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The heart has a very high energy demand but very little energy reserves. In order to sustain contractile function, the heart has to continually produce a large amount of ATP. The heart utilizes free fatty acids mainly and carbohydrates to some extent as substrates for making energy and any change in this energy supply can seriously compromise cardiac function. It has emerged that alterations in cardiac energy metabolism are a major contributor to the development of a number of different forms of heart disease. It is also now known that optimizing energy metabolism in the heart is a viable and important approach to treating various forms of heart disease. Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism at molecular, transcriptional and physiological levels. It also describes how alterations in energy metabolism contribute to the development of heart dysfunction and how optimization of energy metabolism can be used to treat heart disease. The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of mitochondrial oxidative metabolism on cardiac energetics. The treatment of heart disease by optimizing energy metabolism is also discussed, which includes increasing overall energy production as well as increasing the efficiency of energy production and switching energy substrate preference of the heart. This book will be a valuable source of information to graduate students, postdoctoral fellows, and investigators in the field of experimental cardiology as well as biochemists, physiologists, pharmacologists, cardiologists, cardiovascular surgeons and other health professionals.
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The Scientists Guide to Cardiac Metabolism combines the basic concepts of substrate metabolism, regulation, and interaction within the cell and the organism to provide a comprehensive introduction into the basics of cardiac metabolism. This important reference is the perfect tool for newcomers in cardiac metabolism, providing a basic understanding of the metabolic processes and enabling the newcomer to immediately communicate with the expert as substrate/energy metabolism becomes part of projects. The book is written by established experts in the field, bringing together all the concepts of cardiac metabolism, its regulation, and the impact of disease. Provides a quick and comprehensive introduction into cardiac metabolism Contains an integrated view on cardiac metabolism and its interrelation in metabolism with other organs Presents insights into substrate metabolism in relation to intracellular organization and structure as well as whole organ function Includes historical perspectives that reference important investigators that have contributed to the development of the field
During the last years the understanding for the aetiology of cardiomyopathies could be greatly improved. A great deal of information has accumulated in the field of inherited metabolic diseases, which provides a new basis for our understanding of many heart muscle problems and their corresponding clinical disease entities. This book is meant to give the reader a comprehensive overview of the cardiological manifestations of inborn errors of metabolism. Latest information, such as cardiomyopathy in Fabry disease or in patients with CDG-syndrome is included. It should be helpful, not only to cardiologists, paediatricians, internists and general practicioners, but also to all those interested in a better understanding of the metabolic basis of clinical disease entities.
ATP plays a central role in the two leading causes of cardiac morbidity and mortality in the western world: ischemia and heart failure. We are in our infancy applying what is known about biology and chemistry of ATP toward developing effective therapies for these diseases. In this volume, the current understanding of the chemistry and biology of ATP specifically in the cardiomyocyte is presented. New insights into ATP have been gleaned using biophysical techniques allowing dynamic measurement of chemical events in the intact beating heart and using new animal models in which cardiac proteins are either over expressed, deleted or harbor specific mutations. This book provides a summary of the basic understanding and includes illustrations of why ATP and the Heart is important to both the clinician and scientist.
Heart failure continues to be a major public health problem in the United States with close to half a million new cases diagnosed each year. Moreover, deaths from heart failure are on the increase, in part because of advances in the treatment of other fatal diseases, and in part from the prevalence of lifestyles indifferent to the risk factors for heart disease. This is not to say that no progress has been made in the treatment of heart failure. While for many years treatment was confined to the management of the symptoms, in recent years with the advent of ACE inhibitor and ß blacker therapies, real improvements in cardiac function and life expectancy have been achieved (Volume 4B, Leier). On a more basic level, enormous advances have been made in describing many of the changes in structure and function of the heart and the parallel neurohumoral and circulatory adaptations that occur during the onset of failure. These advances have been made not only by using various animal models of heart failure, but also using fresh failing human heart tissue, which has become readily available for experimental investigation since the advent of cardiac transplantation.Understanding the significance of many of these changes that occur during the transition to failure and the role they play in the etiology of failure is, however, a much more difficult task. These are exciting times in heart failure research. It is as though many of the pieces of the jigsaw puzzle are available but the puzzle has yet to be assembled. The objective of these volumes is to bring together some advances that have been made in recent years in defining one aspect of the failing heart, that is, the role of altered metabolism, in order to facilitate assembly of the puzzle.
