Relevant bibliographies by topics / Heart disease; Cardiac metabolism

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Heart disease; Cardiac metabolism'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Heart disease; Cardiac metabolism"

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Lopaschuk, Gary D., John R. Ussher, Clifford D. L. Folmes, Jagdip S. Jaswal, and William C. Stanley. "Myocardial Fatty Acid Metabolism in Health and Disease." Physiological Reviews 90, no. 1 (January 2010): 207–58. http://dx.doi.org/10.1152/physrev.00015.2009.

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There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the β-oxidation of long-chain fatty acids. The control of fatty acid β-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via β-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and β-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid β-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid β-oxidation and how alterations in fatty acid β-oxidation can contribute to heart disease. The implications of inhibiting fatty acid β-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.
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Vatner, Stephen F., Misun Park, Lin Yan, Grace J. Lee, Lo Lai, Kousaku Iwatsubo, Yoshihiro Ishikawa, Jeffrey Pessin, and Dorothy E. Vatner. "Adenylyl cyclase type 5 in cardiac disease, metabolism, and aging." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 1 (July 1, 2013): H1—H8. http://dx.doi.org/10.1152/ajpheart.00080.2013.

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G protein-coupled receptor/adenylyl cyclase (AC)/cAMP signaling is crucial for all cellular responses to physiological and pathophysiological stimuli. There are nine isoforms of membrane-bound AC, with type 5 being one of the two major isoforms in the heart. Since the role of AC in the heart in regulating cAMP and acute changes in inotropic and chronotropic state are well known, this review will address our current understanding of the distinct regulatory role of the AC5 isoform in response to chronic stress. Transgenic overexpression of AC5 in cardiomyocytes of the heart (AC5-Tg) improves baseline cardiac function but impairs the ability of the heart to withstand stress. For example, chronic catecholamine stimulation induces cardiomyopathy, which is more severe in AC5-Tg mice, mediated through the AC5/sirtuin 1/forkhead box O3a pathway. Conversely, disrupting AC5, i.e., AC5 knockout, protects the heart from chronic catecholamine cardiomyopathy as well as the cardiomyopathies resulting from chronic pressure overload or aging. Moreover, AC5 knockout results in a 30% increase in a healthy life span, resembling the most widely studied model of longevity, i.e., calorie restriction. These two models of longevity share similar gene regulation in the heart, muscle, liver, and brain in that they are both protected against diabetes, obesity, and diabetic and aging cardiomyopathy. A pharmacological inhibitor of AC5 also provides protection against cardiac stress, diabetes, and obesity. Thus AC5 inhibition has novel, potential therapeutic applicability to several diseases not only in the heart but also in aging, diabetes, and obesity.
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Lakhal-Littleton, Samira. "Ferroportin Mediated Control of Iron Metabolism and Disease." Blood 128, no. 22 (December 2, 2016): SCI—21—SCI—21. http://dx.doi.org/10.1182/blood.v128.22.sci-21.sci-21.

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Abstract Ferroportin, the only known mammalian iron export protein, releases iron from the duodenum, reticuloendothelial system and liver, the sites of iron absorption, recycling and storage respectively. By downregulating ferroportin, the liver-derived hormone hepcidin controls systemic iron availability in response to erythroid demand and inflammation. This ferroportin/hepcidin axis has long been recognized as essential for systemic iron homeostasis. However, both ferroportin and hepcidin are found in tissues not recognized for their role in systemic iron control, such as the heart, the kidney, the brain and the placenta. Co-existence within the same tissue suggests a possible function for hepcidin and ferroportin in local iron homeostasis. However, this hypothesis has not been formally explored. Using mouse models with cardiac-specific manipulation of hepcidin and ferroportin, we have uncovered a role for the cardiac hepcidin/ferroportin axis in cell-autonomous iron homeostasis within cardiomyocytes. Disruption of this cardiac pathway leads to fatal cardiac dysfunction, even against a background of normal systemic iron homeostasis. One the one hand, loss of cardiac ferroportin causes by fatal cardiac iron overload that is preventable by dietary iron restriction 1. On the other hand, loss of cardiac hepcidin or of cardiac hepcidin responsiveness causes fatal cardiomyocyte iron deficiency that is preventable by intravenous iron administration. Comparative study of cardiac iron homeostasis and function in cardiac versus systemic models of ferroportin/hepcidin disruption provides insight into the interplay between systemic and cellular iron homeostasis. A role for the hepcidin/ferroportin axis in cell-autonomous iron control, demonstrated here in the context of the heart, has not previously been described in any other tissue. A pertinent question is whether our findings in the heart extend to other tissues that express both hepcidin and ferroportin, such as the kidney, brain and placenta. Disturbances in iron homeostasis are of clinical importance in cardiovascular disease, renal failure, neurodegeneration and developmental defects. Our findings have two clinically relevant implications: a) that disruption of the local hepcidin/ferroportin axis may in itself have a disease-modifying effect, and b) that therapeutic strategies developed to target the systemic hepcidin/ferroportin axis may have off-target effects relating to local iron control within some tissues. Reference 1.Lakhal-Littleton S, Wolna M, Carr C, et al. Cardiac ferroportin regulates cellular iron homeostasis and is important for cardiac function. PNAS. 2015; 10;112(10):3164-3169. Disclosures No relevant conflicts of interest to declare.
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Deslauriers, Roxanne, and Valery V. Kupriyanov. "Cardiac magnetic resonance spectroscopy." Biochemistry and Cell Biology 76, no. 2-3 (May 1, 1998): 510–21. http://dx.doi.org/10.1139/o98-016.

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The article reviews cardiac magnetic resonance spectroscopy (MRS) in Canada. 31P MRS has been used to study cardiac energetics and intracellular pH in hearts subjected to ischemia-reperfusion and to evaluate the effects of pharmacological interventions. 23Na, 87Rb, and 7Li MRS have provided unique probes to study ion balance and fluxes in intact tissue under normal and stressful physiological conditions. 1H MRS has been used to monitor the accumulation of lactate and lipids in hearts subjected to ischemia-reperfusion and follow the effects of diet on cardiac lipid levels and function. The isolated rat heart has been used most commonly to study the effects of pharmacological agents on energy balance, pH, ion fluxes, and contractile function of the heart subjected to ischemia-reperfusion. The pig heart has been developed as an alternative to the rodent heart because its metabolism is more similar to that of the human heart. Human atrial appendages have been useful in evaluating the effects of preservation strategies (temperature, composition of preservation solutions) on energy levels. The pig heart model has been useful in evaluating the effects of preservation solutions on cardiac function of hearts destined for transplantation. An isolated blood-perfused pig heart model has been developed to assess the effects of cardioplegic strategies on the preservation of contractile function of hearts following surgery on the heart. An in vivo canine model has been used to study myocardial infarction and the effects of therapies to reduce the infarct zones and areas of the heart at risk of infarction. Studies of human hearts in vivo have provided insight into the metabolic adaptations that occur in individuals living at high altitudes.Key words: ion transport, metabolism, heart disease, organ preservation, drug effects.
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Lopaschuk, Gary D. "Treating ischemic heart disease by pharmacologically improving cardiac energy metabolism." American Journal of Cardiology 82, no. 5 (September 1998): 14K—17K. http://dx.doi.org/10.1016/s0002-9149(98)00532-3.

