UID:
almahu_9949697321102882
Format:
1 online resource (221 p.)
Edition:
1st ed.
ISBN:
0-12-800485-1
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0-12-800039-2
Content:
Inflammation in Heart Failure, edited by W. Matthijs Blankesteijn and Raffaele Altara, is the first book in a decade to provide an in-depth assessment on the causes, symptoms, progression and treatments of cardiac inflammation and related conditions. This reference uses two decades of research to introduce new methods for identifying inflammatory benchmarks from early onset to chronic heart failure and specifically emphasizes the importance of classifying at-risk subgroups within large populations while determining the patterns of cytokines in such classifications. Further, the book details c
Note:
Description based upon print version of record.
,
Front Cover; Inflammation in Heart Failure; Copyright; Contents; Contributors; Preface; Section 1: Pathophysiology of the Inflammatory Response in Heart Failure; Chapter 1: Inflammation in Heart Failure with Preserved Ejection Fraction; 1.1. Introduction; 1.2. Consequences of Limited Understanding of Pathophysiology in HFpEF; 1.3. Underlying Causes of HFpEF; 1.4. Adaptive Mechanisms in HFpEF; 1.5. Inflammation in HFpEF; 1.5.1. Inflammation in HFpEF Animal Studies; 1.5.1.1. Interactions with Other Systems; 1.5.2. Inflammation in HFpEF Human Studies
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1.6. Oxidative Stress, Endothelial Dysfunction and Microvascular Disease1.6.1. Potential Implications for Treatment of HFpEF; 1.7. Conclusions; References; Chapter 2: Role of the Innate Immune System in Ischemic Heart Failure; 2.1. Introduction; 2.2. Initiation of the Immune Response; 2.2.1. Receptors; 2.2.2. Complement; 2.2.3. Oxidative Stress; 2.2.3.1. ROS Generation Post- MI ; 2.2.3.2. Role of Oxidative Stress for Cardiac Necrosis and Inflammation; 2.2.4. Mechanical Stimuli; 2.3. Effectors of Innate Immunity; 2.3.1. Cytokines; 2.3.1.1. Cytokine Effects on Cardiomyocyte Survival
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2.3.1.2. Cytokines Influence Granulation Tissue Formation and Vascular Remodeling Post-injury2.3.1.3. Cytokines Modulate Scar Tissue Formation After Injury; 2.3.1.4. Cytokines and ROS ; 2.3.1.5. Cytokines in Inflammation Resolution; 2.3.2. Cellular Effectors; 2.3.2.1. Leukocyte Recruitment; 2.3.2.2. Neutrophils; 2.3.2.2.1. Neutrophil-Mediated Cardiac Injury; 2.3.2.2.1.1. Reactive Oxygen Species; 2.3.2.2.1.2. Granule Toxicity; 2.3.2.3. Mononuclear Cells; 2.3.2.3.1. Monocytes; 2.3.2.3.2. Macrophages; 2.4. Reverse Remodeling
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2.5. Clinical Implications: Is There a Causal Link Between Dysequilibrated Inflammation and Remodeling?References; Chapter 3: The Role of Inflammation in Myocardial Infarction; 3.1. Introduction; 3.2. Role of the Inflammatory Response Before MI; 3.2.1. Development of the Atherosclerotic Plaque; 3.2.2. Immune Cells Involved; 3.2.3. Maturation and Rupture of the Atherosclerotic Plaque; 3.3. The Role of the Inflammatory Response in MI; 3.3.1. MI and Wound Healing; 3.3.2. Humoral Immune Response Post-MI; 3.3.2.1. Cytokines; 3.3.2.2. Chemokines; 3.3.3. Cellular Immune Response Post-MI
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3.3.3.1. Leukocytes3.3.3.2. Monocytes; 3.3.3.3. Macrophages; 3.3.3.4. Nonimmune Cells; 3.3.4. Other Factors Modulating the Immune Response Post-MI; 3.4. Inflammation as a Pharmacological and Biocellular Target; 3.4.1. Therapy Aimed at Inflammation Before MI; 3.4.1.1. Current Pharmacotherapy Targeting Inflammation Before MI; 3.4.1.1.1. Statins; 3.4.1.1.2. Hypoglycemic Agents; 3.4.1.1.3. Renin Angiotensin System Targeting; 3.4.1.1.4. P2Y 12 Receptor Inhibitors; 3.4.1.2. Novel Strategies Targeting Inflammation Before MI; 3.4.2. Therapy Aimed at Inflammation After MI
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3.4.2.1. Current Pharmacotherapy Targeting Inflammation After MI
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English
Additional Edition:
ISBN 1-336-00887-3
Language:
English