Ian M.C. Dixon - Böcker

This work is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the book is a continuous discussion of subcellular mechanisms of heart failure and its treatment, the presentation has been divided into three sections: the opening section on the subcellular basis of heart failure includes discussions of cytokines, signal transduction, metabolism, extracellular matrix, organ level changes and newer approaches to understanding the pathogenesis of heart failure. The second section focuses on the pathophysiological aspects of cardiomyopathies and their treatment. In the final section, medical, surgical and pharmacological approaches to the treatment of heart failure are discussed in clinical and animal laboratory settings.

The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure. Over the intervening decades, a complete characterization of the renin-angiotensin system (RAS) has been achieved, and our understanding of its biochemistry and physiology has led to the directed development of agents such as ACE inhibitors and receptor antagonists capable of controlling hypertension. More recently, it was shown that angiotensin II is secreted within certain tissues, and that these tissue-specific systems operate independently of the systemic RAS. The novel concept that angiotensin II regulates a number of cardiovascular processes that are unrelated to blood pressure has renewed the interest of both basic and clinical scientists in angiotensin II. The association between angiotensin II and cardiac growth, in particular, has indicated that therapies in use for hypertension may have direct application to the treatment of heart failure. This book focuses on developments in the molecular biology, cellular physiology and structure-function relationships of angiotensin II and its receptors.In addition, this volume covers the therapeutic uses for angiotensin receptor antagonists and considers their potential future applications. This volume aims to be a valuable resource for scientists, practising clinicians and students who are attempting to extend their knowledge in the field of hypertension and heart failure, and who are devoted to improving cardiovascular health.

The importance of the developmental approach for experimental and clinical cardiology is indisputable. Clinical-epidemiological studies have clearly shown that the risk factors of serious cardiovascular diseases, such as atherosclerosis and ischemic heart disease, are already present during the early phases of ontogenetic development. Furthermore, congenital cardiovascular malformations remain the single largest cause of infant mortality from congenital defects in industrial countries. It is therefore not surprising that the interest of theoretical and clinical cardiologists in the developmental approach keeps increasing. Advances in molecular biology accelerated this trend substantially. This book is based on contributions presented at the international symposium The Developing Heart in Prague in May 2000. It should stimulate the curiosity of cardiovascular scientists in gaining insight into the mechanisms of normal and pathological development.

The focus of this special issue of "Molecular and Cellular Biochemistry" is the underlying mechanisms that regulate cardiac growth. The new information provided in the issue can be utilized to design new treatment modalities that will reduce the incidence of cardiac failure, which will improve quality of life in patients with chronic heart disease.

The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth.

The World Heart Congress with a focus on "Frontiers in Cardiovascular Health" held in Winnipeg during July 6-11, 2001, made a unique attempt to bring these specialists together to brainstorm and map out the course of action for cardiovascular research and health in the next century.

Mechanisms of Heart Failure is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the entire book is one continuous discussion of subcellular mechanisms of heart failure and its treatment, the presentation has been divided into three sections: the opening section on the subcellular basis of heart failure includes discussions of cytokines, signal transduction, metabolism, extracellular matrix, organ level changes and newer approaches to understanding the pathogenesis of heart failure. The second section focuses on the pathophysiological aspects of cardiomyopathies and their treatment. In the final section, medical, surgical and pharmacological approaches to the treatment of heart failure are discussed in clinical and animal laboratory settings.

The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure.

The unique biology of cardiac fibroblasts and related cells, such as cardiac myofibroblasts and valvular interstitial cells, distinguish them from other fibroblastic cells, a concept that is only beginning to be widely appreciated. Further, the natural signals that stimulate and inhibit cardiac fibrosis within these cells are not well understood. This volume compiles articles that address the molecular mechanisms that control the synthesis and secretion of the cardiac ECM. The book showcases chapters that highlight discussion of role of Transforming Growth Factor β (TGFβ), an important fibrogenic cytokine and its downstream effectors SMAD in many cardiac diseases. Further, the contributions highlight information to discuss endogenous inhibitors of cardiac fibrosis, as well as advances in tissue engineering specific to matrix in the heart. Finally, discussions of unifying mechanisms of matrix remodeling in valves and myocardium are presented.The mechanisms involved in the stimulation of cardiac fibrosis are not fully understood. In most cases the marginal attenuation of cardiac fibrosis as a result of a given therapy is a beneficial side-effect linked to other primary effects on other cells, especially cardiomyocytes. Very few drugs or agents are known to affect the function and dysfunction of cardiac fibroblasts and myofibroblasts alone. The book helps to translate the information gathered within to allow us to alter the course of fibrogenic events that are typical of cardiac fibrosis, and thereby reduce their burden on the patient and on society itself.