functionalized macromers and triblock-copolymers of poly(trimethylene carbonate) and poly(ethylene glycol). The new membranes have Young’s moduli in the hydrated state ranging from 18 kPa (healthy tissue) to 2.5 MPa (pathological tissue), and are suitable for cell contraction studies using human pluripotent stem-cell-derived cardiomyocytes. The membranes with higher hydrophilicity have low drug adsorption and low Young’s moduli and could be suitable for drug screening applications.

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Jaccard, Arnaud, Anne Cypierre, Annick Rousseau, Fatima Yagoubi, Julie Abraham, Annie Lefebvre, Elisabeth Vidal, Dominique Bordessoule, and Véronique Loustaud-Ratti. "Transient Elastography (FibroScan®) for Noninvasive Assessment of Liver Amyloidosis." Blood 114, no. 22 (November 20, 2009): 4894. http://dx.doi.org/10.1182/blood.v114.22.4894.4894.

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Abstract Abstract 4894 Background Liver involvement is frequent in AL amyloidosis patients, and is found in 70% of cases in autopsy series. Histologic diagnosis of amyloid deposition is mandatory, preferably by biopsies of non-hepatic tissue, liver biopsy being associated with an increased risk of bleeding. FibroScan, a non invasive method for measuring liver stiffness, is used to measure liver fibrosis in patients with viral hepatitis. We postulated that amyloid liver deposition in AL could enhance liver stiffness and that may help for the diagnosis of liver amyloidosis. Methods 41 consecutive AL patients with systemic disease seen at the French Reference Center for AL amyloidosis were analyzed: 17 had liver AL, 23 cardiac AL, and 13 no liver or cardiac involvement according to the criteria defined by the Tours Consensus Opinion on Amyloidosis (2005). All had liver stiffness measured by FibroScan simultaneously with 76 controls: 16 healthy controls, 10 multiple myeloma and 50 consecutive patients chronically infected with hepatitis C virus (HCV). According to the manufacturer's criteria, liver stiffness was interpretable in 32 (78%) of AL patients and in 68 (89%) of the control group. The Mann Whitney test with Bonferroni correction for multiple comparisons was used to compare the interpretable liver stiffness values between the groups. Results The liver stiffness was not statistically different between the healthy (median 4,6 range 2,8-6,5 KPa) and the myeloma controls (median 5,4 range 3,3-11,9 KPa) and both were considered as the negative control group. The negative control group had a liver stiffness significantly different from the HCV group (median 6,8 range 2,9-69,1 KPa, p<0.001), but not from the AL group without liver or cardiac involvement (median 6,1 range 4,2-17,5 KPa, p=0,25). The liver stiffness of AL patients with liver (with or without cardiac) involvement, was significantly higher (median 27,4 range 10,3-75 KPa) than the one of the negative control group (p<0.001), or the HCV group (p=0.001), and the AL group without liver or cardiac involvement (p=0.001). The relationship between AL liver involvement and the liver stiffness value was tested using ROC curve analysis with an optimal cut-off value of 9,8 KPa, a sensitivity of 100% (95%CI71,5 - 100,0), a specificity of 75.6% (95%CI64,6 - 84,7) and a ROC AUC of 0.92 (p=0.0001). In order to favour specificity for the diagnosis of AL liver involvement in non specific clinical situations, we chose the cut-off value of 17.5 KPa (specificity 94,87% (95%CI87,4 - 98,6), sensitivity 63,64% (95%CI30,8 - 89,1). Conclusion FibroScan is a useful non invasive tool which may suggest that a patient with undefined signs (enlarged liver, asymptomatic cholestasis, isolated monoclonal gammopathy) has liver amyloidosis and may help to define liver involvement in patients with proven amyloidosis, especially when liver stiffness reaches the cut-off value of 17,5 KPa. Disclosures No relevant conflicts of interest to declare.

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Leijendekker, W. J., W. D. Gao, and H. E. ter Keurs. "Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (March 1, 1990): H861—H869. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h861.

