Готові списки джерел за темами / Aortic valve abnormalities; calcification; nitric oxide

Добірка наукової літератури з теми "Aortic valve abnormalities; calcification; nitric oxide"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Aortic valve abnormalities; calcification; nitric oxide"

El Accaoui, Ramzi N., Sarah T. Gould, Georges P. Hajj, Yi Chu, Melissa K. Davis, Diane C. Kraft, Donald D. Lund, et al. "Aortic valve sclerosis in mice deficient in endothelial nitric oxide synthase." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 9 (May 1, 2014): H1302—H1313. http://dx.doi.org/10.1152/ajpheart.00392.2013.

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Risk factors for fibrocalcific aortic valve disease (FCAVD) are associated with systemic decreases in bioavailability of endothelium-derived nitric oxide (EDNO). In patients with bicuspid aortic valve (BAV), vascular expression of endothelial nitric oxide synthase (eNOS) is decreased, and eNOS−/− mice have increased prevalence of BAV. The goal of this study was to test the hypotheses that EDNO attenuates profibrotic actions of valve interstitial cells (VICs) in vitro and that EDNO deficiency accelerates development of FCAVD in vivo. As a result of the study, coculture of VICs with aortic valve endothelial cells (vlvECs) significantly decreased VIC activation, a critical early phase of FCAVD. Inhibition of VIC activation by vlvECs was attenuated by NG-nitro-l-arginine methyl ester or indomethacin. Coculture with vlvECs attenuated VIC expression of matrix metalloproteinase-9, which depended on stiffness of the culture matrix. Coculture with vlvECs preferentially inhibited collagen-3, compared with collagen-1, gene expression. BAV occurred in 30% of eNOS−/− mice. At age 6 mo, collagen was increased in both bicuspid and trileaflet eNOS−/− aortic valves, compared with wild-type valves. At 18 mo, total collagen was similar in eNOS−/− and wild-type mice, but collagen-3 was preferentially increased in eNOS−/− mice. Calcification and apoptosis were significantly increased in BAV of eNOS−/− mice at ages 6 and 18 mo. Remarkably, these histological changes were not accompanied by physiologically significant valve stenosis or regurgitation. In conclusion, coculture with vlvECs inhibits specific profibrotic VIC processes. In vivo, eNOS deficiency produces fibrosis in both trileaflet and BAVs but produces calcification only in BAVs.

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Rajamannan, N. M. "Atorvastatin inhibits calcification and enhances nitric oxide synthase production in the hypercholesterolaemic aortic valve." Heart 91, no. 6 (June 1, 2005): 806–10. http://dx.doi.org/10.1136/hrt.2003.029785.

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Choi, Bongkun, Eun-Young Kim, Ji-Eun Kim, Soyoon Oh, Si-On Park, Sang-Min Kim, Hyuksu Choi, Jae-Kwan Song, and Eun-Ju Chang. "Evogliptin Suppresses Calcific Aortic Valve Disease by Attenuating Inflammation, Fibrosis, and Calcification." Cells 10, no. 1 (January 1, 2021): 57. http://dx.doi.org/10.3390/cells10010057.

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Calcific aortic valve disease (CAVD) accompanies inflammatory cell infiltration, fibrosis, and ultimately calcification of the valve leaflets. We previously demonstrated that dipeptidyl peptidase-4 (DPP-4) is responsible for the progression of aortic valvular calcification in CAVD animal models. As evogliptin, one of the DPP-4 inhibitors displays high specific accumulation in cardiac tissue, we here evaluated its therapeutic potency for attenuating valvular calcification in CAVD animal models. Evogliptin administration markedly reduced calcific deposition accompanied by a reduction in proinflammatory cytokine expression in endothelial nitric oxide synthase-deficient mice in vivo, and significantly ameliorated the mineralization of the primary human valvular interstitial cells (VICs), with a reduction in the mRNA expression of bone-associated and fibrosis-related genes in vitro. In addition, evogliptin ameliorated the rate of change in the transaortic peak velocity and mean pressure gradients in our rabbit model as assessed by echocardiography. Importantly, evogliptin administration in a rabbit model was found to suppress the effects of a high-cholesterol diet and of vitamin D2-driven fibrosis in association with a reduction in macrophage infiltration and calcific deposition in aortic valves. These results have indicated that evogliptin prohibits inflammatory cytokine expression, fibrosis, and calcification in a CAVD animal model, suggesting its potential as a selective therapeutic agent for the inhibition of valvular calcification during CAVD progression.

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Parra-Izquierdo, Iván, Tania Sánchez-Bayuela, Javier López, Cristina Gómez, Enrique Pérez-Riesgo, J. Alberto San Román, Mariano Sánchez Crespo, Magdi Yacoub, Adrian H. Chester, and Carmen García-Rodríguez. "Interferons Are Pro-Inflammatory Cytokines in Sheared-Stressed Human Aortic Valve Endothelial Cells." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10605. http://dx.doi.org/10.3390/ijms221910605.

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Calcific aortic valve disease (CAVD) is an athero-inflammatory process. Growing evidence supports the inflammation-driven calcification model, mediated by cytokines such as interferons (IFNs) and tumor necrosis factor (TNF)-α. Our goal was investigating IFNs’ effects in human aortic valve endothelial cells (VEC) and the potential differences between aortic (aVEC) and ventricular (vVEC) side cells. The endothelial phenotype was analyzed by Western blot, qPCR, ELISA, monocyte adhesion, and migration assays. In mixed VEC populations, IFNs promoted the activation of signal transducers and activators of transcription-1 and nuclear factor-κB, and the subsequent up-regulation of pro-inflammatory molecules. Side-specific VEC were activated with IFN-γ and TNF-α in an orbital shaker flow system. TNF-α, but not IFN-γ, induced hypoxia-inducible factor (HIF)-1α stabilization or endothelial nitric oxide synthase downregulation. Additionally, IFN-γ inhibited TNF-α–induced migration of aVEC. Also, IFN-γ triggered cytokine secretion and adhesion molecule expression in aVEC and vVEC. Finally, aVEC were more prone to cytokine-mediated monocyte adhesion under multiaxial flow conditions as compared with uniaxial flow. In conclusion, IFNs promote inflammation and reduce TNF-α–mediated migration in human VEC. Moreover, monocyte adhesion was higher in inflamed aVEC sheared under multiaxial flow, which may be relevant to understanding the initial stages of CAVD.

