Inflammation in Heart Failure (eBook)

Raffaele Altara, Matthijs Blankesteijn (Herausgeber)

eBook Download: PDF | EPUB

2014 | 1. Auflage
220 Seiten
Elsevier Science (Verlag)
978-0-12-800485-2 (ISBN)

Infos

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 clinical applications of the pathophysiological mechanisms of heart failure, diagnosis and therapeutic strategies. Inflammation in Heart Failure's breadth of subject matter, easy-to-follow structure, portability, and high-quality illustrations create an accessible benefit for researchers, clinicians and students. - Presents updated information and research on the relevant inflammatory mediators of heart failure to aid in targeting future translational research as well as the improvement of early diagnosis and treatment - Provides research into better understanding the different inflammatory mediators that signal the underlying diseases that potentially lead to heart failure - Contains 20 years of research, offering a brief overview of the topic leading to current opinions on, and treatment of, heart failure - Provides a structured, systematic and balanced overview of the role of inflammation in heart failure making it a useful resource for researchers and clinicians, as well as those studying cardiovascular diseases

Inhalt

Front Cover 1
Inflammation in Heart Failure 4
Copyright 5
Contents 6
Contributors 10
Preface 12
Section 1: Pathophysiology of the Inflammatory Response in Heart Failure 14
Chapter 1: Inflammation in Heart Failure with Preserved Ejection Fraction 16
1.1. Introduction 16
1.2. Consequences of Limited Understanding of Pathophysiology in HFpEF 16
1.3. Underlying Causes of HFpEF 17
1.4. Adaptive Mechanisms in HFpEF 19
1.5. Inflammation in HFpEF 20
1.5.1. Inflammation in HFpEF Animal Studies 20
1.5.1.1. Interactions with Other Systems 21
1.5.2. Inflammation in HFpEF Human Studies 22
1.6. Oxidative Stress, Endothelial Dysfunction and Microvascular Disease 23
1.6.1. Potential Implications for Treatment of HFpEF 25
1.7. Conclusions 26
References 26
Chapter 2: Role of the Innate Immune System in Ischemic Heart Failure 32
2.1. Introduction 32
2.2. Initiation of the Immune Response 33
2.2.1. Receptors 33
2.2.2. Complement 34
2.2.3. Oxidative Stress 35
2.2.3.1. ROS Generation Post- MI 35
2.2.3.2. Role of Oxidative Stress for Cardiac Necrosis and Inflammation 35
2.2.4. Mechanical Stimuli 36
2.3. Effectors of Innate Immunity 36
2.3.1. Cytokines 36
2.3.1.1. Cytokine Effects on Cardiomyocyte Survival 37
2.3.1.2. Cytokines Influence Granulation Tissue Formation and Vascular Remodeling Post-injury 38
2.3.1.3. Cytokines Modulate Scar Tissue Formation After Injury 38
2.3.1.4. Cytokines and ROS 39
2.3.1.5. Cytokines in Inflammation Resolution 39
2.3.2. Cellular Effectors 40
2.3.2.1. Leukocyte Recruitment 40
2.3.2.2. Neutrophils 40
2.3.2.2.1. Neutrophil-Mediated Cardiac Injury 41
2.3.2.2.1.1. Reactive Oxygen Species 41
2.3.2.2.1.2. Granule Toxicity 42
2.3.2.3. Mononuclear Cells 43
2.3.2.3.1. Monocytes 43
2.3.2.3.2. Macrophages 44
2.4. Reverse Remodeling 44
2.5. Clinical Implications: Is There a Causal Link Between Dysequilibrated Inflammation and Remodeling? 45
References 45
Chapter 3: The Role of Inflammation in Myocardial Infarction 52
3.1. Introduction 52
3.2. Role of the Inflammatory Response Before MI 53
3.2.1. Development of the Atherosclerotic Plaque 53
3.2.2. Immune Cells Involved 53