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Dolinsky, Vernon W., and Jason R. B. Dyck. "Role of AMP-activated protein kinase in healthy and diseased hearts." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (December 2006): H2557—H2569. http://dx.doi.org/10.1152/ajpheart.00329.2006.

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The heart is capable of utilizing a variety of substrates to produce the necessary ATP for cardiac function. AMP-activated protein kinase (AMPK) has emerged as a key regulator of cellular energy homeostasis and coordinates multiple catabolic and anabolic pathways in the heart. During times of acute metabolic stresses, cardiac AMPK activation seems to be primarily involved in increasing energy-generating pathways to maintain or restore intracellular ATP levels. In acute situations such as mild ischemia or short durations of severe ischemia, activation of cardiac AMPK appears to be necessary for cardiac myocyte function and survival by stimulating ATP generation via increased glycolysis and accelerated fatty acid oxidation. Whereas AMPK activation may be essential for adaptation of cardiac energy metabolism to acute and/or minor metabolic stresses, it is unknown whether AMPK activation becomes maladaptive in certain chronic disease states and/or extreme energetic stresses. However, alterations in cardiac AMPK activity are associated with a number of cardiovascular-related diseases such as pathological cardiac hypertrophy, myocardial ischemia, glycogen storage cardiomyopathy, and Wolff-Parkinson-White syndrome, suggesting the possibility of a maladaptive role. Although the precise role AMPK plays in the diseased heart is still in question, it is clear that AMPK is a major regulator of cardiac energy metabolism. The consequences of alterations in AMPK activity and subsequent cardiac energy metabolism in the healthy and the diseased heart will be discussed.
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Selthofer-Relatić, K., A. Kibel, D. Delić-Brkljačić, and I. Bošnjak. "Cardiac Obesity and Cardiac Cachexia: Is There a Pathophysiological Link?" Journal of Obesity 2019 (September 2, 2019): 1–7. http://dx.doi.org/10.1155/2019/9854085.

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Obesity is a risk factor for cardiometabolic and vascular diseases like arterial hypertension, diabetes mellitus type 2, dyslipidaemia, and atherosclerosis. A special role in obesity-related syndromes is played by cardiac visceral obesity, which includes epicardial adipose tissue and intramyocardial fat, leading to cardiac steatosis; hypertensive heart disease; atherosclerosis of epicardial coronary artery disease; and ischemic cardiomyopathy, cardiac microcirculatory dysfunction, diabetic cardiomyopathy, and atrial fibrillation. Cardiac expression of these changes in any given patient is unique and multimodal, varying in clinical settings and level of expressed changes, with heart failure development depending on pathophysiological mechanisms with preserved, midrange, or reduced ejection fraction. Progressive heart failure with misbalanced metabolic and catabolic processes will change muscle, bone, and fat mass and function, with possible changes in the cardiac fat state from excessive accumulation to reduction and cardiac cachexia with a worse prognosis. The question we address is whether cardiac obesity or cardiac cachexia is to be more feared.
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Lena, Alessia, Nicole Ebner, and Markus S. Anker. "Cardiac cachexia." European Heart Journal Supplements 21, Supplement_L (December 1, 2019): L24—L27. http://dx.doi.org/10.1093/eurheartj/suz241.

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Abstract Cachexia is a multifactorial disease characterized by a pathologic shift of metabolism towards a more catabolic state. It frequently occurs in patients with chronic diseases such as chronic heart failure and is especially common in the elderly. In patients at risk, cardiac cachexia is found in about 10% of heart failure patients. The negative impact of cardiac cachexia on mortality, morbidity, and quality of life demonstrates the urgent need to find new effective therapies against cardiac cachexia. Furthermore, exercise training and nutritional support can help patients with cardiac cachexia. Despite ongoing efforts to find new therapies for cachexia treatment, also new preventive strategies are needed.
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Gao, Chen, and Yibin Wang. "mRNA Metabolism in Cardiac Development and Disease: Life After Transcription." Physiological Reviews 100, no. 2 (April 1, 2020): 673–94. http://dx.doi.org/10.1152/physrev.00007.2019.

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The central dogma of molecular biology illustrates the importance of mRNAs as critical mediators between genetic information encoded at the DNA level and proteomes/metabolomes that determine the diverse functional outcome at the cellular and organ levels. Although the total number of protein-producing (coding) genes in the mammalian genome is ~20,000, it is evident that the intricate processes of cardiac development and the highly regulated physiological regulation in the normal heart, as well as the complex manifestation of pathological remodeling in a diseased heart, would require a much higher degree of complexity at the transcriptome level and beyond. Indeed, in addition to an extensive regulatory scheme implemented at the level of transcription, the complexity of transcript processing following transcription is dramatically increased. RNA processing includes post-transcriptional modification, alternative splicing, editing and transportation, ribosomal loading, and degradation. While transcriptional control of cardiac genes has been a major focus of investigation in recent decades, a great deal of progress has recently been made in our understanding of how post-transcriptional regulation of mRNA contributes to transcriptome complexity. In this review, we highlight some of the key molecular processes and major players in RNA maturation and post-transcriptional regulation. In addition, we provide an update to the recent progress made in the discovery of RNA processing regulators implicated in cardiac development and disease. While post-transcriptional modulation is a complex and challenging problem to study, recent technological advancements are paving the way for a new era of exciting discoveries and potential clinical translation in the context of cardiac biology and heart disease.
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Vaillant, Fanny, Benjamin Lauzier, Matthieu Ruiz, Yanfen Shi, Dominic Lachance, Marie-Eve Rivard, Virginie Bolduc, Eric Thorin, Jean-Claude Tardif, and Christine Des Rosiers. "Ivabradine and metoprolol differentially affect cardiac glucose metabolism despite similar heart rate reduction in a mouse model of dyslipidemia." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 4 (October 1, 2016): H991—H1003. http://dx.doi.org/10.1152/ajpheart.00789.2015.