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Andre, E., E. Yaniz-Galende, C. Hamilton, G. J. Dusting, N. Hellen, CE Poulet, M. Diez Cunado, et al. "Poster session 1Cell growth, differentiation and stem cells - Heart72Understanding the metabolism of cardiac progenitor cells: a first step towards controlling their proliferation and differentiation?73Expression of pw1/peg3 identifies a new cardiac adult stem cell population involved in post-myocardial infarction remodeling74Long-term stimulation of iPS-derived cardiomyocytes using optogenetic techniques to promote phenotypic changes in E-C coupling75Benefits of electrical stimulation on differentiation and maturation of cardiomyocytes from human induced pluripotent stem cells76Constitutive beta-adrenoceptor-mediated cAMP production controls spontaneous automaticity of human induced pluripotent stem cell-derived cardiomyocytes77Formation and stability of T-tubules in cardiomyocytes78Identification of miRNAs promoting human cardiomyocyte proliferation by regulating Hippo pathway79A direct comparison of foetal to adult epicardial cell activation reveals distinct differences relevant for the post-injury response80Role of neuropilins in zebrafish heart regeneration81Highly efficient immunomagnetic purification of cardiomyocytes derived from human pluripotent stem cells82Cardiac progenitor cells posses a molecular circadian clock and display large 24-hour oscillations in proliferation and stress tolerance83Influence of sirolimus and everolimus on bone marrow-derived mesenchymal stem cell biology84Endoglin is important for epicardial behaviour following cardiac injuryCell death and apoptosis - Heart87Ultrastructural alterations reflecting Ca2+ handling and cell-to-cell coupling disorders precede occurrence of severe arrhythmias in intact animal heart88Urocortin-1 promotes cardioprotection through ERK1/2 and EPAC pathways: role in apoptosis and necrosis89Expression p38 MAPK and Cas-3 in myocardium LV of rats with experimental heart failure at melatonin and enalapril introductionTranscriptional control and RNA species - Heart92Accumulation of beta-amyloid 1-40 in HF patients: the role of lncRNA BACE1-AS93Role of miR-182 in zebrafish and mouse models of Holt-Oram syndrome94Mir-27 distinctly regulates muscle-enriched transcription factors and growth factors in cardiac and skeletal muscle cells95AF risk factors impair PITX2 expression leading to Wnt-microRNA-ion channel remodelingCytokines and cellular inflammation - Heart98Post-infarct survival depends on the interplay of monocytes, neutrophils and interferon gamma in a mouse model of myocardial Infarction99Inflammatory cd11b/c cells play a protective role in compensated cardiac hypertrophy by promoting an orai3-related pro-survival signal100Anti-inflammatory effects of endothelin receptor blockade in the atrial tissue of spontaneously hypertensive rats101Mesenchymal stromal cells reduce NLRP3 inflammasome activity in Coxsackievirus B3-induced myocarditis102Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis103The impact of regulatory T lymphocytes on long-term mortality in patients with chronic heart failure104Temporal dynamics of dendritic cells after ST-elevation myocardial infarction relate with improvement of myocardial functionGrowth factors and neurohormones - Heart107Preconditioning of hypertrophied heart: miR-1 and IGF-1 crosstalk108Modulation of catecholamine secretion from human adrenal chromaffin cells by manipulation of G protein-coupled receptor kinase-2 activity109Evaluation of cyclic adenosin-3,5- monophosphate and neurohormones in patients with chronic heart failureNitric oxide and reactive oxygen species - Heart112Hydrogen sulfide donor inhibits oxidative and nitrosative stress, cardiohemodynamics disturbances and restores cNOS coupling in old rats113Role and mechanisms of action of aldehydes produced by monoamine oxidase A in cardiomyocyte death and heart failure114Exercise training has contrasting effects in myocardial infarction and pressure-overload due to different endothelial nitric oxide synthase regulation115S-Nitroso Human Serum Albumin dose-dependently leads to vasodilation and alters reactive hyperaemia in coronary arteries of an isolated mouse heart model116Modulating endothelial nitric oxide synthase with folic acid attenuates doxorubicin-induced cardiomyopathy119Effects of long-term very high intensity exercise on aortic structure and function in an animal model120Electron paramagnetic resonance spectroscopy quantification of nitrosylated hemoglobin (HbNO) as an index of vascular nitric oxide bioavailability in vivo121Deletion of repressor activator protein 1 impairs acetylcholine-induced relaxation due to production of reactive oxygen speciesExtracellular matrix and fibrosis - Heart124MicroRNA-19b is associated with myocardial collagen cross-linking in patients with severe aortic stenosis. Potential usefulness as a circulating biomarker125A new ex vivo model to study cardiac fibrosis126Heterogeneity of fibrosis and fibroblast differentiation in the left ventricle after myocardial infarction127Effect of carbohydrate metabolism degree compensation to the level of galectin-3 changes in hypertensive patients with chronic heart failure and type 2 diabetes mellitus128Statin paradox in association with calcification of bicuspid aortic valve interstitial cells129Cardiac function remains impaired despite reversible cardiac fibrosis after healed experimental viral myocarditisIon channels, ion exchangers and cellular electrophysiology - Heart132Identifying a novel role for PMCA1 (Atp2b1) in heart rhythm instability133Mutations of the caveolin-3 gene as a predisposing factor for cardiac arrhythmias134The human sinoatrial node action potential: time for a computational model135iPSC-derived cardiomyocytes as a model to dissect ion current alterations of genetic atrial fibrillation136Postextrasystolic potentiation in healthy and diseased hearts: effects of the site of origin and coupling interval of the preceding extrasystole137Absence of Nav1.8-based (late) sodium current in rabbit cardiomyocytes and human iPSC-CMs138hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit cellular electrophysiological abnormalitiesMicrocirculation141Atherogenic indices, collagen type IV turnover and the development of microvascular complications- study in diabetics with arterial hypertension142Changes in the microvasculature and blood viscosity in women with rheumatoid arthritis, hypercholesterolemia and hypertensionAtherosclerosis145Shear stress regulates endothelial autophagy: consequences on endothelial senescence and atherogenesis146Obstructive sleep apnea causes aortic remodeling in a chronic murine model147Aortic perivascular adipose tissue displays an aged phenotype in early and late atherosclerosis in ApoE-/- mice148A systematic evaluation of the cellular innate immune response during the process of human atherosclerosis149Inhibition of Coagulation factor Xa increases plaque stability and attenuates the onset and progression of atherosclerotic plaque in apolipoprotein e-deficient mice150Regulatory CD4+ T cells from patients with atherosclerosis display pro-inflammatory skewing and enhanced suppression function151Hypoxia-inducible factor (HIF)-1alpha regulates macrophage energy metabolism by mediating miRNAs152Extracellular S100A4 is a key player of smooth muscle cell phenotypic transition: implications in atherosclerosis153Microparticles of healthy origins improve atherosclerosis-associated endothelial progenitor cell dysfunction via microRNA transfer154Arterial remodeling and metabolism impairment in early atherosclerosis155Role of pannexin1 in atherosclerotic plaque formationCalcium fluxes and excitation-contraction coupling158Amphiphysin II induces tubule formation in cardiac cells159Interleukin 1 beta regulation of connexin 43 in cardiac fibroblasts and the effects of adult cardiac myocyte:fibroblast co-culture on myocyte contraction160T-tubular electrical defects contribute to blunted beta-adrenergic response in heart failure161Beat-to-beat variability of intracellular Ca2+ dynamics of Purkinje cells in the infarct border zone of the mouse heart revealed by rapid-scanning confocal microscopy162The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: a study on transgenic mouse models with different mutations163Synthesis of cADPR and NAADP by intracellular CD38 in heart: role in inotropic and arrhythmogenic effects of beta-adrenoceptor signalingContractile apparatus166Towards an engineered heart tissue model of HCM using hiPSC expressing the ACTC E99K mutation167Diastolic mechanical load delays structural and functional deterioration of ultrathin adult heart slices in culture168Structural investigation of the cardiac troponin complex by molecular dynamics169Exercise training restores myocardial and oxidative skeletal muscle function from myocardial infarction heart failure ratsOxygen sensing, ischaemia and reperfusion172A novel antibody specific to full-length stromal derived factor-1 alpha reveals that remote conditioning induces its cleavage by endothelial dipeptidyl peptidase 4173Attenuation of myocardial and vascular arginase activity by vagal nerve stimulation via a mechanism involving alpha-7 nicotinic receptor during cardiac ischemia and reperfusion174Novel nanoparticle-mediated medicine for myocardial ischemia-reperfusion injury simultaneously targeting mitochondrial injury and myocardial inflammation175Acetylcholine plays a key role in myocardial ischaemic preconditioning via recruitment of intrinsic cardiac ganglia176The role of nitric oxide and VEGFR-2 signaling in post ischemic revascularization and muscle recovery in aged hypercholesterolemic mice177Efficacy of ischemic preconditioning to protect the human myocardium: the role of clinical conditions and treatmentsCardiomyopathies and fibrosis180Plakophilin-2 haploinsufficiency leads to impaired canonical Wnt signaling in ARVC patient181Improved technique for customized, easier, safer and more reliable transverse aortic arch banding and debanding in mice as a model of pressure overload hypertrophy182Late sodium current inhibitors for the treatment of inducible obstruction and diastolic dysfunction in hypertrophic cardiomyopathy: a study on human myocardium183Angiotensin II receptor antagonist fimasartan has protective role of left ventricular fibrosis and remodeling in the rat ischemic heart184Role of High-Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts activities and heart function after myocardial infarction185Atrial remodeling in hypertrophic cardiomyopathy: insights from mouse models carrying different mutations in cTnT186Electrophysiological abnormalities in ventricular cardiomyocytes from a Maine Coon cat with hypertrophic cardiomyopathy: effects of ranolazine187ZBTB17 is a novel cardiomyopathy candidate gene and regulates autophagy in the heart188Inhibition of SRSF4 in cardiomyocytes induces left ventricular hypertrophy189Molecular characterization of a novel cardiomyopathy related desmin frame shift mutation190Autonomic characterisation of electro-mechanical remodeling in an in-vitro leporine model of heart failure191Modulation of Ca2+-regulatory function by three novel mutations in TNNI3 associated with severe infant restrictive cardiomyopathyAging194The aging impact on cardiac mesenchymal like stromal cells (S+P+)195Reversal of premature aging markers after bariatric surgery196Sex-associated differences in vascular remodeling during aging: role of renin-angiotensin system197Role of the receptor for advanced glycation end-products (RAGE) in age dependent left ventricle dysfunctionsGenetics and epigenetics200hsa-miR-21-5p as a key factor in aortic remodeling during aneurysm formation201Co-inheritance of mutations associated with arrhythmogenic and hypertrophic cardiomyopathy in two Italian families202Lamin a/c hot spot codon 190: form various amino acid substitutions to clinical effects203Treatment with aspirin and atorvastatin attenuate cardiac injury induced by rat chest irradiation: Implication of myocardial miR-1, miR-21, connexin-43 and PKCGenomics, proteomics, metabolomics, lipidomics and glycomics206Differential phosphorylation of desmin at serines 27 and 31 drives the accumulation of preamyloid oligomers in heart failure207Potential role of kinase Akt2 in the reduced recovery of type 2 diabetic hearts subjected to ischemia / reperfusion injury208A proteomics comparison of extracellular matrix remodelling in porcine coronary arteries upon stent implantationMetabolism, diabetes mellitus and obesity211Targeting grk2 as therapeutic strategy for cancer associated to diabetes212Effects of salbutamol on large arterial stiffness in patients with metabolic syndrome213Circulating microRNA-1 and microRNA-133a: potential biomarkers of myocardial steatosis in type 2 diabetes mellitus214Anti-inflammatory nutrigenomic effects of hydroxytyrosol in human adipocytes - protective mechanisms of mediterranean diets in obesity-related inflammation215Alterations in the metal content of different cardiac regions within a rat model of diabetic cardiomyopathyTissue engineering218A novel conductive patch for application in cardiac tissue engineering219Establishment of a simplified and improved workflow from neonatal heart dissociation to cardiomyocyte purification and characterization220Effects of flexible substrate on cardiomyocytes cell culture221Mechanical stretching on cardiac adipose progenitors upregulates sarcomere-related genes." Cardiovascular Research 111, suppl 1 (July 1, 2016): S16—S42. http://dx.doi.org/10.1093/cvr/cvw135.