3.2.3. Maturation and Rupture of the Atherosclerotic Plaque 54
3.3. The Role of the Inflammatory Response in MI 54
3.3.1. MI and Wound Healing 54
3.3.2. Humoral Immune Response Post-MI 56
3.3.2.1. Cytokines 56
3.3.2.2. Chemokines 57
3.3.3. Cellular Immune Response Post-MI 57
3.3.3.1. Leukocytes 58
3.3.3.2. Monocytes 58
3.3.3.3. Macrophages 58
3.3.3.4. Nonimmune Cells 59
3.3.4. Other Factors Modulating the Immune Response Post-MI 59
3.4. Inflammation as a Pharmacological and Biocellular Target 60
3.4.1. Therapy Aimed at Inflammation Before MI 60
3.4.1.1. Current Pharmacotherapy Targeting Inflammation Before MI 60
3.4.1.1.1. Statins 61
3.4.1.1.2. Hypoglycemic Agents 61
3.4.1.1.3. Renin Angiotensin System Targeting 61
3.4.1.1.4. P2Y 12 Receptor Inhibitors 62
3.4.1.2. Novel Strategies Targeting Inflammation Before MI 62
3.4.2. Therapy Aimed at Inflammation After MI 63
3.4.2.1. Current Pharmacotherapy Targeting Inflammation After MI 63
3.4.2.1.1. Statins 63
3.4.2.1.2. RAS Targeting 65
3.4.2.1.3. Mineralocorticoid Receptor Antagonists 65
3.4.2.1.4. Beta-Blockers 65
3.4.2.1.5. Antiplatelet Agents 66
3.4.2.2. Novel Strategies Targeting Inflammation After MI 66
3.5. Conclusions 69
References 70
Chapter 4: Cross Talk Between Inflammation and Extracellular Matrix Following Myocardial Infarction 80
4.1. Introduction 80
4.2. Roles of Inflammation in the MI Setting 81
4.2.1. Neutrophil Degranulation 81
4.2.2. Macrophage Activation 81
4.3. CYTOKINE AND CHEMOKINE ROLES IN LV REMODELING 82
4.3.1. Cytokines Regulate Fibroblast Phenotype and Function 82
4.3.2. Chemokines Regulate LV Remodeling 82
4.4. MMP ROLES IN THE INFARCTED MYOCARDIUM 82
4.4.1. MMPs 82
4.4.2. MMP -1 83
4.4.3. MMP -2 83
4.4.4. MMP -3 83
4.4.5. MMP -7 84
4.4.6. MMP -8 84
4.4.7. MMP -9 84
4.4.8. MMP -13 84
4.4.9. MMP -14 84
4.4.10. MMP -28 84
4.5. ECM Roles in the MI Setting 85
4.5.1. Structural ECM 85
4.5.2. Collagens 85
4.5.3. Fibronectin 86
4.5.4. Laminins 86
4.5.5. Matricellular Proteins 86
4.5.6. CCNs 86
4.5.7. Osteopontin 87
4.5.8. Periostin 87
4.5.9. SPARC 87
4.5.10. Tenascin-C 87
4.5.11. Thrombospondin-1 88
4.6. Matricryptins: ECM Fragments with Biological Activity 88
4.7. Future Directions 88
4.8. Conclusions 89
Acknowledgments 89
References 89
Chapter 5: Cross Talk Between Brain and Inflammation 94
5.1. Cardiovascular Disease and Brain Disorders 94
5.1.1. Introduction 94
5.1.2. Brain Disorders Leading to Cardiovascular Disease 94
5.1.3. Cardiovascular Disease Leading to Brain Disorders 95
5.1.4. Inflammation as the Link in Neurocardiac Interaction 95
5.2. Cross Talk Between Brain and Cardiovascular System 96
5.2.1. Cardiovascular Regulation and the Brain 96
5.2.2. Inflammation 97
5.2.2.1. Circulating Cytokines 97
5.2.2.2. Autonomic Nervous System 98
5.2.2.2.1. Sympathetic Activation 99
5.2.2.2.2. Parasympathetic Inhibition 99
5.2.2.2.3. Synergism 100
5.2.2.3. Cytokine Functions in the Brain 100
5.3. Conclusions 101
References 101
Chapter 6: Translation of Animal Models into Clinical Practice: Application to Heart Failure 106
6.1. Introduction 106
6.2. Animal Models of Acquired Cardiomyopathy 107
6.2.1. Models of Ischemia-Reperfusion and Infarction 107
6.2.1.1. Small Rodent Models 108
6.2.1.2. Large-Animal Models 108
6.2.2. Animal Models of Pressure and Volume Overload 109
6.2.2.1. The Mouse Model of Transverse Aortic Constriction 109
6.2.2.2. The Rat Model of Aortic Constriction 109
