Nobuakira Takeda - Böcker

This volume brings together leading basic scientists and clinicians, presenting new approaches to the complex problem of heart failure, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. This book is intended for clinical and experimental cardiologists.

Whenever the heart is challenged with an increased workload for a prolonged period, it responds by increasing its muscle mass - a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situations such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss) and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. This text compiles state-of-the-art presentations in the area of molecular biology, cellular physiology and signal transduction in cardiac hypertrophy and heart failure to help in the formulation of new concepts and approaches for stimulating research. The book contains two sections: "Mechanisms of Cardiac Hypertrophy", and "Cardiac Failure in the Hypertrophied Heart". It is hoped that both students and scientists, as well as clinical and experimental cardiologists, will find this book useful in understanding the molecular and cellular events underlying the development of cardiac hypertrophy and the transition from cardiac hypertrophy to heart failure.

The last three decades of the 20th century saw impressive progress in the field of pathogenesis, prevention and therapy of ischemic heart disease which resulted in a marked decline in mortality in the Western World. However, the incidence of this devastating disease is on the rise in developing countries. This volume is organized into two sections: pathophysiologic mechanisms of ischemia-reperfusion injury; and preconditioning and protection of ischemia-reperfusion injury it contains late-1990s information concerning the current concepts of ischemia-reperfusion injury, the sequence of events resulting in the loss of contractile dysfunction, and mechanisms of cardioprotection by several drugs as well as the role of ischemic preconditioning in attenuating problems associated with ischemia-reperfusion injury.

Evidence suggests that the ischemic preconditioning response is a multi-factorial process consisting of an initial early trigger, an intermediate mediator, and an end effector. Each of these steps in is now its own intense area of investigation. The need to render the heart ischemic for a brief period to invoke the preconditioning response is currently the major factor limiting clinical application of this powerful cardioprotective strategy. Research efforts have utilized brief exposures to pharmacological agents, in lieu of a brief preconditioning ischemia, to trigger/mimic the ischemic preconditioning-induced response. The World Heart Congress held in Winnipeg in July 2001 provided a forum for the presentation of insights into the basic mechanisms of ischemia and reperfusion injury, as well as novel strategies to protect the heart from cell death, ventricular arrhythmias, and contractile dysfunction. Many pioneers in the fields of ischemia-reperfusion injury and preconditioning-induced protection presented there and the chapters in this book represent selected papers from these symposia.

Pathophysiology of Heart Failure brings together leading basic scientists and clinicians, presenting new approaches to this complex problem, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. Audience: Clinical and experimental cardiologists will find the book a helpful source of ideas and inspiration.

Current evidence suggests that the ischemic preconditioning response is a multi-factorial process consisting of an initial early trigger, an intermediate mediator, and an end effector.

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa­ tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under­ the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid­ linked signal transduction pathways are activated in some specific manner depend­ ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.