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Garcia-Martinez, V., C. Lopez Sanchez, W. Hamed, W. Hamed, JH Hsu, R. Ferrer-Lorente, Maryam Alshamrani, et al. "Poster session 2Morphogenetic mechanisms290MiR-133 regulates retinoic acid pathway during early cardiac chamber specification291Bmp2 regulates atrial differentiation through miR-130 during early heart looping formationDevelopmental genetics294Association of deletion allele of insertion/deletion polymorphism in alpha 2B adrenoceptor gene and hypertension with or without type 2 diabetes mellitus295Association of G1359A polymorphism of the endocannabinoid type 1 receptor (CNR1) with coronary artery disease (CAD) with type 2 diabetes mellitusCell growth, differentiation and stem cells - Vascular298Gamma-secretase inhibitor prevents proliferation and migration of ductus arteriosus smooth muscle cells: a role of Notch signaling in postnatal closure of ductus arteriosus299Mesenchymal stromal-like cells (MLCs) derived from induced pluripotent stem (iPS) cells: a promising therapeutic option to promote neovascularization300Sonic Hedgehog promotes mesenchymal stem cell differentiation to vascular smooth muscle cells in cardiovacsular disease301Proinflammatory cytokine secretion and epigenetic modification in endothelial cells treated LPS-GinfivalisCell death and apoptosis - Vascular304Mitophagy acts as a safeguard mechanism against human vascular smooth muscle cell apoptosis induced by atherogenic lipidsTranscriptional control and RNA species - Vascular307MicroRNA-34a role in vascular calcification308Local delivery of a miR-146a inhibitor utilizing a clinically applicable approach attenuates neointima formation after vascular injury309Long noncoding RNA landscape of hypoxic endothelial cells310Specific circulating microRNAs levels associate with hypertension, hyperglycemia and dysfunctional HDL in acute coronary syndrome patientsCytokines and cellular inflammation - Vascular313Phosphodiesterase5A up-regulation in vascular endothelium under pro-inflammatory conditions: a newly disclosed anti-inflammatory activity for the omega-3polyunsaturated aatty acid docosahexaenoic acid314Cardiovascular risk modifying with extra-low dose anticytokine drugs in rhematoid arthritis315Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation316Lymphocytic myocarditis coincides with increased plaque inflammation and plaque hemorrhage in coronary arteries, facilitating myocardial infarction317Serum osteoprotegerin level predictsdeclined numerous of circulating endothelial- derived and mononuclear-derived progenitor cells in patients with metabolic syndromeGrowth factors and neurohormones - Vascular320Effect of gastrin-releasing peptide (GRP) on vascular inflammationSignal transduction - Heart323A new synthetic peptide regulates hypertrophy in vitro through means of the inhibition of nfkb324Inducible fibroblast-specific knockout of p38 alpha map kinase is cardioprotective in a mouse model of isoproterenol-induced cardiac hypertrophy325Regulation of beta-adrenoceptor-evoked inotropic responses by inhibitory G protein, adenylyl cyclase isoforms 5 and 6 and phosphodiesterases326Binding to RGS3 and stimulation of M2 muscarinic acetylcholine receptors modulates the substrate specificity of p190RhoGAP in cardiac myocytes327Cardiac regulation of post-translational modifications, parylation and deacetylation in LMNA dilated cardiomyopathy mouse model328Beta-adrenergic regulation of the b56delta/pp2a holoenzyme in cardiac myocytes through b56delta phosphorylation at serine 573Nitric oxide and reactive oxygen species - Vascular331Oxidative stress-induced miR-200c disrupts the regulatory loop among SIRT1, FOXO1 and eNOS332Antioxidant therapy prevents oxidative stress-induced endothelial dysfunction and Enhances Wound Healing333Morphological and biochemical characterization of red blood cell in coronary artery diseaseCytoskeleton and mechanotransduction - Heart336Novel myosin activator, JSH compounds, increased myocardial contractility without chronotropic effect in ratsExtracellular matrix and fibrosis - Vascular339Ablation of Toll-like receptor 9 causes cardiac rupture after myocardial infarction by attenuating proliferation and differentiation of cardiac fibroblasts340Altered vascular remodeling in the mouse hind limb ischemia model in Factor VII activating protease (FSAP) deficiencyVasculogenesis, angiogenesis and arteriogenesis343Pro-angiogenic effects of proly-hydroxylase inhibitors and their potential for use in a novel strategy of therapeutic angiogenesis for coronary total occlusion344Nrf2 drives angiogenesis in transcription-independent manner: new function of the master regulator of oxidative stress response345Angiogenic gene therapy, despite efficient vascular growth, is not able to improve muscle function in normoxic or chronically ischemic rabbit hindlimbs -role of capillary arterialization and shunting346Effect of PAR-1 inhibition on collateral vessel growth in the murine hind limb model347Quaking is a key regulator of endothelial cell differentiation, neovascularization and angiogenesis348"Emerging angiogenesis" in the chick chorioallantoic membrane (CAM). An in vivo study349Exosomes from cardiomyocyte progenitor cells and mesenchymal stem cells stimulate angiogenesis in vitro and in vivo via EMMPRINEndothelium352Reciprocal regulation of GRK2 and bradykinin receptor stimulation modulate Ca2+ intracellular level in endothelial cells353The roles of bone morphogenetic proteins 9 and 10 in endothelial inflammation and atherosclerosis354The contribution of GPR55 to the L-alpha-lysophosphatidylinositol-induced vasorelaxation in isolated human pulmonary arteries355The endothelial protective ACE inhibitor Zofenoprilat exerts anti-inflammatory activities through H2S production356A new class of glycomimetic drugs to prevent free fatty acid-induced endothelial dysfunction357Endothelial progenitor cells to apoptotic endothelial cell-derived microparticles ration differentiatesas preserved from reduced ejection fractionheart failure358Proosteogenic genes are activated in endothelial cells of patients with thoracic aortic aneurysm359Endothelin ETB receptors mediate relaxing responses to insulin in pericardial resistance arteries from patients with cardiovascular disease (CVD)Smooth muscle and pericytes362CX3CR1 positive myeloid cells regulate vascular smooth muscle tone by inducing calcium oscillations via activation of IP3 receptors363A novel function of PI3Kg on cAMP regulation, role in arterial wall hyperplasia through modulation of smooth muscle cells proliferation364NRP1 and NRP2 play important roles in the development of neointimal hyperplasia in vivo365Azithromycin induces autophagy in aortic smooth muscle cellsCoagulation, thrombosis and platelets368The real time in vivo evaluation of platelet-dependent aldosterone prothrombotic action in mice369Development of a method for in vivo detection of active thrombi in mice370The antiplatelet effects of structural analogs of the taurine chloramine371The influence of heparin anticoagulant drugs on functional state of human platelets372Regulation of platelet aggregation and adenosine diphosphate