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Inflammation in heart failure /
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 in...
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | , |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
Amsterdam :
Academic Press,
[2015]
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| Temas: | |
| Acceso en línea: | Texto completo |
Tabla de Contenidos:
- 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.
- 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.
- 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.
- 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.
- 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.