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While heart rate reduction (HRR) is a target for the management of patients with heart disease, contradictory results were reported using ivabradine, which selectively inhibits the pacemaker If current, vs. β-blockers like metoprolol. This study aimed at testing whether similar HRR with ivabradine vs. metoprolol differentially modulates cardiac energy substrate metabolism, a factor determinant for cardiac function, in a mouse model of dyslipidemia (hApoB+/+;LDLR−/−). Following a longitudinal study design, we used 3- and 6-mo-old mice, untreated or treated for 3 mo with ivabradine or metoprolol. Cardiac function was evaluated in vivo and ex vivo in working hearts perfused with 13C-labeled substrates to assess substrate fluxes through energy metabolic pathways. Compared with 3-mo-old, 6-mo-old dyslipidemic mice had similar cardiac hemodynamics in vivo but impaired ( P < 0.001) contractile function (aortic flow: −45%; cardiac output: −34%; stroke volume: −35%) and glycolysis (−24%) ex vivo. Despite inducing a similar 10% HRR, ivabradine-treated hearts displayed significantly higher stroke volume values and glycolysis vs. their metoprolol-treated counterparts ex vivo, values for the ivabradine group being often not significantly different from 3-mo-old mice. Further analyses highlighted additional significant cardiac alterations with disease progression, namely in the total tissue level of proteins modified by O-linked N-acetylglucosamine ( O-GlcNAc), whose formation is governed by glucose metabolism via the hexosamine biosynthetic pathway, which showed a similar pattern with ivabradine vs. metoprolol treatment. Collectively, our results emphasize the implication of alterations in cardiac glucose metabolism and signaling linked to disease progression in our mouse model. Despite similar HRR, ivabradine, but not metoprolol, preserved cardiac function and glucose metabolism during disease progression.
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Dissertations / Theses on the topic "Heart disease; Cardiac metabolism"

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Hopkins, James Charles Alex. "Myocardial glycogen, glucose uptake and insulin sensitivity : interrelations and changes with disease." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363766.

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Luongo, Timothy Scott. "The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/437718.

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Biomedical Sciences
Ph.D.
The high metabolic demand of the heart makes it essential that an efficient and tightly controlled system be in place to regulate energy production. Contractility is mediated by a variable flux in intracellular calcium (iCa2+), which is proposed to be integrated into mitochondria to regulate cardiac energetics. Moreover, mitochondrial Ca2+ (mCa2+)-overload is known to activate the mitochondrial permeability transition pore (MPTP) and induce cell death. However, the true function of cardiac mCa2+ in physiology remains unknown. Recent studies have reported that the Mcu gene encodes the channel-forming portion of the mitochondrial calcium uniporter (MCU) and is required for mCa2+ uptake (Baughman et al., 2011; De Stefani, Raffaello, Teardo, Szabo, & Rizzuto, 2011). To examine the role of mCa2+ in the heart, we generated a conditional, cardiac-specific knockout model and deleted Mcu in adult mice (Mcu-cKO). Loss of Mcu protected against myocardial ischemia-reperfusion (IR) (40 min occlusion of the left coronary artery (LCA) followed by 24h reperfusion) injury by preventing the activation of the MPTP. We observed a 45% reduction in infarct size per area-at-risk and a 65% reduction in cardiac troponin-I serum levels from 24h post-IR. In addition, while we found no baseline phenotype or change in baseline mCa2+ content, Mcu-cKO mice lacked contractile responsiveness to β-adrenergic receptor stimulation (isoproterenol infusion) as assessed by invasive hemodynamics, and, in parallel, were unable to activate mitochondrial dehydrogenases, thereby decreasing tricarboxylic acid (TCA) cycle flux and cardiac NADH. We found that Mcu-cKO mice had a 3-fold increase in pyruvate dehydrogenase (PDH) phosphorylation and a 50% decrease in PDH activity post-isoproterenol infusion. Further experimental analyses in isolated adult cardiomyocytes confirmed a lack of energetic responsiveness to acute sympathetic stress (isoproterenol failure to mediate an increase in oxidative phosphorylation capacity) supporting the hypothesis that the physiological function of the MCU in the heart is to modulate Ca2+-dependent metabolism during the ‘fight or flight’ response. However, questions still remain on how basal mCa2+ levels are regulated and if it contributes to cardiac disease. The mitochondrial sodium/calcium exchanger (mNCX) is hypothesized as the primary mechanism of mCa2+ efflux, but to date no study has confirmed its identity or function in an in vivo system (Palty et al., 2010). To investigate the role of mNCX in the heart, we generated mutant mice with loxP sites flanking exons 5-7 of the candidate gene, Slc8b1, and crossed them with a tamoxifen-inducible, cardiomyocyte-specific, αMHC-Cre mouse to delete mNCX in the adult heart (mNCX-cKO). Biophysical study of cardiomyocytes isolated from mNCX-cKO mice revealed a significant reduction in mCa2+ efflux rate. Tamoxifen-induced deletion of Slc8b1 in adult hearts caused sudden death with less than 15% of mice surviving after 10 days. Echocardiographic evaluation of mNCX-cKO hearts 3d post-tamoxifen revealed significant left ventricular (LV) remodeling, characterized by significant dilation and a substantial decrease in function. In addition, mNCX-cKO hearts exhibited increased reactive oxygen species generation when assessed by DHE imaging of live myocardial tissue and mitoSOX Red imaging in isolated adult cardiomyocytes. Using an Evan’s blue dye exclusion technique, we found that mNCX-cKO hearts displayed significant sarcolemmal rupture (~8% of all myocytes at a single time point 3d post-tamoxifen), indicative of cellular necrosis. To rescue the sudden death phenotype and acute loss of cells, we crossed our mNCX-cKO mice with the cyclophilin d (a mediator of MPTP-opening) knockout mice. mNCX-cKO x CypD-KO mice had a significant improvement in survival and LV-function. In addition, loss of MPTP activation also rescued mitochondrial pathology on the subcellular level. Since deletion of mNCX was detrimental on cardiac function, we thought that increasing mNCX could protect cardiomyocytes by reducing mCa2+-overload during cardiac disease. To test this, we generated a conditional, cardiac-specific mNCX overexpression mouse model (mNCX-Tg) to assess if increasing mCa2+ efflux would prevent cardiac injury in multiple pathological surgical models. mNCX-Tg and controls were subjected to in vivo IR injury followed by 24h reperfusion and myocardial infarction (MI) (permanent LCA ligation). mNCX-Tg mice displayed reduced cell death (a 43% reduction in infarct size 24h post-IR and a 33% reduction in scar size 4w post-MI), preserved LV function, a reduction in ROS generation, and a decrease in numerous HF indices. For the first time, we showed that mNCX is essential for maintenance of the mCa2+ microdomain in cardiomyocytes and that mNCX represents a novel therapeutic target in HF.
Temple University--Theses
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Steeples, Violetta Rae. "Metabolic modulation through deletion of hypoxia-inducible factor-1α and fumarate hydratase in the heart." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:f546ca24-6226-4846-b492-30de26836e94.