release by d dimer in acute coronary syndrome (in vitro study)Oxygen sensing, ischaemia and reperfusion375Sirtuin 5 mediates brain injury in a mouse model of cerebral ischemia-reperfusion376Abscisic acid: a new player in cardiomyocyte protection from ischaemia?377Protective effects of ultramicronized palmitoylethanolamide (PEA-um) in myocardial ischaemia and reperfusion injury in vivo378Identification of stem cell-derived cardiomyocytes using cardiac specific markers and additional testing of these cells in simulated ischemia/reperfusion system379Single-dose intravenous metformin treatment could afford significant protection of the injured rat kidney in an experimental model of ischemia-reperfusion380Cardiotoxicity of long acting muscarinic receptor antagonists used for chronic obstructive pulmonary disease381Dependence antioxidant potential on the concentration of amino acids382The impact of ischemia-reperfusion on physiological parameters,apoptosis and ultrastructure of rabbit myocardium with experimental aterosclerosisMitochondria and energetics385MicroRNA-1 dependent regulation of mitochondrial calcium uniporter (MCU) in normal and hypertrophied hearts386Mitochondrial homeostasis and cardioprotection: common targets for desmin and aB-crystallin387Overexpression of mitofusin-2 (Mfn2) and associated mitochondrial dysfunction in the diabetic heart388NO-dependent prevention of permeability transition pore (MPTP) opening by H2S and its regulation of Ca2+ accumulation in rat heart mitochondria389G protein coupled receptor kinase 2 (GRK2) is fundamental in recovering mitochondrial morphology and function after exposure to ionizing radiation (IR)Gender issues392Sex differences in pulmonary vascular control; focus on the nitric oxide pathwayAging395Heart failure with preserved ejection fraction develops when feeding western diet to senescence-accelerated mice396Cardiovascular markers as predictors of cognitive decline in elderly hypertensive patients397Changes in connexin43 in old rats with volume overload chronic heart failureGenetics and epigenetics400Calcium content in the aortic valve is associated with 1G>2G matrix metalloproteinase 1 polymorphism401Neuropeptide receptor gene s (NPSR1) polymorphism and sleep disturbances402Endothelin-1 gene Lys198Asn polymorphism in men with essential hypertension complicated and uncomplicated with chronic heart failure403Association of common polymorphisms of the lipoprotein lipase and pon1 genes with the metabolic syndrome in a sample of community participantsGenomics, proteomics, metabolomics, lipidomics and glycomics405Gene expression quantification using multiplexed color-coded probe pairs to determine RNA content in sporadic cardiac myxoma406Large-scale phosphorylation study of the type 2 diabetic heart subjected to ischemia / reperfusion injury407Transcriptome-based identification of new anti-inflammatory properties of the olive oil hydroxytyrosol in vascular endothelial cell under basal and proinflammatory conditions408Gene polymorphisms combinations and risk of myocardial infarctionComputer modelling, bioinformatics and big data411Comparison of the repolarization reserve in three state-of-the-art models of the human ventricular action potentialMetabolism, diabetes mellitus and obesity414Endothelial monocyte-activating polypeptide-II improves heart function in type -I Diabetes mellitus415Admission glucose level is independent predictor of impaired left ventricular function in patients with acute myocardial infarction: a two dimensional speckle-tracking echocardiography study416Association between biochemical markers of lipid profile and inflammatory reaction and stiffness of the vascular wall in hypertensive patients with abdominal obesity417Multiple common co-morbidities produce left ventricular diastolic dysfunction associated with coronary microvascular dysfunction, oxidative stress and myocardial stiffening418Investigating the cardiovascular effects of antiretroviral drugs in a lean and high fat/sucrose diet rat model of obesity419Statins in the treatment of non-alcoholic steatohepatitis (NASH). Our experience from a 2-year prospective study in Constanta County, Romania420Epicardial adipose tissue as a predictor of cardiovascular outcome in patients with ACS undergoing PCI?Arterial and pulmonary hypertension423Dependence between heart rhythm disorers and ID polymorphism of ACE gene in hypertensive patients424Molecular mechanisms underlying the beneficial effects of Urocortin 2 in pulmonary arterial hypertension425Inhibition of TGf-b axis and action of renin-angiotensin system in human ascending aorta aneurysms426Early signs of microcirculation and macrocirculation abnormalities in prehypertension427Vascular smooth muscle cell-expressed Tie-2 controls vascular tone428Cardiac and vascular remodelling in the development of chronic thrombo-embolic pulmonary hypertension in a novel swine modelBiomarkers431Arrhythmogenic cardiomyopathy: a new, non invasive biomarker432Can circulating microRNAs distinguish type 1 and type 2 myocardial infarction?433Design of a high-throughput multiplex proteomics assay to identify left ventricular diastolic dysfunction in diabetes434Monocyte-derived and P-selectin-carrying microparticles are differently modified by a low fat diet in patients with cardiovascular risk factors who will and who will not develop a cardiovascular event435Red blood cell distribution width assessment by polychromatic interference microscopy of thin films in chronic heart failure436Invasive and noninvasive evaluation of quality of radiofrequency-induced cardiac denervation in patients with atrial fibrillation437The effect of therapeutic hypothermia on the level of brain derived neurotrophic factor (BDNF) in sera following cardiopulmonary resustitation438Novel biomarkers to predict outcome in patients with heart failure and severe aortic stenosis439Biological factors linking depression and anxiety to cardiovascular disease440Troponins and myoglobin dynamic at coronary arteries graftingInvasive, non-invasive and molecular imaging443Diet composition effects on the genetic typing of the mouse ob mutation: a micro-ultrasound characterization of cardiac function, macro and micro circulation and liver steatosis444Characterization of pig coronary and rabbit aortic lesions using IV-OCT quantitative analysis: correlations with histologyGene therapy and cell therapy447Enhancing the survival and angiogenic potential of mouse atrial mesenchymal cells448VCAM-1 expression in experimental myocardial infarction and its relation to bone marrow-derived mononuclear cell retentionTissue engineering451Advanced multi layered scaffold that increases the maturity of stem cell-derived human cardiomyocytes452Response of engineered heart tissue to simulated ischemia/reperfusion in the presence of acute hyperglycemic conditions453Serum albumin hydrogels prevent de-differentiation of neonatal cardiomyocytes454A novel paintbrush technique for transfer of low viscosity ultraviolet light curable cyan methacrylate on saline immersed in-vitro sheep heart." Cardiovascular Research 111, suppl 1 (July 1, 2016): S56—S81. http://dx.doi.org/10.1093/cvr/cvw149.