6.2.2.3. Spontaneous Hypertensive Rats 109
6.2.2.4. Large-Animal Models 109
6.2.3. Animal Models of Toxic Cardiomyopathy 110
6.2.4. Models of Sepsis-Associated LV Dysfunction 110
6.3. Animal Models of Genetic Cardiomyopathies 111
6.4. Improvements in Animal Models ( Table 6.2) 112
References 113
Section 2: Inflammatory Biomarkers 116
Chapter 7: Inflammatory Biomarkers in Post-infarction Heart Failure and Cardiac Remodeling 118
7.1. Introduction 118
7.2. The Role of the Inflammatory Response in Repair and Remodeling of the Infarcted Heart 119
7.3. Specific Inflammatory Biomarkers as Predictors of Post-infarction Remodeling 120
7.3.1. General Markers of Inflammation 120
7.3.1.1. C-Reactive Protein 120
7.3.1.2. Myeloperoxidase 121
7.3.2. Cytokines ( Table 7.2) 122
7.3.2.1. The TNF - a System 122
7.3.2.2. IL -6 123
7.3.2.3. The Expanding Role of ST2 123
7.3.2.4. The Role of Growth Differentiation Factor-15, a TGF - ß Family Member 123
7.3.2.5. Chemokines 124
7.3.3. The Matrix 124
7.3.3.1. Matrix Metalloproteinases 124
7.3.3.2. Matricellular Proteins 125
7.3.3.2.1. Galectin-3 125
7.3.3.2.2. Tenascin-C 125
7.3.4. Indicators of Cellular Activation 125
7.4. Implementation of Biomarker-Based Strategies in Patients with Myocardial Infarction 125
References 126
Chapter 8: Technological Aspects of Measuring Inflammatory Markers 130
8.1. Immunoassays Development and New Directions 130
8.2. Methodology and Instrumentation 130
8.2.1. Solid Phase/Planar Assays 131
8.2.1.1. Multiplexed ELISA 132
8.2.1.2. Electrochemical Multiplexed ELISA 132
8.2.1.3. Membrane-Based Assay 134
8.2.2. Suspension Array Technology/Bead-Based Immunoassays 135
8.2.2.1. Cytometric Bead Assay 135
8.2.2.2. Luminex Screening and Performance Assays 137
8.3. MIA Implementation 137
8.3.1. Sampling Qualified Specimen for MIA 137
8.3.2. Analytical Challenges and Clinical Utility 137
8.3.2.1. Cytokines/Biomarkers Stability 137
8.3.2.2. The Importance of Validation 138
8.3.2.2.1. Case 1 138
8.3.2.2.2. Case 2 139
8.3.2.3. The IL-6 Case (Systematic Review) 139
8.4. The Immunoassay Market: Opportunities and Issues 141
Acknowledgments 142
References 142
Chapter 9: Molecular Imaging to Identify the Vulnerable Plaque: From Basic Research to Clinical Practice 144
9.1. Introduction 144
9.2. Molecular Imaging of Inflammation 146
9.2.1. Preclinical 146
9.2.2. Clinical 146
9.3. Molecular Imaging of Cell Death 147
9.3.1. Preclinical 147
9.3.2. Clinical 148
9.4. Molecular Imaging of Remodeling 148
9.4.1. Preclinical 148
9.5. Molecular Imaging of Thrombosis 149
9.5.1. Preclinical 149
9.6. Molecular Imaging of (Micro) Calcification 150
9.6.1. Preclinical 150
9.6.2. Clinical 150
9.7. Socioeconomic Impact of Molecular Imaging 150
9.8. Conclusion and Future Perspectives 151
References 151
Section 3: Targeting of the Inflammatory Response 156
Chapter 10: Mineralcorticoid Receptor Antagonists 158
10.1. Introduction 158
10.2. Molecular Basis for the Clinical Use of MR Antagonist in HF 158
10.2.1. Generalities 159
10.2.2. Inflammation 160
10.2.3. Cardiac Fibrosis 161
10.3. Pharmacology of Mineralcorticoid Receptor Antagonist 161
10.4. Clinical Evidences 162
10.4.1. Systolic HF 162
10.4.2. Diastolic HF 162
10.4.3. Arrhythmias 163
10.5. Conclusion and Future Perspectives 163
References 163
Chapter 11: PPARs as Modulators of Cardiac Metabolism and Inflammation 168
11.1. Introduction 168
11.2. Peroxisome Proliferator-Activated Receptors 169