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The stiffness of rat cardiac trabeculae was measured in vitro to distinguish between an increase in unstimulated force (Fu) caused by rapid cycling of cross bridges or caused by rigor bridges during hypoxia. The force was measured with a strain gauge, the sarcomere length was determined by laser diffraction techniques, and muscle length was controlled by means of a motor. Stiffness was analyzed by using small (less than 1% of muscle length) sinusoidal length perturbations of 1 and 100 Hz. The stiffness at 100 Hz increased linearly with force during tetani at a varied [Sr2+] (0.25-10 mM) in the Krebs-Henseleit (K-H) buffer, but remained virtually unchanged at 1 Hz. In contrast, the stiffness of both the passive muscle and the muscle exposed to either CN- or to PO2 less than 1.5 mmHg up to development of maximal Fu (Fumax) was similar at 1- and 100-Hz perturbations. Less profound hypoxia (PO2 6-10 mmHg) resulted in spontaneous sarcomere activity during the rise in Fu, and an increase in the ratio of stiffness at 100 Hz to stiffness at 1 Hz was detected. When oxidative phosphorylation was inhibited by CN- (2 mM) while the muscle was stimulated in the absence of both Ca2+ and Na+ (choline+substituted), the addition of Na+ at the time at which Fu had reached 30-40% of Fumax did not affect the rate of rise of Fu. These results show that the development of Fu during more complete anoxia in rat trabeculae is completely due to the formation of rigor links and that Ca2(+)-dependent cross-bridge activation can contribute to the rise in Fu during less severe hypoxia.

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Winau, Lea, Rocio Hinojar Baydes, Axel Braner, Ulrich Drott, Harald Burkhardt, Shirish Sangle, David P. D’Cruz, et al. "High-sensitive troponin is associated with subclinical imaging biosignature of inflammatory cardiovascular involvement in systemic lupus erythematosus." Annals of the Rheumatic Diseases 77, no. 11 (August 4, 2018): 1590–98. http://dx.doi.org/10.1136/annrheumdis-2018-213661.

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BackgroundCardiovascular (CV) involvement in patients with systemic lupus erythematosus (SLE) is presumably subclinical for the major part of its evolution. We evaluated the associations between high-sensitive troponin T (hs-TropT), a sensitive marker of myocardial injury, and CV involvement using cardiac magnetic resonance (CMR).Methods and resultsThis is a two-centre (London and Frankfurt) CMR imaging study at 3.0 Tesla of consecutive 92 patients with SLE free of cardiac symptoms, undergoing screening for cardiac involvement. Venous samples were drawn and analysed post-hoc for cardiac biomarkers, including hs-TropT, high-sensitive C reactive protein and N-terminal pro brain natriuretic peptide. Compared with age-matched/gender-matched non-SLE controls (n=78), patients had significantly raised cardiac biomarker levels, native T1 and T2, aortic and ventricular stiffness, and reduced global longitudinal strain (p<0.01). In SLE, hs-TropT was significantly and independently associated with native T2, followed by the models including native T1 and aortic stiffness (Χ2 0.462, p<0.01). There were no relationships between hs-TropT and age, gender, CV risk factors, duration of systemic disease, cardiac structure or function, or late gadolinium enhancement.ConclusionsPatients with SLE have a high prevalence of subclinical myocardial injury as demonstrated by raised high-sensitive troponin levels. CMR with T2 mapping reveals myocardial oedema as the strongest predictor of hs-TropT release, underscoring the inflammatory interstitial remodelling as the main mechanism of injury. Patients without active myocardial inflammation demonstrate diffuse interstitial remodelling and increased vascular stiffness. These findings substantiate the role of CMR in screening of subclinical cardiac involvement.Trial registration numerNCT02407197; Results.

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Di Lisi, Daniela, Filippo Brighina, Girolamo Manno, Francesco Comparato, Vincenzo Di Stefano, Francesca Macaione, Giuseppe Damerino, et al. "Hereditary Transthyretin Amyloidosis: How to Differentiate Carriers and Patients Using Speckle-Tracking Echocardiography." Diagnostics 13, no. 24 (December 9, 2023): 3634. http://dx.doi.org/10.3390/diagnostics13243634.