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Liu, Zongtao, Nianguo Dong, Haipeng Hui, Yixuan Wang, Fayun Liu, Li Xu, Ming Liu, et al. "Endothelial cell-derived tetrahydrobiopterin prevents aortic valve calcification." European Heart Journal, February 9, 2022. http://dx.doi.org/10.1093/eurheartj/ehac037.

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Abstract Aims Tetrahydrobiopterin (BH4) is a critical determinant of the biological function of endothelial nitric oxide synthase. The present study was to investigate the role of valvular endothelial cell (VEC)-derived BH4 in aortic valve calcification. Methods and results Plasma and aortic valve BH4 concentrations and the BH4:BH2 ratio were significantly lower in calcific aortic valve disease patients than in controls. There was a significant decrease of the two key enzymes of BH4 biosynthesis, guanosine 5′-triphosphate cyclohydrolase I (GCH1) and dihydrofolate reductase (DHFR), in calcified aortic valves compared with the normal ones. Endothelial cell-specific deficiency of Gch1 in Apoe−/− (Apoe−/−Gch1fl/flTie2Cre) mice showed a marked increase in transvalvular peak jet velocity, calcium deposition, runt-related transcription factor 2 (Runx2), dihydroethidium (DHE), and 3-nitrotyrosine (3-NT) levels in aortic valve leaflets compared with Apoe−/−Gch1fl/fl mice after a 24-week western diet (WD) challenge. Oxidized LDL (ox-LDL) induced osteoblastic differentiation of valvular interstitial cells (VICs) co-cultured with either si-GCH1- or si-DHFR-transfected VECs, while the effects could be abolished by BH4 supplementation. Deficiency of BH4 in VECs caused peroxynitrite formation increase and 3-NT protein increase under ox-LDL stimulation in VICs. SIN-1, the peroxynitrite generator, significantly up-regulated alkaline phosphatase (ALP) and Runx2 expression in VICs via tyrosine nitration of dynamin-related protein 1 (DRP1) at Y628. Finally, folic acid (FA) significantly attenuated aortic valve calcification in WD-fed Apoe−/− mice through increasing DHFR and salvaging BH4 biosynthesis. Conclusion The reduction in endothelial-dependent BH4 levels promoted peroxynitrite formation, which subsequently resulted in DRP1 tyrosine nitration and osteoblastic differentiation of VICs, thereby leading to aortic valve calcification. Supplementation of FA in diet attenuated hypercholesterolaemia-induced aortic valve calcification by salvaging BH4 bioavailability. Key question Tetrahydrobiopterin (BH4) insufficiency-dependent endothelial nitric oxide synthase dysfunction mediates endothelial dysfunction and leads to vascular diseases. The role of BH4 in aortic valve calcification has not been explored. Key finding Tetrahydrobiopterin and guanosine 5′-triphosphate cyclohydrolase I are reduced in calcified aortic valves. Endothelial cell-specific deficiency of Gch1 promotes murine aortic valve calcification. Tetrahydrobiopterin reduction in valvular endothelial cells promotes valvular interstitial cells (VICs) osteogenesis via ONOO− formation. Folic acid suppresses murine aortic valve calcification by salvaging BH4 bioavailability. Take-home message Tetrahydrobiopterin is closely associated with the development of aortic valve calcification. Valvular endothelial cells dysfunction leads to ONOO− formation, resulting in osteoblastic differentiation of VICs. Salvaging BH4 bioavailability may be a potential therapeutic strategy for aortic valve calcification.

