This book bridges the gap between fundamental and translational research in the area of heart disease. It describes a multidisciplinary approach, and demonstrates biochemical mechanisms associated with dysregulation of redox signaling, which leads heart disease. Presenting recent studies on improved forms of ROS scavenging enzymes; specific inhibitors for different ROS generating enzymes; and oxidant induced signaling pathways and their antagonists that allow subtle modulation of redox signaling, it also discusses the spatial and temporal aspects of oxidative stress in the cardiovascular system, which are of vital importance in developing better strategies for treating heart disease. Each chapter offers researchers valuable insights into identifying targets for drug development for different types of heart disease.

One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.

This book aims to provide a comprehensive review of the most up-to-date knowledge of the sources and molecular mechanisms of oxidative stress, and its role in disease and cancer. It also focuses on the novel agents and methods that can be employed to prevent oxidative stress and associated diseases.The authors first review the most recent data on the basic mechanisms of oxidative stress. The second section discusses oxidative stress leading to several diseases and cancers, and in the third section, the strategies employed in the prevention and treatment of oxidative stress-related diseases are discussed.

This book aims to clarify the potential association between frailty and cardiovascular disease in older people. Covering the biological as well as the clinical point of view, it allows researchers and clinicians to discover the significance of this topic. The contributions cover the most important aspects in the potential relationship between frailty and cardiovascular disease. In particular, authoritative authors in this field have clarified the definition and the epidemiology of frailty and cardiovascular disease in older people. A large part of the volume is dedicated to the biological mechanisms of frailty and cardiovascular disease, trying to find those in common between these two conditions. Since this book is dedicated to both researchers and clinicians, we have proposed some chapters to the importance of comprehensive geriatric assessment in the evaluation and treatment of cardiovascular diseases and frailty. In this regard, the importance of geriatric evaluation in cardiac surgery for older people is well covered. Finally, the importance of cardiac rehabilitation and physical exercise is summarized, being, actually, the most important treatments for both frailty and cardiovascular disease. Written by many well-known and widely published experts in their respective fields, this book will appeal to a wide readership such as researchers in the field and clinicians, especially suited in geriatric medicine and cardiology who, every day, face frail older patients.

This book systematically focuses on central sleep apneas, analyzing their relationship especially with heart failure and discussing recent research results and emerging treatment strategies based on feedback modulation. The opening chapters present historical background information on Cheyne-Stokes respiration (CSR), clarify terminology, and explain the mechanics and chemistry of respiration. Following a description of the physiology of respiration, the pathophysiology underlying central apneas in different disorders and particularly in heart failure is discussed. The similarities and differences of obstructive and central apneas are then considered. The book looks beyond the concept of sleep apnea to daytime CSR and periodic breathing during effort and contrasts the opposing views of CSR as a compensatory phenomenon or as detrimental to the failing heart. The diagnostic tools currently in use for the detection of CSR are thoroughly reviewed, with guidance on interpretation of findings. The book concludes by describing the various forms of treatment that are available for CSR and by explaining how to select patients for treatment.

The role of oxidative stress in human disease has become an area of intense interest. Free radicals, a normal product of metabolism, exist in all aerobic cells in balance with biochemical antioxidants. Environmental stress increases the levels of free radicals drastically, thereby disturbing the equilibrium between free radical production and the antioxidant capability causing oxidative stress. Over the years, ROS has been implicated in the pathologies of various diseases like cancer, neurological disorder, cardiovascular diseases rheumatoid arthritis, diabetes etc. This book provides an in depth critical state-of-art reviews from established investigators on free radicals, ROS associated pathogenesis of human diseases, biomarkers of oxidative damage, antioxidants, phytonutrients and other related health concerns of modern society. The present book is aimed at graduate students, researchers in academia, industry and clinicians with the interest in redox biology. Special attention has been devoted to the topic of ROS signalling, oxidative stress induced human pathologies & antioxidative therapies. The book consists of four parts in specified topics based on the current literatures for the better understanding of the readers with respect to their subject-wise interests. The first section of the book provides an overview about the ROS production and their measuring tools and techniques followed by the mechanisms involved in the oxidative stress in the second section. The third section describes the involvement of oxidative stress in different human diseases and the last section focuses on the different strategies to ameliorate oxidative stress induced stress.

This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.