Inflammation in Heart Failure.

By: Blankesteijn, MatthijsContributor(s): Altara, RaffaelePublisher: San Diego : Elsevier Science & Technology, 2014Copyright date: ©2015Description: 1 online resource (221 pages)Content type: text Media type: computer Carrier type: online resourceISBN: 9780128004852Subject(s): Heart failure -- Diagnosis.;Inflammation -- Alternative treatmentGenre/Form: Electronic books. Additional physical formats: Print version:: Inflammation in Heart FailureDDC classification: 616.129 LOC classification: RC685.C53 -- .I54 2015ebOnline resources: Click to View
Contents:
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 Disease -- 1.6.1. 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-injury -- 2.3.1.3. 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. Leukocytes -- 3.3.3.2. 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 -- 3.4.2.1. Current Pharmacotherapy Targeting Inflammation After MI -- 3.4.2.1.1. Statins -- 3.4.2.1.2. RAS Targeting -- 3.4.2.1.3. Mineralocorticoid Receptor Antagonists -- 3.4.2.1.4. Beta-Blockers -- 3.4.2.1.5. Antiplatelet Agents -- 3.4.2.2. Novel Strategies Targeting Inflammation After MI -- 3.5. Conclusions -- References -- Chapter 4: Cross Talk Between Inflammation and Extracellular Matrix Following Myocardial Infarction -- 4.1. Introduction -- 4.2. Roles of Inflammation in the MI Setting -- 4.2.1. Neutrophil Degranulation -- 4.2.2. Macrophage Activation -- 4.3. CYTOKINE AND CHEMOKINE ROLES IN LV REMODELING -- 4.3.1. Cytokines Regulate Fibroblast Phenotype and Function -- 4.3.2. Chemokines Regulate LV Remodeling -- 4.4. MMP ROLES IN THE INFARCTED MYOCARDIUM.
4.4.1. MMPs -- 4.4.2. MMP -1 -- 4.4.3. MMP -2 -- 4.4.4. MMP -3 -- 4.4.5. MMP -7 -- 4.4.6. MMP -8 -- 4.4.7. MMP -9 -- 4.4.8. MMP -13 -- 4.4.9. MMP -14 -- 4.4.10. MMP -28 -- 4.5. ECM Roles in the MI Setting -- 4.5.1. Structural ECM -- 4.5.2. Collagens -- 4.5.3. Fibronectin -- 4.5.4. Laminins -- 4.5.5. Matricellular Proteins -- 4.5.6. CCNs -- 4.5.7. Osteopontin -- 4.5.8. Periostin -- 4.5.9. SPARC -- 4.5.10. Tenascin-C -- 4.5.11. Thrombospondin-1 -- 4.6. Matricryptins: ECM Fragments with Biological Activity -- 4.7. Future Directions -- 4.8. Conclusions -- Acknowledgments -- References -- Chapter 5: Cross Talk Between Brain and Inflammation -- 5.1. Cardiovascular Disease and Brain Disorders -- 5.1.1. Introduction -- 5.1.2. Brain Disorders Leading to Cardiovascular Disease -- 5.1.3. Cardiovascular Disease Leading to Brain Disorders -- 5.1.4. Inflammation as the Link in Neurocardiac Interaction -- 5.2. Cross Talk Between Brain and Cardiovascular System -- 5.2.1. Cardiovascular Regulation and the Brain -- 5.2.2. Inflammation -- 5.2.2.1. Circulating Cytokines -- 5.2.2.2. Autonomic Nervous System -- 5.2.2.2.1. Sympathetic Activation -- 5.2.2.2.2. Parasympathetic Inhibition -- 5.2.2.2.3. Synergism -- 5.2.2.3. Cytokine Functions in the Brain -- 5.3. Conclusions -- References -- Chapter 6: Translation of Animal Models into Clinical Practice: Application to Heart Failure -- 6.1. Introduction -- 6.2. Animal Models of Acquired Cardiomyopathy -- 6.2.1. Models of Ischemia-Reperfusion and Infarction -- 6.2.1.1. Small Rodent Models -- 6.2.1.2. Large-Animal Models -- 6.2.2. Animal Models of Pressure and Volume Overload -- 6.2.2.1. The Mouse Model of Transverse Aortic Constriction -- 6.2.2.2. The Rat Model of Aortic Constriction -- 6.2.2.3. Spontaneous Hypertensive Rats -- 6.2.2.4. Large-Animal Models -- 6.2.3. Animal Models of Toxic Cardiomyopathy.
6.2.4. Models of Sepsis-Associated LV Dysfunction -- 6.3. Animal Models of Genetic Cardiomyopathies -- 6.4. Improvements in Animal Models ( Table 6.2) -- References -- Section 2: Inflammatory Biomarkers -- Chapter 7: Inflammatory Biomarkers in Post-infarction Heart Failure and Cardiac Remodeling -- 7.1. Introduction -- 7.2. The Role of the Inflammatory Response in Repair and Remodeling of the Infarcted Heart -- 7.3. Specific Inflammatory Biomarkers as Predictors of Post-infarction Remodeling -- 7.3.1. General Markers of Inflammation -- 7.3.1.1. C-Reactive Protein -- 7.3.1.2. Myeloperoxidase -- 7.3.2. Cytokines ( Table 7.2) -- 7.3.2.1. The TNF - α System -- 7.3.2.2. IL -6 -- 7.3.2.3. The Expanding Role of ST2 -- 7.3.2.4. The Role of Growth Differentiation Factor-15, a TGF - β Family Member -- 7.3.2.5. Chemokines -- 7.3.3. The Matrix -- 7.3.3.1. Matrix Metalloproteinases -- 7.3.3.2. Matricellular Proteins -- 7.3.3.2.1. Galectin-3 -- 7.3.3.2.2. Tenascin-C -- 7.3.4. Indicators of Cellular Activation -- 7.4. Implementation of Biomarker-Based Strategies in Patients with Myocardial Infarction -- References -- Chapter 8: Technological Aspects of Measuring Inflammatory Markers -- 8.1. Immunoassays Development and New Directions -- 8.2. Methodology and Instrumentation -- 8.2.1. Solid Phase/Planar Assays -- 8.2.1.1. Multiplexed ELISA -- 8.2.1.2. Electrochemical Multiplexed ELISA -- 8.2.1.3. Membrane-Based Assay -- 8.2.2. Suspension Array Technology/Bead-Based Immunoassays -- 8.2.2.1. Cytometric Bead Assay -- 8.2.2.2. Luminex Screening and Performance Assays -- 8.3. MIA Implementation -- 8.3.1. Sampling Qualified Specimen for MIA -- 8.3.2. Analytical Challenges and Clinical Utility -- 8.3.2.1. Cytokines/Biomarkers Stability -- 8.3.2.2. The Importance of Validation -- 8.3.2.2.1. Case 1 -- 8.3.2.2.2. Case 2 -- 8.3.2.3. The IL-6 Case (Systematic Review).
8.4. The Immunoassay Market: Opportunities and Issues -- Acknowledgments -- References -- Chapter 9: Molecular Imaging to Identify the Vulnerable Plaque: From Basic Research to Clinical Practice -- 9.1. Introduction -- 9.2. Molecular Imaging of Inflammation -- 9.2.1. Preclinical -- 9.2.2. Clinical -- 9.3. Molecular Imaging of Cell Death -- 9.3.1. Preclinical -- 9.3.2. Clinical -- 9.4. Molecular Imaging of Remodeling -- 9.4.1. Preclinical -- 9.5. Molecular Imaging of Thrombosis -- 9.5.1. Preclinical -- 9.6. Molecular Imaging of (Micro) Calcification -- 9.6.1. Preclinical -- 9.6.2. Clinical -- 9.7. Socioeconomic Impact of Molecular Imaging -- 9.8. Conclusion and Future Perspectives -- References -- Section 3: Targeting of the Inflammatory Response -- Chapter 10: Mineralcorticoid Receptor Antagonists -- 10.1. Introduction -- 10.2. Molecular Basis for the Clinical Use of MR Antagonist in HF -- 10.2.1. Generalities -- 10.2.2. Inflammation -- 10.2.3. Cardiac Fibrosis -- 10.3. Pharmacology of Mineralcorticoid Receptor Antagonist -- 10.4. Clinical Evidences -- 10.4.1. Systolic HF -- 10.4.2. Diastolic HF -- 10.4.3. Arrhythmias -- 10.5. Conclusion and Future Perspectives -- References -- Chapter 11: PPARs as Modulators of Cardiac Metabolism and Inflammation -- 11.1. Introduction -- 11.2. Peroxisome Proliferator-Activated Receptors -- 11.3. PPARs and the Control of Cardiac Energy Metabolism -- 11.3.1. Role of PPAR α -- 11.3.2. Role of PPAR β / δ -- 11.3.3. Role of PPAR γ -- 11.4. PPARs and Cardiac Inflammation -- 11.4.1. PPAR α -- 11.4.2. PPAR β / δ -- 11.4.3. PPAR γ -- 11.5. Cross Talk Between Cardiac Metabolism and Inflammation -- 11.5.1. Modulation of Inflammation/Metabolism by PPARs -- 11.5.2. Sirt1 Couples Inflammation and Metabolism in the Heart -- 11.5.3. The FGF21 Autocrine Pathway -- 11.6. PPAR Agonists and Heart Failure Treatment.
11.7. Conclusions and Perspectives.
Summary: 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.
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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 Disease -- 1.6.1. 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-injury -- 2.3.1.3. 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. Leukocytes -- 3.3.3.2. 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 -- 3.4.2.1. Current Pharmacotherapy Targeting Inflammation After MI -- 3.4.2.1.1. Statins -- 3.4.2.1.2. RAS Targeting -- 3.4.2.1.3. Mineralocorticoid Receptor Antagonists -- 3.4.2.1.4. Beta-Blockers -- 3.4.2.1.5. Antiplatelet Agents -- 3.4.2.2. Novel Strategies Targeting Inflammation After MI -- 3.5. Conclusions -- References -- Chapter 4: Cross Talk Between Inflammation and Extracellular Matrix Following Myocardial Infarction -- 4.1. Introduction -- 4.2. Roles of Inflammation in the MI Setting -- 4.2.1. Neutrophil Degranulation -- 4.2.2. Macrophage Activation -- 4.3. CYTOKINE AND CHEMOKINE ROLES IN LV REMODELING -- 4.3.1. Cytokines Regulate Fibroblast Phenotype and Function -- 4.3.2. Chemokines Regulate LV Remodeling -- 4.4. MMP ROLES IN THE INFARCTED MYOCARDIUM.

