Atherosclerosis And Oxidant Stress A New Perspective

Vascular injury is initiated by oxidant injury to the vessel wall. This volume is organized around the role of oxidant damage in this disease process and provides a collection of the most recent studies, representing various disciplines that can serve as the basis for further improvements in our understanding and control of cardiovascular and cerebral vascular 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 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.

New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.

Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient, First Edition, is the first comprehensive text to focus on important biomechanical studies conducted in the last decade that have increased our understanding of coronary atherosclerotic plaque initiation, growth, and rupture, as well as improving the design of medical devices and clinical interventions, including surgical procedures. The book provides students, researchers, engineers, clinicians, and interventional cardiologists with an overview of the main topics related to the biomechanics of atherosclerosis, in a single volume written by several experts in the field. This volume is part of the Biomechanics of Living Organs book series. The biomechanics of human soft tissues and organs has been an emerging research field since the publication of Y.C. Fung’s original book series in the 1990s. The publication of such books entirely dedicated to a specific biomechanical subject is necessary to advance scientific research in the field of biomechanics and to transfer important knowledge to future generations. Therefore, this series of volumes on the biomechanics of living organs has been created. This series began in July 2017 with the publication of a first volume on the fundamentals of Hyperelastic Constitutive Laws for Finite Element Modeling of Living Organs. The current volume on the Biomechanics of Coronary Atherosclerotic Plaque, is the latest in this new series. Presents the main computational fluid dynamic studies performed, describing blood flow in healthy and pathological artery branches, including in coronary bifurcations Highlights the correlation between plaque initiation regions and blood shear stress amplitude Discusses the main biomechanical and mechanobiological models to highlight the importance of quantifying the residual and peak cap stresses and the presence of μ-calcifications to evaluate the risk of plaque rupture Introduces the most recent intravascular imaging biomarker techniques (elastography, palpography and modulography)

Human aging is a complex phenomenon. This state-of-the-art book discusses the role of free radicals in aging in different animal models, as well as the relevance of free radicals on age-related diseases and pathological conditions in humans (following an introduction section of the basics and theory of free radicals). In addition, the major interventions trials of antioxidant supplements in age-related disease, cancer and so forth are reviewed and discussed.

Availability of advanced computational technology has fundamentally altered the investigative paradigm in the field of biomechanics. Armed with sophisticated computational tools, researchers are seeking answers to fundamental questions by exploring complex biomechanical phenomena at the molecular, cellular, tissue and organ levels. The computational armamentarium includes such diverse tools as the ab initio quantum mechanical and molecular dynamics methods at the atomistic scales and the finite element, boundary element, meshfree as well as immersed boundary and lattice-Boltzmann methods at the continuum scales. Multiscale methods that link various scales are also being developed. While most applications require forward analysis, e.g., finding deformations and stresses as a result of loading, others involve determination of constitutive parameters based on tissue imaging and inverse analysis. This book provides a glimpse of the diverse and important roles that modern computational technology is playing in various areas of biomechanics including biofluids and mass transfer, cardiovascular mechanics, musculoskeletal mechanics, soft tissue mechanics, and biomolecular mechanics.

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.