11.3. PPARs and the Control of Cardiac Energy Metabolism 170
11.3.1. Role of PPAR a 170
11.3.2. Role of PPAR ß / d 171
11.3.3. Role of PPAR . 171
11.4. PPARs and Cardiac Inflammation 172
11.4.1. PPAR a 172
11.4.2. PPAR ß / d 172
11.4.3. PPAR . 173
11.5. Cross Talk Between Cardiac Metabolism and Inflammation 173
11.5.1. Modulation of Inflammation/Metabolism by PPARs 173
11.5.2. Sirt1 Couples Inflammation and Metabolism in the Heart 174
11.5.3. The FGF21 Autocrine Pathway 175
11.6. PPAR Agonists and Heart Failure Treatment 175
11.7. Conclusions and Perspectives 176
References 176
Chapter 12: Inflammatory Modulation by Statins and Heart Failure: From Pharmacological Data to Clinical Evidence 182
12.1. Inflammation and Immune Cells 182
12.2. Endothelial Cells 184
12.3. Cardiomyocytes 185
12.4. Fibroblasts 186
12.5. A Summary of the Clinical Evidence 186
References 187
Chapter 13. Small but Smart: microRNAs in the Center of Inflammatory Processes During Cardiovascular Diseases, the Metabolic 192
13.1. Introduction 192
13.2. Role of Inflammation-Related microRNAs in HF 193
13.3. microRNAs as Regulators of the Inflammatory Response During Atherogenesis 194
13.3.1. MicroRNAs Modulate Inflammatory Function of ECs 194
13.3.2. MicroRNAs Modulate the Macrophage Response to Oxidized LDL 195
13.4. microRNAs in the Metabolic Syndrome 195
13.5. Circulating microRNA Profiles of Cardiovascular Diseases 196
13.5.1. Circulating microRNA Profiles of Cardiac Disease 196
13.5.2. Circulating microRNA Profiles of Vascular Disease 196
13.5.3. Circulating microRNA Profiles of Diabetes 197
13.5.4. Functional Roles for Circulating microRNAs 197
13.6. Aging, Inflammation, and HF: Are There Shared microRNAs? 199
13.7. Conclusions and Future Perspectives 200
Acknowledgments 200
References 201
Chapter 14: The Role of Cytokines in Clinical Heart Failure 204
14.1. Role of Inflammation in the Pathogenesis of HF 204
14.1.1. Effects of Cytokines on LV Function 204
14.1.2. Effects of Proinflammatory Cytokines on LV Remodeling 205
14.2. Inflammation as a Therapeutic Target in HF 206
14.2.1. Anti-inflammatory Therapies 206
14.2.1.1. Transcriptional Suppression of Proinflammatory Cytokines 206
14.2.1.2. Translational Suppression of Proinflammatory Cytokines 206
14.2.1.3. Targeted Anti-cytokine Approaches Using Biological Response Modifiers 209
14.2.1.3.1. Soluble TNF Receptors 209
14.2.1.3.2. Monoclonal Antibodies 210
14.2.1.3.3. IL-1 Receptor Antagonist 211
14.2.1.4. Other Anti-inflammatory Agents 212
14.2.1.4.1. Statins 212
14.2.1.4.2. N-3 Polyunsaturated Fatty Acids 212
14.2.1.4.3. Oxypurinol 212
14.2.2. Immunomodulation 212
14.2.2.1. Intravenous Immuoglobulin 213
14.2.2.2. Methotrexate 213
14.2.2.3. Immune Modulation Therapy 213
14.3. Summary and Future Directions 214
Acknowledgments 214
Reference 215
Index 218

Produkt-Details

• Erscheint lt. Verlag: 5.12.2014
• Sprache: englisch
• Themenwelt: Sachbuch/Ratgeber ► Gesundheit / Leben / Psychologie
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete ► Dermatologie
• Themenwelt: Medizinische Fachgebiete ► Innere Medizin ► Kardiologie / Angiologie
• Themenwelt: Studium ► 1. Studienabschnitt (Vorklinik) ► Physiologie
• Themenwelt: Studium ► 2. Studienabschnitt (Klinik) ► Pharmakologie / Toxikologie
• Themenwelt: Studium ► Querschnittsbereiche ► Infektiologie / Immunologie
• ISBN-10: 0-12-800485-1 / 0128004851
• ISBN-13: 978-0-12-800485-2 / 9780128004852