A board-certified cardiologist discusses the importance of energy metabolism on cardiovascular health and the positive impact three energy-supplying nutrients--CoQ10, Carnitine, and Ribose--have on the cardiovascular system.
This book presents a multidisciplinary approach to cardiac mechanotransduction. The chapters depict the many faces of the topic, from membrane and ion channel level to mechanics, biochemical signaling and regulation via hormone systems. Cardiac Mechanotransduction is of interest to basic life sciences, like physiology, biochemistry and pharmacology, but also to clinicians working with heart-related problems, such as cardiologists and internists.
Heart failure is a serious cardiovascular disease that develops following a variety of insults to the heart including hypertrophy and myocardial infarction. While it is clear that heart failure is associated with changes in cardiac energy metabolism, it remains unclear if, and how, such changes might contribute to left ventricular (LV) contractile dysfunction. Two distinct hypotheses have been advanced to link changes in energy metabolism with heart failure: 1) there is a state of energetic crisis / starvation, where rates of energy metabolism decrease and thereby cause LV failure, or 2) there is inefficiency in energy utilization where more energy is required to produce external work. Inefficiency may be due to mismatched rates of glycolysis and glucose oxidation that leads to intracellular proton accumulation resulting in Na+ and Ca2+ overload. Recently, drug-induced modulation of rates of carbohydrate and fat metabolism has been proposed as a new approach for the treatment of LV dysfunction and heart failure. Such metabolic modulation can also be achieved experimentally by the use of genetically-modified experimental animals. This thesis compared the metabolic profile of remodeled post-infarction mouse hearts with normal hearts, studied the response of these hearts to ex vivo ischemia reperfusion (IR) and the ability of metabolic modulation to limit the deterioration of metabolic efficiency and LV dysfunction following myocardial infarction. Using coronary artery ligation, we created a mouse model of post-infarction remodeled heart failure that we verified using in vivo echocardiographic examination. Using ex vivo heart perfusion in the isolated working mode, we provided evidence that CAL hearts are metabolically inefficient rather than energy starved and that mismatched glucose metabolism is a possible contributor to metabolic inefficiency. Using malonyl CoA decarboxylase deficient (MCD-KO) mice that are known to have better matching of glucose metabolism, we confirmed that this metabolic intervention improved glucose matching, metabolic efficiency and limited functional deterioration in CAL hearts. We also studied the response of CAL hearts to ex vivo IR. We showed that CAL hearts have better functional recovery and limited functional deterioration following IR in comparison to SHAM hearts. This was associated with reduced ischemic glycogenolysis, lack of acceleration in fatty acid oxidation during reperfusion and increased triacylglycerol accumulation in reperfused CAL hearts. We provided evidence that mitochondrial mass, Ca2+ handling proteins and AMPK activity are unchanged and are unlikely to contribute to the observed response of CAL hearts to IR. This thesis also studied the potential for further protection of CAL hearts after IR via pharmacologic improvement of the match of glucose oxidation using dichloroacetate (DCA). We showed that in presence of lactate, DCA did not stimulate glucose oxidation, improve functional recovery or improve the match of glucose metabolism. We also showed that in absence of lactate, DCA was able to stimulate glucose oxidation but this was not enough to improve the matching of glucose metabolism. This thesis also discussed differences between mouse and rat heart metabolism that may explain the lack of response to DCA in mouse hearts. Similarly, we studied the possible improvement of metabolic efficiency in CAL hearts via acute ex vivo MCD inhibition but this acute intervention was not sufficient to produce benefit.