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Majumdar, Uddalak, Sathiyanarayanan Manivannan, Madhumita Basu, Yukie Ueyama, Mark C. Blaser, Emily Cameron, Michael R. McDermott, et al. "Nitric oxide prevents aortic valve calcification by S-nitrosylation of USP9X to activate NOTCH signaling." Science Advances 7, no. 6 (February 3, 2021). http://dx.doi.org/10.1126/sciadv.abe3706.

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Sanchez, Sandra, Mercedes Castro, Alberto Cook Calvete, María Delgado Marín, Ignacio Hernandez Navarro, Jose Lopez-Menendez, Carlos Zaragoza, and Marta Saura. "Abstract P1069: Integrin Linked Kinase Controls Human Valve Endotelial Cells Pro-osteogenic Activation In A TFG-b/NO Dependent Manner." Circulation Research 131, Suppl_1 (August 5, 2022). http://dx.doi.org/10.1161/res.131.suppl_1.p1069.

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Calcific aortic valve disease (CAVD) is expected in the aging population. CAVD physiopathology arises from endothelial dysfunction leading to lipid accumulation, inflammation, and osteogenic transformation. Many studies suggest that valve endothelial cells (VECs) undergoing EndMT may differentiate into osteoblastic interstitial cells. We previously showed that Integrin linked kinase (ILK) regulates vasomotor function by preventing endothelial nitric oxide synthase uncoupling. ILK expression in vascular endothelium plays an essential cardioprotective role. Moreover, we have found a significant negative correlation between human valve protein levels of ILK and the osteogenic marker Runx2 and BMP2 in 70 patients with calcific aortic stenosis, a higher decrease at the endothelial level. We hypothesized that Endothelial ILK plays a protective role in human valve endothelial cells osteogenic transition. Isolation of human valve endothelial cells from the aortic (aortic hVECs) and ventricular sides (ventricular hVECs) show a specific ILK decrease in the aortic hVECs from calcific compared to non-calcified valve (p<0.05). Silencing ILK expression in hVECs decreased NO production and increased ROS (Reactive Oxygen Species) production as early as 72 hours. After five days of silencing ILK, hVEC express myofibroblast markers SM22a, α-SMA, MMP12, MMP9, and SNAI 1 while losing the endothelial markers (CD31, and vWF (p<0.01). ILK silenced hVECs (siILK-hVECs) express the osteogenic marker RunX2 indicating osteogenic differentiation and developed calcified nodules. Cell treatment with Noggin, a BMP2 antagonist, did not reverse the increase of Runx2, thus excluding the implication of the BMP2/RUNX2 axis. However, silk-hVECs showed an increase in phosphorylated-SMAD 2, suggesting a TFG-β -dependent mechanism. Treatment of siILK-hVECs with the NO donor DETA-NO decreased Smad 2 activation and RunX2. Moreover, DETA-NO treated siILK hVECs cultured in pro-osteogenic media did not develop calcification. Collectively, our results point to a crucial role of ILK in keeping human valve endothelial cell phenotype preventing valve calcification in a Nitric Oxide-TFGβ1 dependent manner. Financed by the Regional European fund “a way to achieve Europe.” JCCM SBPLY/19/180501/000055S and ISCIII PI20/00930