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Hypoxia inducible factor-1α (HIF-1α) plays a critical role in the oxygen homeostasis of all metazoans. HIF-1α is a master transcriptional regulator which coordinates the adaptive response to low oxygen tension. Through activation of a plethora of downstream target genes, HIF-1α facilitates oxygenation by promoting angiogenesis and blood vessel dilation, in addition to modulating metabolic pathways to inhibit oxidative phosphorylation and promote glycolytic energy production. Given the critical roles of hypoxia, insufficient blood supply and perturbed energetics in the pathogenesis of cardiovascular disorders, notably ischaemic heart disease, therapeutic modulation of HIF-1α is of significant clinical interest. Previous studies have demonstrated an acute cardioprotective role for both endogenous and supraphysiological HIF-1α signalling in the context of myocardial ischaemia. In contrast, chronic supraphysiological HIF-1α activation in the unstressed heart has been shown to induce cardiac dysfunction. To address the effect of chronic endogenous HIF-1α activation post-myocardial infarction (MI), the present work employed a murine coronary artery ligation (CAL) model in conjunction with temporally-inducible, cardiac-specific deletion of Hif-1α. While CAL surgery successfully modelled myocardial infarction – eliciting substantial adverse cardiac remodelling and contractile dysfunction – there was no evidence of chronic HIF-1α activation by CAL in HIF knockout or control left ventricular samples. In keeping with this, chronic ablation of Hif-1α (from 2 weeks post-CAL) had no discernible additional effect upon cardiac function. Overall, these findings do not support a potential therapeutic role for inhibition of HIF-1α signalling in the chronic phase post-MI. The fundamental tricarboxylic acid (TCA) cycle enzyme fumarate hydratase (FH) converts fumarate to malate. FH deficiency is associated with smooth muscle and kidney tumours which exhibit normoxic HIF signalling due to fumarate accumulation. To investigate the potential for fumarate accumulation to elicit protective HIF signalling, a cardiac-specific Fh1 null mouse was developed through Cre-loxP recombination. Strikingly, despite interruption of the TCA cycle in a highly metabolically demanding organ, cardiac Fh1 null mice were viable, fertile and survived into adulthood, demonstrating the remarkable metabolic plasticity of the heart. However, by 3-4 months Fh1 null mice develop a lethal cardiomyopathy characterised by cardiac hypertrophy, ventricular dilatation and contractile dysfunction. Despite lack of a pseudohypoxic response, Fh1 null hearts did exhibit another phenomenon observed in FH-deficient cancers and also attributed to fumarate accumulation – activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2) antioxidant pathway. Heterozygous, but not homozygous, somatic deletion of Nrf2 extended the life expectancy of cardiac Fh1 null mice. Exploration of redox status revealed a more reductive environment in Fh1 null hearts than controls. As a corollary, inhibition of the rate limiting enzyme of the pentose phosphate pathway – a major source of cellular reducing equivalents – with dehydroepiandrosterone conferred striking amelioration of the Fh1 null cardiomyopathy, suggesting a possible pathogenic role for reductive stress. While loss of mitochondrial Fh1 activity and subsequent TCA cycle dysfunction likely contribute to the Fh1 null phenotype, the importance of cytosolic FH was unclear. To clarify this, FH was expressed specifically in the cytosol in vivo. This was sufficient to substantially rescue the Fh1 null cardiomyopathy, supporting a role for cytosolic FH disruption in its pathogenesis. Taken together, these findings highlight the potential for reductive stress to contribute to cardiac dysfunction and suggest a function for cytosolic FH in cardiac metabolic homeostasis.
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Mahmod, Masliza. "Multiparametric cardiovascular magnetic resonance for the assessment of cardiac function and metabolism in hypertrophy and heart failure." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:ff24c167-e00d-4c6d-9809-82203979ba7a.

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Both hypertrophied and failing hearts are characterised by pathological left ventricular (LV) remodelling, impaired myocardial energy status and alteration in substrate metabolism. Cardiac magnetic resonance imaging (CMR) and magnetic resonance spectroscopy (MRS) are powerful tools in the characterisation of these disease conditions. More recent techniques have allowed assessment of myocardial steatosis using 1H-MRS and tissue oxygenation using blood oxygen level dependent (BOLD) CMR. In hypertrophy and heart failure, studies on steatosis and the relationship with other parameters such as myocardial function and fibrosis, especially in humans are limited. I therefore investigated the presence of steatosis in severe aortic stenosis (AS) and dilated cardiomyopathy (DCM), and further assessed its relation to contractile function. This study found that myocardial triglyceride (TG) content is increased in both symptomatic and asymptomatic AS patients (lipid/water ratio 0.89±0.42% in symptomatic AS; 0.75±0.36% in asymptomatic AS vs. controls 0.45±0.17%, both p<0.05) and DCM patients (lipid/ratio 0.64±0.44% vs. controls 0.40±0.13%, p=0.03). Circumferential strain was lower in both AS (-16.4±2.5% in symptomatic AS; -18.9±2.9% in asymptomatic AS vs. controls 20.7±2.0%, both p<0.05) and DCM patients (-12.3±3.4% vs. controls -20.9±1.7%, p<0.001). In AS, myocardial contractility is related to the degree of steatosis, and were both reversible following aortic valve replacement (AVR), lipid/water ratio 0.92±0.41% vs. pre AVR 0.45±0.17%, p=0.04 and circumferential strain -17.2±2.0% vs. pre AVR -19.5±3.2%, p=0.04. A novel finding of this study was significant correlation of MRS-measured TG content with histological staining of TG of the myocardium, taken from endomyocardial biopsy during AVR. In DCM, myocardial TG was independently associated with LV dilatation and correlated significantly with hepatic TG, which suggests that both cardiac and hepatic steatosis might be a common feature in the failing heart. Additionally, although the hypertrophied heart is characterised by impaired perfusion, it is unknown if this is severe enough to translate into tissue deoxygenation and ischaemia. I assessed this by using adenosine vasodilator stress test and BOLD-CMR in patients with severe AS. It was found that AS patients had reduced perfusion (myocardial perfusion reserve index-MPRI 1.0±0.3 vs. controls 1.7±0.3, p<0.001), and blunted tissue oxygenation (blood-oxygen level dependent-BOLD signal intensity-SI change 4.8±9.6% vs. controls 18.2±11.6%, p=0.001) during stress. Importantly, there was a substantial improvement in perfusion and oxygenation towards normal after AVR, MPRI 1.5±0.4, p=0.005 vs. pre AVR and BOLD SI change 16.4±7.0%, p=0.014 vs. pre AVR. Overall, the work in this thesis supports the powerful role of CMR in assessing LV function and elucidating metabolic mechanisms in the hypertrophied and failing heart.
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Dewan, Aaraf. "A Unique Role for Sarcolemmal Membrane Associated Protein Isoform 1 (SLMAP1) as a Regulator of Cardiac Metabolism and Endosomal Recycling." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35088.