4.4.1. MMPs -- 4.4.2. MMP -1 -- 4.4.3. MMP -2 -- 4.4.4. MMP -3 -- 4.4.5. MMP -7 -- 4.4.6. MMP -8 -- 4.4.7. MMP -9 -- 4.4.8. MMP -13 -- 4.4.9. MMP -14 -- 4.4.10. MMP -28 -- 4.5. ECM Roles in the MI Setting -- 4.5.1. Structural ECM -- 4.5.2. Collagens -- 4.5.3. Fibronectin -- 4.5.4. Laminins -- 4.5.5. Matricellular Proteins -- 4.5.6. CCNs -- 4.5.7. Osteopontin -- 4.5.8. Periostin -- 4.5.9. SPARC -- 4.5.10. Tenascin-C -- 4.5.11. Thrombospondin-1 -- 4.6. Matricryptins: ECM Fragments with Biological Activity -- 4.7. Future Directions -- 4.8. Conclusions -- Acknowledgments -- References -- Chapter 5: Cross Talk Between Brain and Inflammation -- 5.1. Cardiovascular Disease and Brain Disorders -- 5.1.1. Introduction -- 5.1.2. Brain Disorders Leading to Cardiovascular Disease -- 5.1.3. Cardiovascular Disease Leading to Brain Disorders -- 5.1.4. Inflammation as the Link in Neurocardiac Interaction -- 5.2. Cross Talk Between Brain and Cardiovascular System -- 5.2.1. Cardiovascular Regulation and the Brain -- 5.2.2. Inflammation -- 5.2.2.1. Circulating Cytokines -- 5.2.2.2. Autonomic Nervous System -- 5.2.2.2.1. Sympathetic Activation -- 5.2.2.2.2. Parasympathetic Inhibition -- 5.2.2.2.3. Synergism -- 5.2.2.3. Cytokine Functions in the Brain -- 5.3. Conclusions -- References -- Chapter 6: Translation of Animal Models into Clinical Practice: Application to Heart Failure -- 6.1. Introduction -- 6.2. Animal Models of Acquired Cardiomyopathy -- 6.2.1. Models of Ischemia-Reperfusion and Infarction -- 6.2.1.1. Small Rodent Models -- 6.2.1.2. Large-Animal Models -- 6.2.2. Animal Models of Pressure and Volume Overload -- 6.2.2.1. The Mouse Model of Transverse Aortic Constriction -- 6.2.2.2. The Rat Model of Aortic Constriction -- 6.2.2.3. Spontaneous Hypertensive Rats -- 6.2.2.4. Large-Animal Models -- 6.2.3. Animal Models of Toxic Cardiomyopathy.