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Background: Hereditary transthyretin amyloidosis is a rare disease caused by transthyretin (TTR) gene mutations. The aim of our study was to identify early signs of cardiac involvement in patients with a TTR gene mutation in order to differentiate carriers from patients with neurological or cardiac disease. Methods: A case–control study was carried out on 31 subjects with the TTR mutation. Patients were divided into three groups: 23% with cardiac amyloidosis and polyneuropathy (group A), 42% with only polyneuropathy (group B) and 35% carriers (group C). Speckle-tracking echocardiography (left-ventricular global longitudinal strain—GLS, atrial stiffness) was performed in all patients. The apical/basal longitudinal strain ratio (SAB) and relative apical sparing (RAS) were assessed in all subjects. Results: Analyzing groups C and B, we only found a significant difference in the SAB (p-value 0.001) and RAS (p-value 0.039). These parameters were significantly more impaired in group A compared to group B (SAB p-value 0.008; RAS p-value 0.002). Also, atrial stiffness was significantly impaired in groups A and B compared to group C. Conclusions: Our study suggests the diagnostic role of the SAB and RAS in cardiac amyloidosis. The SAB and RAS showed a gradual increase from carriers to patients with neurological and cardiac diseases. Thus, these parameters, in addition to atrial stiffness, could be used to monitor carriers. More extensive data are needed.

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Balani, Kantesh, Flavia C. Brito, Lidia Kos, and Arvind Agarwal. "Melanocyte pigmentation stiffens murine cardiac tricuspid valve leaflet." Journal of The Royal Society Interface 6, no. 40 (July 8, 2009): 1097–102. http://dx.doi.org/10.1098/rsif.2009.0174.

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Pigmentation of murine cardiac tricuspid valve leaflet is associated with melanocyte concentration, which affects its stiffness. Owing to its biological and viscoelastic nature, estimation of the in situ stiffness measurement becomes a challenging task. Therefore, quasi-static and nanodynamic mechanical analysis of the leaflets of the mouse tricuspid valve is performed in the current work. The mechanical properties along the leaflet vary with the degree of pigmentation. Pigmented regions of the valve leaflet that contain melanocytes displayed higher storage modulus (7–10 GPa) than non-pigmented areas (2.5–4 GPa). These results suggest that the presence of melanocytes affects the viscoelastic properties of the mouse atrioventricular valves and are important for their proper functioning in the organism.

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Hu, Min, Shen Wang, Dan Wang, Qinhao Lai, Xiaoying Chen, Shiwei Duan, Mengke Zhao, and Junhao Huang. "Combined moderate and high intensity exercise with dietary restriction improves cardiac autonomic function associated with a reduction in central and systemic arterial stiffness in obese adults: a clinical trial." PeerJ 5 (October 5, 2017): e3900. http://dx.doi.org/10.7717/peerj.3900.

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Objective The present study aimed to assess the effects of exercise with dietary restriction on cardiac autonomic activity, arterial stiffness, and cardiovascular biomarkers in obese individuals. Methods Seventeen obese adults completed an 8-week exercise and dietary program. Anthropometry, body composition, and multiple biochemical markers were measured. We used carotid-femoral pulse wave velocity (cfPWV), brachial-ankle pulse wave velocity (baPWV), central blood pressure, and augmentation index (AIx) to assess arterial stiffness. To determine cardiac autonomic activity, heart rate variability (HRV) was analyzed by standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive normal-to-normal intervals (RMSSD), total power (TF), low-frequency power in normalized units (LFnu), high-frequency power in normalized units (HFnu), and low-frequency power/high-frequency power (LF/HF). Results Following the exercise and diet intervention, obese subjects had significant reductions in body weight, body mass index, body fat percentage, brachial systolic blood pressure, and resting heart rate, and they had shown improvements in blood chemistry markers such as lipid profiles, insulin, and high-sensitivity C-reactive protein. There was a significant reduction in both cfPWV and baPWV following the intervention when compared to baseline levels. Moreover, the AIx and aortic systolic blood pressure were significantly reduced after the intervention. The diet and exercise intervention significantly increased cardiac autonomic modulation (determined by improved SDNN, RMSSD, TP LF, HF, and LF/HF), which was partly due to changes in heart rate, insulin resistance, and the inflammatory pattern. Furthermore, we observed a correlation between enhanced cardiac autonomic modulation (LF/HF) and decreased arterial stiffness, as measured by central cfPWV and systemic baPWV. Discussion An 8-week combined intervention of diet and exercise is effective in improving cardiac autonomic function in obese adults, with an associated decrease in central and systemic arterial stiffness.