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Majumdar, Uddalak, Talita Z. Choudhury, Sathiyanarayanan Manivannan, Yukie Ueyama, Madhumita Basu, and Vidu Garg. "Single-cell RNA-sequencing analysis of aortic valve interstitial cells demonstrates the regulation of integrin signaling by nitric oxide." Frontiers in Cardiovascular Medicine 9 (October 25, 2022). http://dx.doi.org/10.3389/fcvm.2022.742850.

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Calcific aortic valve disease (CAVD) is an increasingly prevalent condition among the elderly population that is associated with significant morbidity and mortality. Insufficient understanding of the underlying disease mechanisms has hindered the development of pharmacologic therapies for CAVD. Recently, we described nitric oxide (NO) mediated S-nitrosylation as a novel mechanism for preventing the calcific process. We demonstrated that NO donor or an S-nitrosylating agent, S-nitrosoglutathione (GSNO), inhibits spontaneous calcification in porcine aortic valve interstitial cells (pAVICs) and this was supported by single-cell RNA sequencing (scRNAseq) that demonstrated NO donor and GSNO inhibited myofibroblast activation of pAVICs. Here, we investigated novel signaling pathways that are critical for the calcification of pAVICs that are altered by NO and GSNO by performing an in-depth analysis of the scRNA-seq dataset. Transcriptomic analysis revealed 1,247 differentially expressed genes in pAVICs after NO donor or GSNO treatment compared to untreated cells. Pathway-based analysis of the differentially expressed genes revealed an overrepresentation of the integrin signaling pathway, along with the Rho GTPase, Wnt, TGF-β, and p53 signaling pathways. We demonstrate that ITGA8 and VCL, two of the identified genes from the integrin signaling pathway, which are known to regulate cell-extracellular matrix (ECM) communication and focal adhesion, were upregulated in both in vitro and in vivo calcific conditions. Reduced expression of these genes after treatment with NO donor suggests that NO inhibits calcification by targeting myofibroblast adhesion and ECM remodeling. In addition, withdrawal of NO donor after 3 days of exposure revealed that NO-mediated transcriptional and translational regulation is a transient event and requires continuous NO exposure to inhibit calcification. Overall, our data suggest that NO and S-nitrosylation regulate the integrin signaling pathway to maintain healthy cell-ECM interaction and prevent CAVD.

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Дисертації з теми "Aortic valve abnormalities; calcification; nitric oxide"

Hua, Xiang. "Effects of nitric oxide on aortic valve calcification in vitro." Thesis, 2007. http://hdl.handle.net/2440/69462.

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Aortic stenosis is characterized by accelerated aortic valve calcification, but the pathogenesis of this process is poorly understood. The aim of this study was to evaluate the potential impact of nitric oxide supplementation on valve matrix calcification in a tissue culture model, and the interaction between superoxide anion release and the process. Data from the study suggest that superoxide anion release, induced by transforming growth factor beta 1 contributes to calcific formation and that nitric oxide can limit this process.
Thesis (M.Clin.Sc.) -- University of Adelaide, School of Medicine, 2007

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Ngo, Doan Thi Minh. "Pathogenesis of aortic valve stenosis: bench to bedside approach." 2008. http://hdl.handle.net/2440/41887.