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Altered glucose metabolism is the underlying factor in many metabolic disorders, including diabetes. A novel protein recently linked to diabetes through animal and clinical studies is Sarcolemmal Membrane Associated Protein (SLMAP) but its role in metabolism remains undefined. The data here reveals a novel role for SLMAP isoform1 in glucose metabolism within the myocardium. Neonatal cardiomyocytes (NCMs) harvested from hearts of transgenic mice expressing SLMAP1, presented with increased glucose uptake, glycolytic rate, as well as glucose transporter 4 (GLUT4) expressions with minimal impact on lipid metabolism. SLMAP1 expression markedly increased the machinery required for endosomal trafficking of GLUT4 to the membrane within NCMs, accounting for the observed effects on glucose metabolism. The data here indicates SLMAP1 as a unique regulator of glucose metabolism through endosomal regulation of GLUT4 trafficking and suggests it may uniquely serve as a target to limit cardiovascular disease in metabolic disorders such as diabetes.
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Wachowiak, Paul Stephen. "Relationships among Cynical Hostility, Metabolic Syndrome, and Cardiac Structure and Function in Multi-Ethnic Post-Myocardial Infarction Patients: A Structural Modeling Approach." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/291.

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BACKGROUND: Risk factors associated with Metabolic Syndrome (MetS) have been implicated in cardiovascular disease (CVD) development and outcomes. Few studies have investigated relationships between psychological variables, MetS factors, and indices of cardiac structure and function (CSF) among healthy individuals in a single conceptual model. No studies to date have analyzed such relationships in patients with CVD. METHODS: The present study examined associations between cynical hostility (CynHo), MetS factors, and CSF in 186 multi-ethnic post-myocardial infarction (MI) patients. Structural equation modeling was used to test a theory driven model of MetS that had good statistical fit. Primary MetS variables included waist circumference (WC), the homeostatic model of insulin resistance (HOMA-IR), glucose area under the curve (G-AUC), triglycerides (TRIG), high-density lipoprotein cholesterol (HDL-C), and diastolic blood pressures (DBP). Secondary MetS variables included plasminogen activator inhibitor-1 (PAI-1) and a latent inflammation variable comprised of CRP and IL-6. Cardiac function variables were fractional shortening (FS), E/A ratio, and rate-pressure product (RPP). A latent cardiac mass (CM) variable was also created. RESULTS: The final structural model had good model fit (Chi-Square(102)=100.65, p=0.52, CFI=1.00, RMSEA=0.00, and SRMR=0.04). Direct paths were supported between WC and CM and all MetS factors except TRIG and G-AUC. WC was indirectly associated with DBP via CM. The model supported positive direct paths between HOMA-IR and G-AUC, TRIG, and PAI-1, but not inflammation or HDL-C. HOMA-IR demonstrated a direct positive association with RPP and direct inverse associations with FS and E/A ratio. No direct paths were supported between other MetS variables except one between TRIG and HDL-C. CynHo demonstrated a direct positive relationship with HOMA-IR. CONCLUSIONS: Similar to findings in healthy individuals, central adiposity and IR play primary roles in CSF impairment in post-MI patients. Findings suggest that CynHo could promote the progression of metabolic dysfunction and cardiac disease via factors that influence the efficiency of glucose metabolism. Interventions for post-MI patients should take into account both direct and indirect effects of CynHo, central adiposity, and IR on the progression of CVD in this population to reduce adverse outcomes and improve quality of life.
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Cutter, Zachary S. "EFFECTS OF THE NA-CL CO-TRANSPORTER (NCC) IN WESTERN DIET INDUCED METABOLIC AND CARDIAC DYSFUNCTION." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5431.

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Interleukin-18 (IL-18) is a pro-inflammatory cytokine known to be involved in maintaining metabolic homeostasis; however, also capable of inducing cardiac dysfunction. Additionally, IL-18, has been shown to bind to a novel receptor, the Na-Cl Co-transporter (NCC). We hypothesized that NCC mediates IL-18 metabolic and cardiac signaling in mice. Using male C57BL/6J mice, we compared the metabolic and cardiac function changes after at least 8 weeks of high-saturated fat high sugar diet (Western Diet) in NCC knockout (NCCKO), IL-18 knockout (IL-18KO), and wild-type mice. We show that NCCKO mice have significantly increased body weight gain from baseline, no difference in fasting blood glucose, and attenuated cardiac diastolic dysfunction after WD compared to wild-type mice. Collectively, the metabolic and cardiac phenotypes of NCCKO mice resembled that of the IL-18KO mice, indicating that NCC may mediate IL-18 signaling in a mouse model of diet-induced obesity and cardiac dysfunction.
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Dumaresq, Danielle Maia Holanda. "AvaliaÃÃo dos efeitos metabÃlico e oxidativo em cirurgia cardÃaca pediÃtrica: influÃncia da tÃcnica anestÃsica." Universidade Federal do CearÃ, 2006. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=409.