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Shalini Sharma, Vikram Kala, Vivek Sharma, Prerna Panjeta. "Aortic Stiffness is Associated with Cardiac Function and Cerebral Blood Flow Pulsatility in Type2 Diabetes Mellitus." International Journal of Physiology 7, no. 3 (July 25, 2019): 251–56. http://dx.doi.org/10.37506/ijop.v7i3.180.

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Introduction Central hemodynamics has an important role in maintaining appropriate cerebral and other end-organ perfusion and is altered in type2DM. Arterial stiffening is an early phenomenon in patients with type2DM, affecting cardiac function by increasing the cardiac afterload and reducing diastolic coronary artery perfusion, also involving small vessel disease in the brain and subsequent hypoperfusion. Aims and Objectives The aim of present study was to determine whether aortic stiffness affects cardiac function and whether central elastic artery stiffness was associated with cerebral blood flow pulsatility and subsequent, cerebral perfusion in type 2 DM patients. Materials and Method Fifty six patients with type2DM and 60 age-matched healthy volunteers were enrolled. Aortic PWV was measured using non-invasive cardiovascular risk analysis system (Periscope). Cerebral blood flow was measured by using Trans-Cranial Doppler. Results CFPWV of diabetic group showed significantly higher mean values (Group 1=931.00±215.98cm/s Group 2=1241±152.03cm/s) than control subjects (758±151.82). CFPWV was significantly (p value <0.01) increased between two diabetic groups. HbA1c was most significantly correlated to CFPWV (r=1.00, p<0.001) followed by weak correlation between central aortic stiffness quantified by PWV and PI (r=0.5, p>0.01). Conclusion In patients with type2DM, aortic stiffness is significantly associated with pulse pressure, aortic pulse pressure, aortic augmentation pressure as well as with cerebral blood flow pulsatility and subsequent cerebral perfusion, contributing to decreased cardiac function and cerebral hypoperfusion. Aortic PWV and TCD measurement might be useful prognostic marker of cardiac and cerebrovascular disease in type2DM.

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Bupha-Intr, Tepmanas, Ye Win Oo, and Jonggonnee Wattanapermpool. "Increased myocardial stiffness with maintenance of length-dependent calcium activation by female sex hormones in diabetic rats." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1661—H1668. http://dx.doi.org/10.1152/ajpheart.00411.2010.

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A decrease in peak early diastolic filling velocity in postmenopausal women implies a sex hormone-related diastolic dysfunction. The regulatory effect of female sex hormones on cardiac distensibility therefore was evaluated in ovariectomized rats by determining the sarcomere length-passive tension relationship of ventricular skinned fiber preparations. Diabetes also was induced in the rat to assess the protective significance of female sex hormones on diastolic function. While ovariectomy had no effect on myocardial stiffness, collagen content, or titin ratio, a significant increase in myocardial stiffness was observed in diabetic rat only when female sex hormones were intact. The increased stiffness in diabetic-sham rats was accompanied by an elevated collagen content resulting from increases in the levels of procollagen and Smad2. Surprisingly, the increased myocardial stiffness in diabetic-sham rats was accompanied by a shift toward a more compliant N2BA of cardiac titin isoforms. The pCa-active tension relationship was analyzed at fixed sarcomere lengths of 2.0 and 2.3 μm to determine the magnitude of changes in myofilament Ca2+ sensitivity between the two sarcomere lengths. Interestingly, high expression of N2BA titin was associated with a suppressed magnitude of changes in myofilament Ca2+ sensitivity only in the diabetic-ovariectomized condition. Estrogen supplementation in diabetic-ovariectomized rats partially increased myocardial stiffness but completely reversed the change in myofilament Ca2+ sensitivity. These results indicate a restrictive adaptation of myocardium governed by female sex hormones to maintain myofilament activity in compensation to the pathophysiological induction of cardiac dilatation by the diabetic condition.

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Journal articles on the topic 'Cardiac stiffness'

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