Overview

Atherosclerotic cardiovascular disease remains the major cause of death and disability in Western society. The field of atherosclerosis research has grown tremendously over the last forty years, shedding a great deal of light on the contributing factors and natural history of the disorder and enabling strategies for its treatment and prevention. Some of the greatest strides in this field in recent years have derived from advances in molecular biology techniques. These strides were chosen for emphasis in the most recent Princess Lilian symposium, whose proceedings this volume represents. Historically, the Princess Lilian meetings have been small ones aimed at bringing together investigators from diverse specialties to discuss a particular subject. The most recent meeting was no exception and included clinicians, clinical investigators, and research­ ers in basic science. The symposium began with an extensive review of coronary morphopathological findings in patients who died of coronary heart disease. Any rational hypothesis of atherogenesis must take into account clinical findings, and any attempt to bridge the gap between experimental laboratory findings and studies in man is highly desirable. Three chapters focus on endothelial injury: one on the nitric oxide pathway in physiology and pathology, a second on the activation of endothelial cells, and a third on the monocyte and endothelial injury. Still another chapter examines growth factors, in particular the fibroblast growth factor in atherogenesis.

Full Product Details

Author:   Antonio M. Jr. Gotto
Publisher:   Springer London Ltd
Imprint:   Springer London Ltd
Edition:   Softcover reprint of the original 1st ed. 1992
Dimensions:   Width: 17.00cm , Height: 1.00cm , Length: 24.20cm
Weight:   0.354kg
ISBN:  

9781447119111

ISBN 10:   1447119118
Pages:   180
Publication Date:   23 November 2011
Audience:   Professional and scholarly ,  Professional & Vocational
Format:   Paperback
Publisher's Status:   Active
Availability:   Manufactured on demand  
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Table of Contents

1 Morphological Findings in the Coronary Arteries in Fatal Coronary Artery Diseas.- Number of Major Epicardial Coronary Arteries Severely Narrowed in the Various “Coronary Events”.- Quantitative Approach to Atherosclerotic Coronary Artery Disease: Amounts of Narrowing in Each 5-mm Segment of Each of the Four Major Coronary Arteries.- Distribution of Severe Narrowing in Each of the Three Longest Epicardial Coronary Arteries in Fatal Coronary Artery Disease.- Clinical Usefulness of the Quantitative Approach to Coronary Artery Disease.- Significance of Coronary Arterial Thrombus in Transmural Acute Myocardial Infarction.- Cardiac Morphological Findings in Acute Myocardial Infarction Treated with Thrombolytic Therapy.- Composition of Atherosclerotic Plaques in Fatal Coronary Artery Disease.- Effects of Percutaneous Transluminal Coronary Angioplasty on Atherosclerotic Plaques and Relation of Plaque Composition and Arterial Size to Outcome.- Morphological Findings in Saphenous Veins Used as Coronary Arterial Bypass Conduits.- 2 The L-Arginine: Nitric Oxide Pathway in Physiology and Patholog.- The Constitutive Nitric Oxide Synthase.- The Inducible Nitric Oxide Synthase.- Conclusions.- 3 Endothelial Activation: Its Role in Inflammation, Vascular Injury and Atherogenesi.- Endothelial Activation In Vivo.- Endothelial Activation and Endothelial Injury.- Endothelial Activation and Atherogenesis.- Conclusions and Summary.- 4 Basic Fibroblast Growth Factor in Vascular Development and Atherogenesi.- Vascular Injury in Atherosclerosis.- Vascular Balloon Injury and Restenosis.- Platelet-Derived Growth Factors.- Fibroblast Growth Factors.- Expression of bFGF in Vascular Development and Injury.- Prospects for Anti-bFGFs.- Targeted Toxin Therapy.- 5 The Monocyte and Endothelial Injuryin Atherogenesi.- Monocytes and Lesion-Susceptible Areas.- Morphology of Lesion-Susceptible Areas.- Endothelial Transport and intimal Accumulation in S-Areas.- Monocyte Recruitment in Lesion-Susceptible Areas.- 6 Lp [a]: A Lipoprotein Class with Atherothrombotic Potentia.- Structural Properties of Lp [a].- Lp [a] Physiology.- Lp [a] as a Cardiovascular Pathogen.- Considerations on the Thrombo-atherogenicity of Lp [a].- Diagnostic Considerations.- Approaches to Correct High Plasma Levels of Lp [a].- 7 Modified Lipoproteins and Atherogenesi.- Methods.- Results.- Discussion.- 8 The Molecular Biology of Apolipoprotein.- Hepatic Apo B Metabolism.- Structure and Function of Hepatic Apo B-100.- Intestinal Apo B-48 Metabolism.- Conclusions.- 9 Structure and Evolution of the Apolipoprotein and Lipase Gene Familie.- Methods.- The Soluble Apolipoprotein Multigene Family.- Structure and Evolution of the Lipase Gene Family.- Concluding Remarks.- 10 A Gln to Arg Substitution in the Adducin Family of Proteins is a Necessary but not Sufficient Factor for High Blood Pressure in Rats of the Milan Hypertensive Strai.- Results.- Discussion.- 11 Genetic Control of Plasma Lipid, Lipoprotein and Apolipoprotein Levels: From Restriction Fragment Length Polymorphisms to Specific Mutation.- Background.- The Apo B Protein.- The ApoB Gene.- Apo B Protein Polymorphism.- Linkage Disequilibrium.- Apo B Gene Sequencing.- Conclusions.- 12 Receptor Regulation of Lipoprotein Metabolis.- Separate Pathways for Exogenous and Endogenous Lipids.- Postulating a Chylomicron Remnant Receptor.- Studies on Chylomicron Remnant Catabolism.- Characterization of LRP as the Potential Chylomicron Remnant Receptor.- Structural Features of LRP.- Regulation of LRP.- Conclusion.- 13 The High-Density Lipoprotein Recepto.- High-Density Lipoprotein Receptor Hypothesis.- Methods.- High-Density Apolipoproteins Stimulate Translocation and Efflux of Intracellular Sterol.- Intracellular Signals in High-Density Apolipoprotein-Mediated Sterol Translocation and Efflux.- The High-Density Lipoprotein Receptor.- Clinical Implications.- 14 High-Density Lipoprotein Cholesterol, Triglycerides and Coronary Heart Disease.- 15 Apolipoproteins, Reverse Cholesterol Transport and Coronary Heart Diseas.- The Role of the Apo A1/C3/A4 Gene in Association Studies and Cosegregation Studies.- The Role of Apo A-I Mutants.- Molecular Defects in HDL Cholesterol Deficiency Syndromes.- Conclusions.- 16 Cholesterol-Lowering Clinical Trials: Where Do We Go From Here?.- Some Previous Venues.- Future Directions.

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