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Instituto Dr. Josà Frota
A cirurgia cardÃaca pediÃtrica freqÃentemente necessita de circulaÃÃo extracorpÃrea (CEC) durante a intervenÃÃo cirÃrgica. A combinaÃÃo de estresse cirÃrgico e CEC evoca uma resposta inflamatÃria sistÃmica multifatorial, com ativaÃÃo das cascatas humoral e celular. Somado à isto, a CEC proporciona perÃodos de isquemia-reperfusÃo, levando à condiÃÃes favorÃveis para formaÃÃo de radicais livres e criando uma situaÃÃo de desequilÃbrio que à denominada de estresse oxidativo. As espÃcies reativas do oxigÃnio (ERO) formadas durante o perÃodo de isquemia-reperfusÃo, estÃo intensamente implicadas na patogÃnese da disfunÃÃo miocÃrdica transitÃria (stunning heart), da necrose miocÃrdica devido à peroxidaÃÃo lipÃdica severa, da disfunÃÃo vascular, da morte celular programada (apoptose) e das disritmias pÃs-isquÃmicas. A influÃncia da tÃcnica anestÃsica sobre a resposta metabÃlica e oxidativa foi avaliada em um estudo envolvendo 20 crianÃas portadoras de doenÃas cardÃacas congÃnitas, distribuÃdas aleatoriamente em dois grupos: GP, o grupo em que foi utilizado anestesia venosa total com propofol e GS, grupo em que foi utilizado anestesia balanceada com sevoflurano. Foram determinadas as concentraÃÃes plasmÃticas das SubstÃncias Reativas do Ãcido TiobarbitÃrico (TBARS), glutationa, lactato e piruvato em trÃs tempos: T0 apÃs cateterizaÃÃo da artÃria radial, T1, 30 minutos apÃs o inÃcio da CEC e T2 ao tÃrmino do procedimento. Para a avaliaÃÃo dos marcadores estre os tempos em cada grupo, foi usado o teste de Friedman. A comparaÃÃo das mÃdias entre os dois grupos foi feita atravÃs do teste de Wilcoxon. Realizou-se tambÃm a correlaÃÃo de Pearson, para avaliar os marcadores entre os grupos. Valores de p < 0,05 foram considerados significantes. As concentraÃÃes de TBARS, glutationa, lactato e piruvato nÃo se alteraram significantemente nos tempos observados (p>0,05, teste de Friedman). Ao se comparar os valores mÃdios dos marcadores entre os grupos, nÃo se encontrou diferenÃa significante (p>0,05, teste de Wilcoxon). O quociente obtido da relaÃÃo lactato e piruvato (L/P) foi maior que 10 nos dois grupos, sem significÃncia estatÃstica quando comparado os dois grupos. Encontrou-se uma correlaÃÃo de pearson moderada para o TBARS, durante T1(r=0,50; p=0,13) e T2(r=0,51;p=0,12). Durante a CEC (T1), encontrou-se uma correlaÃÃo alta entre os grupos para o lactato (r=0,68; p=0,02), piruvato (r=o,75; p=0,01) e relaÃÃo L/P (r=0,83; p=0,003). A comparaÃÃo do uso de duas tÃcnicas anestÃsicas com mecanismos de aÃÃo distintos permite confrontar propriedades protetoras jà bem estabelecidas dos anestÃsicos venosos e inalatÃrios. As tÃcnicas anestÃsicas investigadas neste estudo, apresentaram comportamentos semelhantes, nÃo havendo aumento de substratos do estresse metabÃlico e oxidativo, durante a correÃÃo cirÃrgica de cardiopatias congÃnitas em crianÃas acianÃticas.
Pediatric cardiac surgery often requires cardiopulmonary bypass (CPB) during the surgical intervention. CPB and surgical stress combination evokes a multifatorial systemic inflammatory response with activation of the humoral and cellular cascade. In addition, CPB provides ischemia-reperfusion periods, leading to favorable conditions to free radical production and creating an imbalance, knew as oxidative stress. Reactive Oxygen Species (ROS) formed during the ischemia-reperfusion period are strongly implicated in the pathogenesis of the transitory myocardial dysfunction (stunning heart), myocardial necrosis, programmed cell death (apoptosis), vascular dysfunction and postischemic dysrhythmias. The anesthetic technique influence on the metabolic and oxidative response was evaluated in 20 children with congenital heart disease, randomized in two groups: GP, group which used venous total anesthesia with propofol, and GS, the group which used balanced anesthesia with sevoflurano. Thiobarbituric acid-reactive substance (TBARS), glutatione, lactate and pyruvate plasmatic concentrations were determined in three times: T0, after radial artery canulation, T1, 30 minutes after CPB start and T2, at the end of procedure. The markers evaluation in the several times and in each group, the Friedman test was used. The Wilcoxon test was used to compare the medians between the groups. Pearson correlation was done to evaluate the markers between the groups. Values of p<0.05 were considered statistically significant. The TBARS, gluthatione, lactate and pyruvate concentrations did not change significantly in the observed times (p>0,05, Friedman test). When the markerâs median values was compared between the groups, it wasnât significant (p>0,05, Wilcoxon test). The quotient of the relationship between lactate and pyruvate (L/P) was greater than 10 in both groups, with no difference statistically significant. There was a moderate Pearson correlation for TBARS, in T1 (r=0,50; p=0,13) e T2(r=0,51;p=0,12). During the CPB (T1), there was a high Pearson correlation between the groups for lactate (r=0,68; p=0,02), piruvato (r=0,75; p=0,01) e L/P rate (r=0,83; p=0,003). The comparison of two anesthetic techniques with distinct action mechanisms, allow confronting inhalator and venous anesthetic protecting proprieties. The anesthetic techniques investigated in this study were similar, without metabolic and oxidative stress substrates augment, in congenital heart disease surgical correction of acianotic children
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Murray, Andrew James. "Control of cardiac metabolism and efficiency." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:858cc1f9-7ba0-4999-a1c8-614a950888c2.

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Quigley, Gillian Margaret. "Inflammation of the heart in heart disease." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/inflammation-of-the-heart-in-heart-disease(eae19e58-aeb4-4673-924e-1dbd1c831fec).html.