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Experiments described in this thesis address the pathogenesis of aortic valve sclerosis/stenosis using a bench to bedside approach. In particular, the thesis begins with development of a technique using ultrasonic backscatter analyses to quantitate the early stages of aortic stenosis. Subsequent chapters utilized this methodology to quantitate aortic valve structural changes in a model and intervention study of aortic stenosis in rabbits. The last chapters are human studies designed to identify factors associated with presence of aortic sclerosis/stenosis; with particular interest in potential association of endothelial dysfunction/inflammation/platelet aggregation with abnormal aortic valve structure quantitated by ultrasonic backscatter. In Chapter 1 (Introduction) the relevant literature is reviewed. Development of ultrasonic backscatter to quantitate aortic sclerosis (Chapter 2) Aortic valve sclerosis (ASc) is detected when there is visual assessment of focal increases in echogenicity of the aortic valve most commonly assessed by echocardiography. However, there is no previously described method to quantitate degree of aortic valve structural abnormality as ASc is not associated with marked hemodynamic obstruction quantifiable by Doppler echocardiography. The current study used ultrasonic backscatter to quantitate aortic valve structural abnormality in patients assessed as having ASc based on valve appearances, compared to young healthy volunteers with normal aortic valves. The results of the study indicate: 1) that the mean levels of aortic valve backscatter in ASc patients are approximately 60% greater than in young healthy volunteers (ie aortic valve backscatter scores ≥ 16dB are not consistent with normal aortic valve structure), 2) ultrasonic backscatter scores in ASc patients are directly correlated with subjective scoring of sclerosis and with a positive trend with transvalvular pressure gradients in patients with mild-moderate aortic stenosis, and most importantly, 3) ultrasonic backscatter is a reproducible technique, with mean differences between estimates based on repeat echocardiograms of 2.3 ± 1.7 (9.1%). These results indicate that ultrasonic backscatter could be used as a quantitative measure of aortic valve structural abnormality in epidemiology and for examination of interventions. In vivo studies Development of an animal model of aortic stenosis with vitamin D2 (Chapter 3) The aim of the study was to develop an appropriate animal model for AS. The study used vitamin D2 alone at 25,000IU/4 days weekly (vit-D2) for 8 weeks to induce AS in rabbits. Results showed that: 1) rabbits in the vit-D2 group had significantly increased in transvalvular velocity and pressure gradients compared to rabbits in the control group (normal chow + drinking water); this was consistent for aortic valve ultrasonic backscatter scores; 2) aortic valve immunohistochemistry/histology showed marked calcification, neutral lipids, macrophage, and leukocyte infiltrations for rabbits in the vit- D2 group (ie consistent with histology of human AS); 3) significant elevation of asymmetric dimethylarginine (ADMA) concentrations in the vit-D2 group occurred compared to controls over the 8 weeks treatment period; the change in ADMA concentrations correlated significantly with the change in transvalvular pressure gradients for rabbits in the vit-D2 group; 4) rabbits in the vit-D2 group had significantly impaired endothelium-dependent acetylcholine-induced aortic relaxation, and this effect was completely abolished by the nitric oxide synthase inhibitor (L-NAME); 5) the addition of 0.5% cholesterol-supplemented diet to the vitamin D2 regimen did not accentuate the development of AS. Thus, treatment with vitamin D2 at 25,000IU/4 days weekly for 8 weeks significantly induced AS with similar aortic valve pathology to that of human AS; therefore, the model is suitable for use in examining potential therapeutic interventions in AS. Effects of ramipril on development of AS in rabbits (Chapter 4) Using this animal model, this study aimed to examine the effects of the angiotensinconverting enzyme inhibitor (ACEi) ramipril on development of AS. Rabbits (n=28) treated for 8 weeks were divided into 2 groups: (a) vitamin D2 alone (n=10) (normal chow + 25,000IU vitamin D2 in drinking water); (b) vitamin D2/Ramipril (n=12) (normal chow+25,000IU vitamin D2/Ramipril (0.5mg/kg) in drinking water). Six further rabbits constituted a normal reference group (no treatment was given). The results for comparisons between vitamin D2/ramipril vs vitamin D2 alone were as follows: 1) ramipril-treated rabbits had significantly less severe hemodynamic obstructions (p<0.05, for both) as assessed by transvalvular velocity, and aortic valve area; with borderline reduction in aortic valve backscatter (p=0.08); 2) ramipril significantly reduced plasma ADMA concentrations; 3) there was improvement in acetylcholine-induced aortic relaxation (p=0.056), with significant improvement in sodium nitroprusside-induced relaxation (p<0.05); 4) there was a strong inverse correlation between acetylcholineinduced aortic relaxation and aortic valve backscatter score (0<0.001), thus providing further evidence of the potential role of nitric oxide in retarding the development of AS in this model. These data provide a strong rationale for the inception of a randomized trial of ACE inhibition as a strategy for limitation of AS progression in humans. Human studies Aortic stenosis is associated with elevated plasma levels of asymmetric dimethylarginine (ADMA) concentrations in humans (Chapter 5). Given the findings that aortic stenosis induced by vitamin D2 in rabbits also caused elevation of plasma ADMA concentrations, a physiological inhibitor of nitric oxide synthase, a mediator and marker of endothelial dysfunction and an indicator of incremental cardiovascular risk. The study sought to determine whether plasma ADMA concentrations are elevated independently of pre-existing coronary risk factors in subjects with at least moderate aortic stenosis (n=42) compared to age-matched patients with normal aortic valves (n=42): as determined both by visual assessment and with aortic valve backscatter scores < 16dB. Results for this study were as follows: 1) plasma ADMA concentrations were not statistically different between the AS and non-AS group (median 0.59 vs 0.54 µmol/L, p=0.13, Mann-Whitney test) on univariate analysis; 2) backward stepwise multiple linear regression showed the presence of AS was a significant predictor of elevated ADMA concentrations (p=0.04, 95% CI =0.001, 0.072). 3) in addition, elevated plasma ADMA concentrations were also associated with history of atrial fibrillation (p=0.009, 95% CI=0.015, 0.100), and negatively associated with creatinine clearance (p=0.01, 95% CI=-0.002, 0.000), and the use of statin therapy (p=0.01, 95% CI=-0.081, -0.011). Therefore, in conclusion, this study found that AS is independently associated with elevation of ADMA concentrations, beyond that implied by “conventional” risk factors for endothelial dysfunction. The clinical status of AS as an incremental marker of cardiovascular risk may reflect ADMA-mediated endothelial dysfunction. Assessment of factors associated with ASc in a random ageing population study (Chapter 6). There have been few clinical studies of factors associated with ASc. Previous population studies have established that ASc is an independent correlate of incremental risk of coronary events. Having established that patients with AS have increased plasma ADMA concentrations (Chapter 5), it was now aimed to determine whether subjects with increased aortic valve backscatter scores (ASc) also have other markers of endothelial dysfunction/NO effects, independent of preexisting coronary risk factors. The study was designed to identify such anomalies, if they existed, on an incremental basis to other putative correlates of ASc, including coronary risk factors, renal dysfunction and vitamin D levels. Random selected subjects (n=253) aged between 51 to 77 years were evaluated. All patients underwent transthoracic echocardiography examination; aortic valve ultrasonic backscatter score (AVBS), was used to quantitate echogenicity of the aortic valve. Conventional coronary risk factors were identified on history. Integrity of NO generation/response was assessed via (i) plasma ADMA concentrations; (ii) inhibition of platelet aggregation by the NO donor sodium nitroprusside (SNP); (iii) aortic augmentation index (AIx), a measure of arterial stiffness/wave reflection. All putative correlations with AVBS were examined by univariate and stepwise multiple linear regression analyses. On the basis of echocardiographic appearances, ASc was present in 63 subjects (25.4%); mean AVBS scores was 14.9±4.6dB (SD) vs 11.2±3.9dB (SD) in the presence vs absence of ASc (p<0.001). Univariate analyses revealed that platelet responsiveness to NO was inversely correlated with AVBS (β=-0.16, p=0.02); but [ADMA] and AIx were not. On multiple linear regression, significant correlates of increased AVBS were: (i) advanced age (β=0.21, p=0.003), (ii) low body mass index (β=-0.23, p=0.001); and (iii) impaired platelet responsiveness to NO (β=-0.16, p=0.02). In Chapter 7, the implications of the overall findings in this thesis are discussed in relation to future perspective.
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Thesis(Ph.D.) -- School of Medicine, 2008

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