6.2.4. Models of Sepsis-Associated LV Dysfunction -- 6.3. Animal Models of Genetic Cardiomyopathies -- 6.4. Improvements in Animal Models ( Table 6.2) -- References -- Section 2: Inflammatory Biomarkers -- Chapter 7: Inflammatory Biomarkers in Post-infarction Heart Failure and Cardiac Remodeling -- 7.1. Introduction -- 7.2. The Role of the Inflammatory Response in Repair and Remodeling of the Infarcted Heart -- 7.3. Specific Inflammatory Biomarkers as Predictors of Post-infarction Remodeling -- 7.3.1. General Markers of Inflammation -- 7.3.1.1. C-Reactive Protein -- 7.3.1.2. Myeloperoxidase -- 7.3.2. Cytokines ( Table 7.2) -- 7.3.2.1. The TNF - α System -- 7.3.2.2. IL -6 -- 7.3.2.3. The Expanding Role of ST2 -- 7.3.2.4. The Role of Growth Differentiation Factor-15, a TGF - β Family Member -- 7.3.2.5. Chemokines -- 7.3.3. The Matrix -- 7.3.3.1. Matrix Metalloproteinases -- 7.3.3.2. Matricellular Proteins -- 7.3.3.2.1. Galectin-3 -- 7.3.3.2.2. Tenascin-C -- 7.3.4. Indicators of Cellular Activation -- 7.4. Implementation of Biomarker-Based Strategies in Patients with Myocardial Infarction -- References -- Chapter 8: Technological Aspects of Measuring Inflammatory Markers -- 8.1. Immunoassays Development and New Directions -- 8.2. Methodology and Instrumentation -- 8.2.1. Solid Phase/Planar Assays -- 8.2.1.1. Multiplexed ELISA -- 8.2.1.2. Electrochemical Multiplexed ELISA -- 8.2.1.3. Membrane-Based Assay -- 8.2.2. Suspension Array Technology/Bead-Based Immunoassays -- 8.2.2.1. Cytometric Bead Assay -- 8.2.2.2. Luminex Screening and Performance Assays -- 8.3. MIA Implementation -- 8.3.1. Sampling Qualified Specimen for MIA -- 8.3.2. Analytical Challenges and Clinical Utility -- 8.3.2.1. Cytokines/Biomarkers Stability -- 8.3.2.2. The Importance of Validation -- 8.3.2.2.1. Case 1 -- 8.3.2.2.2. Case 2 -- 8.3.2.3. The IL-6 Case (Systematic Review).

8.4. The Immunoassay Market: Opportunities and Issues -- Acknowledgments -- References -- Chapter 9: Molecular Imaging to Identify the Vulnerable Plaque: From Basic Research to Clinical Practice -- 9.1. Introduction -- 9.2. Molecular Imaging of Inflammation -- 9.2.1. Preclinical -- 9.2.2. Clinical -- 9.3. Molecular Imaging of Cell Death -- 9.3.1. Preclinical -- 9.3.2. Clinical -- 9.4. Molecular Imaging of Remodeling -- 9.4.1. Preclinical -- 9.5. Molecular Imaging of Thrombosis -- 9.5.1. Preclinical -- 9.6. Molecular Imaging of (Micro) Calcification -- 9.6.1. Preclinical -- 9.6.2. Clinical -- 9.7. Socioeconomic Impact of Molecular Imaging -- 9.8. Conclusion and Future Perspectives -- References -- Section 3: Targeting of the Inflammatory Response -- Chapter 10: Mineralcorticoid Receptor Antagonists -- 10.1. Introduction -- 10.2. Molecular Basis for the Clinical Use of MR Antagonist in HF -- 10.2.1. Generalities -- 10.2.2. Inflammation -- 10.2.3. Cardiac Fibrosis -- 10.3. Pharmacology of Mineralcorticoid Receptor Antagonist -- 10.4. Clinical Evidences -- 10.4.1. Systolic HF -- 10.4.2. Diastolic HF -- 10.4.3. Arrhythmias -- 10.5. Conclusion and Future Perspectives -- References -- Chapter 11: PPARs as Modulators of Cardiac Metabolism and Inflammation -- 11.1. Introduction -- 11.2. Peroxisome Proliferator-Activated Receptors -- 11.3. PPARs and the Control of Cardiac Energy Metabolism -- 11.3.1. Role of PPAR α -- 11.3.2. Role of PPAR β / δ -- 11.3.3. Role of PPAR γ -- 11.4. PPARs and Cardiac Inflammation -- 11.4.1. PPAR α -- 11.4.2. PPAR β / δ -- 11.4.3. PPAR γ -- 11.5. Cross Talk Between Cardiac Metabolism and Inflammation -- 11.5.1. Modulation of Inflammation/Metabolism by PPARs -- 11.5.2. Sirt1 Couples Inflammation and Metabolism in the Heart -- 11.5.3. The FGF21 Autocrine Pathway -- 11.6. PPAR Agonists and Heart Failure Treatment.

11.7. Conclusions and Perspectives.

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.

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Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2019. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.

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