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Heart failure patients have dysfunction of the cardiac conduction system that contributes to a high burden of arrhythmias including atrial fibrillation and sudden cardiac death. Heart failure has been associated with the inflammatory response, but it is unknown if inflammation is playing a role in the remodelling of the cardiac conduction system in heart failure. Inflammation has been shown to be present in the myocardium from failing hearts and it is known to have detrimental effects on cardiac function, inducing fibrosis, remodelling of ion channels and even arrhythmias. However, the effect of inflammation on the cardiac conduction system has not been investigated. The aims of this study were to determine if there is an increase of pro-inflammatory cytokines and inflammatory cells in the cardiac conduction system in heart failure. In addition, to identify if there is possible inflammation-associated fibrosis and apoptosis in the cardiac conduction system in heart failure. To test these aims, three models of heart failure were used: a rat model of pulmonary arterial hypertension, a rabbit model of congestive heart failure and a rat model of myocardial infarction. In the rat model of pulmonary arterial hypertension there was a bradycardia, a prolongation of the QT interval, and an increase in the atrioventricular and ventricular refractory periods, suggesting electrical remodelling in these animals. The rats with pulmonary arterial hypertension displayed an increase in pro-inflammatory cytokines such as interleukins 1β and TGFβ in the right side of the heart, including the sinoatrial node and right Purkinje fibres of the cardiac conduction system. In addition, in these areas, there was an increase in components of the extracellular matrix, including fibronectin, collagen I and vimentin. Histology revealed regions of non-myocyte nuclei, only in the right ventricle of the rats with pulmonary arterial hypertension. Immunohistochemistry demonstrated patches of CD68 and vimentin expression (markers for macrophages and fibroblasts, respectively) in the right side of the heart in these animals. TUNEL staining also revealed an increase in apoptosis in the right side of the heart. In the rabbit model of congestive heart failure, the region most affected by inflammation was the right atrium, while few changes were measured in the ventricles or cardiac conduction system. Although these results are surprising, it is suggested that the atria could be more sensitive to the physical stretch produced in this model. In the rat model of myocardial infarction, there were regions of non-myocyte nuclei in the border zone. This region also had increases in pro-inflammatory and fibrosis markers. In conclusion, this work has presented the novel finding that there can be inflammation in the cardiac conduction system in heart failure. This could be contributing to the arrhythmias seen in heart failure patients. This could possibly lead the way to anti-inflammatories as a possible novel therapeutic for heart failure patients.
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Books on the topic "Heart disease; Cardiac metabolism"

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František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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Abdel-Aleem, Salah, and James E. Lowe, eds. Cardiac Metabolism in Health and Disease. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5687-9.

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Lopaschuk, Gary D., and Naranjan S. Dhalla, eds. Cardiac Energy Metabolism in Health and Disease. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8.

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Butera, Gianfranco, Massimo Chessa, Andreas Eicken, and John Thomson, eds. Cardiac Catheterization for Congenital Heart Disease. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5681-7.

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Butera, Gianfranco, Massimo Chessa, Andreas Eicken, and John Thomson, eds. Cardiac Catheterization for Congenital Heart Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69856-0.

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Elder, Vicci. Cardiac kids. Dayton, Ohio: Dayton Area Heart and Cancer Assoc., 1994.

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Finley, F. G. Life insurance and cardiac disease. [S.l: s.n., 1985.

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Adolescent cardiac issues. Philadelphia, Pennsylvania: Elsevier, 2014.

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Adebo, Dilachew A., ed. Pediatric Cardiac CT in Congenital Heart Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74822-7.

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Book chapters on the topic "Heart disease; Cardiac metabolism"

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Schaap, Frank G., Ger J. van der Vusse, and Jan F. C. Glatz. "Fatty acid-binding proteins in the heart." In Cardiac Metabolism in Health and Disease, 43–51. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5687-9_4.

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Doroshow, J. H. "Anthracycline-Enhanced Cardiac Oxygen Radical Metabolism." In Oxygen Radicals in the Pathophysiology of Heart Disease, 323–32. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1743-2_21.

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Ralphe, J. Carter, and Thomas D. Scholz. "Cardiac Metabolic Protection for the Newborn Heart." In Cardiac Energy Metabolism in Health and Disease, 265–76. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_17.

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Guarini, Giacinta, Alda Huqi, and Mario Marzilli. "Metabolic Therapy for the Ischemic Heart." In Cardiac Energy Metabolism in Health and Disease, 237–48. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_15.

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An, Ding, Min-Suk Kim, and Brian Rodrigues. "AMPK Regulation of Cardiac Metabolism in Heart Disease." In Signal Transduction in the Cardiovascular System in Health and Disease, 397–410. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09552-3_21.

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Taegtmeyer, Heinrich. "A Primer on Carbohydrate Metabolism in the Heart." In Cardiac Energy Metabolism in Health and Disease, 3–14. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_1.

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Doenst, Torsten, Patrick H. Guthrie, and Heinrich Taegtmeyer. "Ischemic preconditioning in rat heart: No correlation between glycogen content and return of function." In Cardiac Metabolism in Health and Disease, 153–61. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5687-9_17.

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Park, Edwards A., and George A. Cook. "Differential regulation in the heart of mitochondrial carnitine palmitoyltransferase-I muscle and liver isoforms." In Cardiac Metabolism in Health and Disease, 27–32. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5687-9_2.

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Hacker, Timothy A., Britta Renstrom, Stephen H. Nellis, and A. James Liedtke. "The role of glucose metabolism in a pig heart model of short-term hibernation." In Cardiac Metabolism in Health and Disease, 75–83. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5687-9_8.

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van der Vusse, Ger J., and Monique J. M. de Groot. "Interrelationship between lactate and cardiac fatty acid metabolism." In Lipid Metabolism in the Healthy and Disease Heart, 11–17. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3514-0_2.

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Conference papers on the topic "Heart disease; Cardiac metabolism"

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Krželj, Vjekoslav, and Ivana Čulo Čagalj. "INHERITED METABOLIC DISORDERS AND HEART DISEASES." In Symposium with International Participation HEART AND … Akademija nauka i umjetnosti Bosne i Hercegovine, 2019. http://dx.doi.org/10.5644/pi2019.181.02.

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Inherited metabolic disorders can cause heart diseases, cardiomyopathy in particular, as well as cardiac arrhythmias, valvular and coronary diseases. More than 40 different inherited metabolic disorders can provoke cardiomyopathy, including lysosomal storage disorders, fatty acid oxidation defects, organic acidemias, amino acidopathies, glycogen storage diseases, congenital disorders of glycosylation as well as peroxisomal and mitochondrial disorders. If identified and diagnosed on time, some of congenital metabolic diseases could be successfully treated. It is important to assume them in cases when heart diseases are etiologically undefined. Rapid technological development has made it easier to establish the diagnosis of these diseases. This article will focus on common inherited metabolic disorders that cause heart diseases, as well as on diseases that might be possible to treat.
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Sodhi, M., R. Brunken, P. Tchou, and DA Culver. "Metabolism-Perfusion Imaging To Predict Disease Activity in Cardiac Sarcoidosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2276.

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Miller, JJ, YB Ding, D. Ball, AZ Lau, and DJ Tyler. "P9 Hyperpolarised ketone body metabolism in the rat heart." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.14.

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Wieshammer, Siegfried, Jens Dreyhaupt, and Beate Basler. "Theophylline Reduces Cardiac Stress In Patients With Lung Disease And Concomitant Heart Disease." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4474.

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Hundertmark, MJ, CT Rodgers, O. Rider, S. Neubauer, and M. Mahmod. "P21 Cardiac metabolism in patients with heart failure with mid-range ejection fraction." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.26.

