The Role of Immune Mechanisms in Cardiovascular Disease

Herausgegeben von Schultheiss, Heinz-Peter; Schwimmbeck, Peter

• Broschiertes Buch

Produktbeschreibung

An involvement of the immune system is suspected in various cardiovascular diseases. Recent advances in the fields of molecular biology, genetics, cell biology, and immunology have made it possible to identify several pathomechanisms. However, still more questions arise with regard to the pathophysiology, diagnosis, and treatment of immunologically mediated cardiovascular diseases. In this book, leading scientists and clinicians from different areas of cardiology present the state-of-the-art knowledge on the involve ment of the immune system in myocardial and vascular diseases. In the field of myocarditis, both the virological and the immunological findings are presented, and the interactions between the virus and the immune system are discussed. Since the cellular immune system and its mediators play an important role in the inflammation by bacteria that cause endocarditis and septic shock, studies investigating the underlying pathomechanisms are de scribed. Another major topic in this volume is the involvement of the immune system in arteriosclerosis and coronary heart disease, which represents an important problem in clinical cardiology. The final chapter addresses the question of therapeutic options, presenting new approaches for a specific and effective therapy based on the current knowledge of immunologically mediated cardiovascular diseases.

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Produktdetails

• Verlag: Springer / Springer Berlin Heidelberg / Springer, Berlin
• Artikelnr. des Verlages: 978-3-540-61358-9
• 1996.
• Seitenzahl: 340
• Erscheinungstermin: 17. Oktober 1996
• Englisch
• Abmessung: 235mm x 155mm x 19mm
• Gewicht: 525g
• ISBN-13: 9783540613589
• ISBN-10: 3540613587
• Artikelnr.: 25313006

Inhaltsangabe

The Immunology of Myocarditis.- Mechanisms and Genetics of Autoimmunity.- Molecular Pathogenesis of Myocarditis and Cardiomyopathy: Analysis of Virus-Receptor Interactions and Tyrosine Phosphorylation Events.- Coxsackievirus Genetics and the Cardiovirulent Viral Phenotype.- Lessons from Animal Models of Viral Myocarditis.- The Role of Cytokines in the Pathogenesis of Myocarditis.- The Role of Heart Infiltrating Cells in Myocyte Injury.- The Significance of T Cell Responses in Human Myocarditis.- The Possible Pathogenic Role of Autoantibodies in Myocarditis and Dilated Cardiomyopathy.- The Adenine Nucleotide Translocator: A Major Autoantigen in Myocarditis and Dilated Cardiomyopathy.- Immunohistochemical Analysis of Inflammatory Heart Disease.- Immunological Mediators in Inflammation of the Heart.- Adhesion Molecule Induction and Expression in Neutrophil-Induced Myocardial Injury.- Molecular Mechanisms of Adhesion of Staphylococcus Aureus to Cardiac Surfaces and Vegetations.- Endotoxins as Potential Mediators of Myocardial Depression.- Immunological Mediators in Arteriosclerosis.- Transplant Associated Coronary Artery Disease.- Role of Ischemia/Reperfusion Injury in Organ Transplantation.- The Role of NO Synthases in Immunological Diseases: Importance for Left Ventricular Function.- The Role of the Endothelium in Atherosclerosis.- Immune and Inflammatory Responses in the Human Atherosclerotic Plaque.- Inflammation in Acute Coronary Syndromes.- Immunological Mechanisms in Myocardial Reperfusion Injury.- Metalloproteinases and Atherosclerotic Plaque Rupture.- Potential Role of Human Cytomegalovirus and Its Interaction with p53 in Coronary Restenosis.- Therapeutic Approaches for Immune-Mediated Cardiovascular Diseases.- Protective Effects of Monoclonal Antibodies to Cell Adhesion Glycoproteins in Models of Cardiac Reperfusion Injury and Leukocyte/Vascular Responses.- Prevention of Arterial Restenosis of Rapamycin and Mycophenolate Mofetil: A New Role for Novel Immunosuppressants in the Prevention of Post-Balloon Angioplasty Restenosis?.- Treatment of Inflammatory Cardiomyopathy with Corticosteroids.- The Genetics of Dilated Cardiomyopathy.- Mechanisms of Allograft Rejection and Therapeutic Options.