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Books on the topic 'Heart disease; Cardiac metabolism'

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

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1

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

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2

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

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3

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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4

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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5

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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6

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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7

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

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8

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

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9

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

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10

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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11

Lerman, Bruce B. Topics in arrhythmias and ischemic heart disease. New York: Demos Medical Pub., 2010.

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12

Butera, Gianfranco, Massimo Chessa, Andreas Eicken, and John D. Thomson, eds. Atlas of Cardiac Catheterization for Congenital Heart Disease. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-72443-0.

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13

Heart disease. Santa Barbara, Calif: Greenwood, an imprint of ABC-CLIO, 2012.

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14

Atlas of congenital cardiac surgery. New York: Churchill Livingstone, 1989.

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15

Feigenbaum, Ernest. Cardiac rehabilitation services. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Center for Health Services Research and Health Care Technology Assessment, 1987.

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16

Care of the intervention cardiac patient. Chichester, West Sussex, England: Wiley, 2007.

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17

van der Vusse, Ger J., and Hans Stam, eds. Lipid Metabolism in the Healthy and Disease Heart. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3514-0.

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18

Cardiac catheterization in congenital heart disease: Pediatric and adult. Malden, Mass: Blackwell Futura, 2005.

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19

Saremi, Farhood, ed. Cardiac CT and MR for Adult Congenital Heart Disease. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8875-0.

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20

Mullins, Charles E., ed. Cardiac Catheterization in Congenital Heart Disease: Pediatric and Adult. Oxford, UK: Blackwell Publishing, 2005. http://dx.doi.org/10.1002/9780470986967.

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21

Chronic cardiac disease: Optimizing therapeutic efficacy in heart failure. London: Whurr, 2002.

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22

Salah, Abdel-aleem, and Lowe James E, eds. Cardiac metabolism in health and disease. Dordrecht: Kluwer Academic Publishers, 1998.

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23

Dhalla, Naranjan S., and Ph.D. Gary D. Lopaschuk. Cardiac Energy Metabolism in Health and Disease. Springer, 2014.

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24

Dhalla, Naranjan S., and Gary D. Lopaschuk. Cardiac Energy Metabolism in Health and Disease. Springer, 2014.

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25

Dhalla, Naranjan S., and Gary D. Lopaschuk. Cardiac Energy Metabolism in Health and Disease. Springer, 2016.

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26

Willis, Monte S., and Cam Patterson. Translational Cardiology: Molecular Basis of Cardiac Metabolism, Cardiac Remodeling, Translational Therapies and Imaging Techniques. Humana Press, 2012.

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27

Willis, Monte S., and Cam Patterson. Translational Cardiology: Molecular Basis of Cardiac Metabolism, Cardiac Remodeling, Translational Therapies and Imaging Techniques. Humana Press, 2014.

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28

Elliott, Perry, and Giuseppe Limongelli. Cardiac Aspects of INHERITED METABOLIC DISEASES. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0070.

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More than 40 inherited metabolic disorders cause heart disease, including fatty acid oxidation defects, glycogen storage disorders, lysosomal storage disorders, peroxisomal diseases, mitochondrial cytopathies, organic acidemias, aminoacidopathies, and congenital disorders of glycosylation. The pattern and severity of cardiac involvement varies between disorders but includes congenital heart diseases, heart muscle diseases, arrhythmias and sudden death, and heart failure. The majority of IMDs are multisystem diseases, but in a few cases cardiac disease is the predominant clinical feature and the main determinant of prognosis. For an increasing number of IEMs there are specific therapies designed to treat or ameliorate the effects of the underlying metabolic defect. In some cases, these therapies have an important effect on the progression of cardiac disease.
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29

Bentham, James R. The genetics of congenital heart disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0022.

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Congenital heart disease (CHD) is defined as a structural cardiac malformation resulting from an abnormality of development; 8% of CHD is inherited in a Mendelian fashion and 12% results from chromosomal imbalance. Recurrence risk and new research suggest that even the remaining 80% of patients without an identifiable familial or syndromic basis for disease may have an identifiable genetic cause. The potential to understand these mechanisms is increasing with the advent of new sequencing techniques which have identified multiple or single rare variants and/or copy number variants clustering in cardiac developmental genes as well as common variants that may also contribute to disease, for example by altering metabolic pathways. Work in model organisms such as mouse and zebrafish has been pivotal in identifying CHD candidate genes. Future challenges involve translating the discoveries made in mouse models to human CHD genetics and manipulating potentially protective pathways to prevent disease.
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30

(Editor), Bohuslav Ost'ádal, and Frantisek Kolár (Editor), eds. Cardiac Ischemia: - From Injury to Protection (Basic Science for the Cardiologist). Springer, 1999.

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31

1945-, Hori M., Janicki Joseph S, and Maruyama Yukio 1941-, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.

