The Cardiomyopathic Heart [antikvár]

Preface Since the coinage of the term cardiomyopathy by Brigden in 1957, investigative cardiologists and pathologists have been classifying all sorts of cardiac diseases in this category, with the exception of coronary artery disease caused by obstruction of coronary vessels. In spite of the confusion regarding the usage of terminology, cardiomyopathies are generally divided into two types—primary cardiomyopathies and secondary cardiomyopathies. Primary cardiomyopathies include diseases affecting the myocardium alone by a process of unknown etiology; secondary cardiomyopathies include diseases of unusual pathogenesis in which the heart is involved in a generalized process underlying the disease. The large number of diseases associated with cardiomyopathy is impressive, so perhaps it is appropriate to use this terminology in a broad sense of the definition. Some of the commonly used terms in this area include congestive cardiomyopathy, hypertrophic cardiomyopathy, dilated cardiomyopathy, genetic cardiomyopathy, ischemic cardiomyopathy, alcoholic cardiomyopathy, diabetic cardiomyopathy, metabolic cardiomyopathy, infective cardiomyopathy, viral cardiomyopathy, catecholamine cardiomyopathy, and adria-mycin cardiomyopathy. Regardless of the pathogenetic factors leading to the development of cardiomyopathy, it is becoming clear that a derangement of cardiac structure and metabolism occurs in cardiomyopathy, and this is usually associated with impaired heart function. Furthermore, hypertrophy of the myocardium is frequently associated with the process of cardiomyopathy. Because of the difficulties in assessing the cellular, metabolic, and molecular mechanisms involved in dysfunction of cardiomyopathic hearts in humans, a wide variety of experimental animal models have been developed. The exact mechanisms leading to the development of heart dysfunction in any experimental model of cardiomyopathys are not clear; however, imbalance of hormonal pattern has been commonly observed. The occurrence of intracellular Ca^ overload is routinely suggested to explain the development of cellular damage and contractile failure in cardiomyopathic hearts. Over the past 30 years much has been written on subcellular and metabolic alterations in different types of cardiomyopathic hearts. It is now timely to examine the literature closely if we are to improve our knowledge concerning the pathophysiology of heart dysfunction in cardiomyopathies. The symposium "Cellular Abnormalities Associated with Cardiomyopathies in Animals," held in Tokyo in May 1992, organized by the Aoto Hospital of the Jikei University under the direction of Professor Makoto Nagano, provided an excellent forum for a meeting of experimental cardiologists and basic scientists to discuss problems related to heart dysfunction in cardiomyopathies. Since cardiomyopathic hamsters have been widely used as an experimental model of heart disease. Part I of this book is devoted to hamster cardiomyopathy. The xxvii