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Kumar, Pramendra, and Vijay Kumar Sharma. "Cardiac Signals Based Methods For Recognizing Heart Disease: A Review." In 2021 Third International Conference on Intelligent Communication Technologies and Virtual Mobile Networks (ICICV). IEEE, 2021. http://dx.doi.org/10.1109/icicv50876.2021.9388448.

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Hendradi, Rimuljo, Achmad Arifin, Mauridhi Hery Purnomo, and Suhendar Gunawan. "Exploration of cardiac valvular hemodynamics by heart sound analysis of hypertensive cardiac disease background patients." In 2012 IEEE International Conference on Computational Intelligence and Cybernetics (CyberneticsCom). IEEE, 2012. http://dx.doi.org/10.1109/cyberneticscom.2012.6381637.

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Baross, Stephanie, Simon Williams, Kathryn Hentges, Andrew Sharrocks, and Bernard Keavney. "BS54 Variation in cardiac long non-coding rnas in congenital heart disease." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.215.

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Kinsella, C., SA Thorne, PF Clift, LE Hudsmith, S. Bowater, R. Vasallo Peraza, JE Perez Torga, and PA Roman Rubio. "30 Managing delivery in women with congenital heart disease: results from the cuban national programme for pregnancy and heart disease." In British Congenital Cardiac Association, Annual meeting abstracts 9–10 November 2017, Great Ormond Street Institute of Child Health, London, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2017-bcca.30.

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Yuliang, Hu, Qiao Junxuan, Wang Haibin, and Wei Xiubo. "Quantized analysis for heart valve disease based on cardiac sound characteristic waveform method." In 2010 2nd International Conference on Signal Processing Systems (ICSPS). IEEE, 2010. http://dx.doi.org/10.1109/icsps.2010.5555596.

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Reports on the topic "Heart disease; Cardiac metabolism"

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Li, Xing-xing, Zong-jing Fan, Jie Cui, Rui Zhuang, Rong-peng Liu, Quan Lin, and Yang Wu. Cardiac rehabilitation of Baduanjin exercise in coronary heart disease after PCI: a protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0065.

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Wang, Cuihua, Gang Liu, Jun Xing, Yahui Wang, Baoli Zhao, and Mingqi Zheng. The effects of high-intensity interval training vs. moderate-intensity continuous training on exercise tolerance and prognosis in Heart Failure and Coronary Artery Disease Cardiac: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0112.

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Treadwell, Jonathan R., James T. Reston, Benjamin Rouse, Joann Fontanarosa, Neha Patel, and Nikhil K. Mull. Automated-Entry Patient-Generated Health Data for Chronic Conditions: The Evidence on Health Outcomes. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepctb38.

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Background. Automated-entry consumer devices that collect and transmit patient-generated health data (PGHD) are being evaluated as potential tools to aid in the management of chronic diseases. The need exists to evaluate the evidence regarding consumer PGHD technologies, particularly for devices that have not gone through Food and Drug Administration evaluation. Purpose. To summarize the research related to automated-entry consumer health technologies that provide PGHD for the prevention or management of 11 chronic diseases. Methods. The project scope was determined through discussions with Key Informants. We searched MEDLINE and EMBASE (via EMBASE.com), In-Process MEDLINE and PubMed unique content (via PubMed.gov), and the Cochrane Database of Systematic Reviews for systematic reviews or controlled trials. We also searched ClinicalTrials.gov for ongoing studies. We assessed risk of bias and extracted data on health outcomes, surrogate outcomes, usability, sustainability, cost-effectiveness outcomes (quantifying the tradeoffs between health effects and cost), process outcomes, and other characteristics related to PGHD technologies. For isolated effects on health outcomes, we classified the results in one of four categories: (1) likely no effect, (2) unclear, (3) possible positive effect, or (4) likely positive effect. When we categorized the data as “unclear” based solely on health outcomes, we then examined and classified surrogate outcomes for that particular clinical condition. Findings. We identified 114 unique studies that met inclusion criteria. The largest number of studies addressed patients with hypertension (51 studies) and obesity (43 studies). Eighty-four trials used a single PGHD device, 23 used 2 PGHD devices, and the other 7 used 3 or more PGHD devices. Pedometers, blood pressure (BP) monitors, and scales were commonly used in the same studies. Overall, we found a “possible positive effect” of PGHD interventions on health outcomes for coronary artery disease, heart failure, and asthma. For obesity, we rated the health outcomes as unclear, and the surrogate outcomes (body mass index/weight) as likely no effect. For hypertension, we rated the health outcomes as unclear, and the surrogate outcomes (systolic BP/diastolic BP) as possible positive effect. For cardiac arrhythmias or conduction abnormalities we rated the health outcomes as unclear and the surrogate outcome (time to arrhythmia detection) as likely positive effect. The findings were “unclear” regarding PGHD interventions for diabetes prevention, sleep apnea, stroke, Parkinson’s disease, and chronic obstructive pulmonary disease. Most studies did not report harms related to PGHD interventions; the relatively few harms reported were minor and transient, with event rates usually comparable to harms in the control groups. Few studies reported cost-effectiveness analyses, and only for PGHD interventions for hypertension, coronary artery disease, and chronic obstructive pulmonary disease; the findings were variable across different chronic conditions and devices. Patient adherence to PGHD interventions was highly variable across studies, but patient acceptance/satisfaction and usability was generally fair to good. However, device engineers independently evaluated consumer wearable and handheld BP monitors and considered the user experience to be poor, while their assessment of smartphone-based electrocardiogram monitors found the user experience to be good. Student volunteers involved in device usability testing of the Weight Watchers Online app found it well-designed and relatively easy to use. Implications. Multiple randomized controlled trials (RCTs) have evaluated some PGHD technologies (e.g., pedometers, scales, BP monitors), particularly for obesity and hypertension, but health outcomes were generally underreported. We found evidence suggesting a possible positive effect of PGHD interventions on health outcomes for four chronic conditions. Lack of reporting of health outcomes and insufficient statistical power to assess these outcomes were the main reasons for “unclear” ratings. The majority of studies on PGHD technologies still focus on non-health-related outcomes. Future RCTs should focus on measurement of health outcomes. Furthermore, future RCTs should be designed to isolate the effect of the PGHD intervention from other components in a multicomponent intervention.
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District chief suffers sudden cardiac death at home after experiencing symptoms consistent with heart disease at his station - Illinois. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, March 2005. http://dx.doi.org/10.26616/nioshfffacef200421.

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