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32

1941-, Maruyama Yukio, Hori M. 1945-, and Janicki Joseph S, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.

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33

Taillefer, Raymond, and Frans J. Th Wackers. Kinetics of Conventional and New Cardiac Radiotracers. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0004.

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The kinetics of radiotracers, that is the mode of uptake, retention and release from the myocardium, are relevant for designing and implementing optimized nuclear cardiac imaging protocols. This chapter addresses the kinetics of commonly used radiotracers for imaging myocardial perfusion, sympathetic neuronal function and cardiac metabolism, both with SPECT and PET cardiac imaging. The optimal timing of imaging after injection either at stress or at rest is determined by rate of uptake in the heart and adjacent organs, as well as the residence time of radiotracers within the myocytes. The efficiency of myocardial extraction over a wide range myocardial blood flows is relevant for reliable detection of obstructive coronary artery disease and absolute quantification of regional myocardial blood flow. For each cardiac imaging agent the cellular mechanism of uptake and its release or retention are discussed with an emphasis on the clinical impact of these parameters.
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34

Bohuslav, Ost̓ádal, Dhalla Naranjan S, Council on Cardiac Metabolism, and International Union of Physiological Sciences. Regional Meeting, eds. Heart function in health and disease: Proceedings of the cardiovascular program sponsored by the Council of Cardiac Metabolism of the International Society and Federation of Cardiology during the Regional Meeting of the International Union of Physiological Sciences, Prague, Czechoslovakia, June 30 - July 5, 1991. Boston: Kluwer Academic Publishers, 1993.

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35

London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.

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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudden death are the most frequent causes of death in ESRD. Cardiomyopathy of overload with development of left ventricular hypertrophy and fibrosis are the most characteristic alterations and major determinants of prognosis. Left ventricular hypertrophy may result in systolic and/or diastolic dysfunction and is a risk factor for arrhythmias, sudden death, heart failure, and myocardial ischaemia. Arterial disease, whether due to atherosclerosis or arteriosclerosis (or both), represents a major contributory factor to the cardiovascular complications. Arterial disease may result in ischaemic complications (ischaemic heart disease, peripheral artery diseases) or arterial stiffening with direct consequences on left ventricular afterload, decreased coronary perfusion, and microvascular abnormalities (inward remodelling and microvessel rarefaction).
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36

Inherited Cardiac Disease. Oxford University Press, USA, 2011.

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37

Kumar, Dhavendra, Pier D. Lambiase, and Perry Elliott. Inherited Cardiac Disease. Oxford University Press, 2020.

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38

Doenst, Torsten, and Michael Schwarzer. Scientist's Guide to Cardiac Metabolism. Elsevier Science & Technology Books, 2015.

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39

Congenital cardiac disease. Philadelphia: Lea & Febiger, 1996.

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40

Cardiac Interventional Procedures Heart Disease. Tim Peters & Co Inc, 1994.

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41

Llarich, Kyle W. Cardiac Examination, Valvular Heart Disease, and Congenital Heart Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0042.

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Despite tremendous technologic advances in medical testing and imaging, physicians must be able to assess patients accurately at the bedside; this assessment allows appropriate, cost-effective, and efficient ordering of tests. Part I of this chapter outlines the salient features of a thorough physical examination, cardiac imaging techniques, and valvular and congenital heart disease. A thorough physical examination includes assessment of jugular venous pressure, arterial pulses, apical impulses, additional cardiac palpitations, and appropriate imaging techniques. Cardiac imaging techniques include contrast angiography, echocardiography, radionuclide imaging, magnetic resonance imaging, electron beam computed tomography and positron emission tomography. Different types of valvular and congenital heart disease are examined.
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42

Abbott, Maude E. Atlas of Congenital Cardiac Disease. McGill-Queen's University Press, 2006.

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43

A, Goldstein Richard, and Dae Michael W. 1950-, eds. Cardiac PET imaging: Congenital heart disease. Reston, Va: Society of Nuclear Medicine, 1998.

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44

A, Fogel Mark, ed. Cardiac MR in congenital heart disease. Chichester, West Sussex, UK: Blackwell Pub., 2009.

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45

M, Dunn Jeffrey, ed. Cardiac valve disease in children. New York, N.Y: Elsevier, 1988.

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46

T, Basson Craig, and Lerman Bruce B, eds. Ischemic heart disease and arrhythmias. New York: Demos Medical Pub., 2010.

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47

Klein, Lloyd W., and James E. Calvin. Resource Utilization in Cardiac Disease. Springer, 2012.

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48

W, Klein Lloyd, and Calvin James E, eds. Resource utilization in cardiac disease. Boston: Klwer Academic Publishers, 1999.

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49

LeWinter, Martin M., Hiroyuki Suga, and Matthew W. Watkins. Cardiac Energetics: From Emax to Pressure-Volume Area. Springer, 2013.

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50

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
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