Excerpt

Broadly speaking, the cause or the etiologic agent responsible for producing atherosclerosis remains unknown. The most widely accepted theory is “Response-to-Injury,” but the initiating injurious agent has yet to be identified. Until the injurious agent is identified, we must treat the symptoms and manifestations produced by the injurious agent rather than the agent itself...a poor bargain for the clinician.

This book attempts to show the nature and characteristics of the injurious agent through study of the gross and microscopic changes taking place in the coronary arteries of patients with and without clinical coronary disease. The specific injurious agent(s) may be unknown, but we can characterize the agent(s) to gain a deeper understanding of the processes involved.

Contents

• Preface
• Acknowledgements
• Introduction
• Chapter 1. The Beginnings. A Multicentric Disease
  • The Injurious Agent
  • Response-to-Injury
  • Proteoglycans and the Extracellular Matrix
  • Adaptive Intimal Thickening
  • Early Atherosclerotic Lesions
  • Advanced Degeneration
  • In Review
  • Unanswered Questions
• Chapter 2. The Smooth Muscle Cell. The Pivot in Atherosclerosis
  • The Fibroproliferative Response
  • Atherosclerotic Fibrous Tissue
  • Other Types of Vascular Fibrous Tissue
  • The Smooth Muscle Cell
  • Degeneration and Necrosis
  • In Review
  • Unanswered Questions
• Chapter 3. Inflammation. A Sign of Active Disease
  • Chronic Inflammation
  • “Active” Inflammatory Atherosclerotic Disease
  • Adventitial Inflammation
  • The Magnitude of Injury
  • Luminal Stenosis and Inflammation
  • Failure of Inflammatory Defenses
  • Natural History of Wall Injury
  • Clinical Manifestations of Atherosclerotic Inflammation
  • In Review
  • Unanswered Questions
• Chapter 4. Atheromas Are Caseous Abscesses
  • The Necrotic Core
  • Size of Atheroma and Luminal Stenosis
  • Atheromas Are Similar to Bacterial Abscesses
  • Proteolytic Enzymes
  • “Exit” Tracts
  • Cleavage Planes
  • Plaque Shoulder Ulcerations
  • Increased Intraplaque Pressure
  • Thermal Heterogeneity
  • In Review
  • Unanswered Questions
• Chapter 5. Calcification: A Physiologic Defense
  • Aging and Vascular Calcification
  • Calcification and Luminal Stenosis
  • Luminal Stenosis without Calcification
  • Calcification Is Similar to Bone Formation
  • Matrix Vesicles
  • Osteoid
  • Osteoid and Atherosclerotic Calcification
  • Normal Bone and Cartilage
  • Evolutionary Purpose
  • Reversibility of Coronary Calcification
  • Sequence of Events
  • In Review
• Chapter 6. Adventitia – The Ultimate Defense
  • Adventitial Thickening over Atherosclerotic Plaques
  • Evolutionary Purpose of Adventitial Thickening
  • Adventitial Resistence to the IA
  • Histologic Features of Adventitial Thickening
  • Significance
  • In Review
• Chapter 7. Surface Erosions
  • Endothelial Vulnerability or Dysfunction
  • Proteolytic Enzymes
  • Longitudinal Spread of the IA
  • Destruction of the Fibrous Cap
  • Absence of Resolution
  • Frequency of Surface Erosions
  • Significance of These Findings
  • In Review
• Chapter 8. Blind Pockets and False Channels
  • False Channels
  • Formation of False Channels
  • Frequency of False Channels
  • Blind Pockets
  • Blind Pockets and Acute Occlusions
  • Clinical Implications
  • In Review
• Chapter 9. Thrombosis and the Injurious Agent
  • Platelets, Injury Repair and Thrombosis
  • Pathologic Hemostasis and Thrombosis
  • Thromboregulatory Control
  • Luminal Stenosis and Thrombosis
  • Wall Injury and Thrombosis
  • Evolutionary Purpose
  • Clinical Implications
  • In Review
• Chapter 10. Chronic Ulcerated Plaques
  • Chronicity of UPs
  • Depth and Extent of UPs
  • UPs and Fibrotic Luminal Stenosis
  • Component versus Complication
  • Early PU Is the Norm
  • Absence of Thrombus
  • In Review
• Chapter 11. What Is the Injurious Agent?
  • Single versus Multiple IAs
  • Mechanism of Progression
  • Evolutionary Purpose
  • Single versus Multiple Infectious Agents
  • Hypothesis
  • Mechanisms of Injury
  • Autoimmunity
  • In Review
• Chapter 12. The Toxic Atheroma
  • The Fundamental Acute Lesion
  • The Toxic Atheroma
  • Embolization of Plaque Tissue
  • Initial Symptoms
  • Downstream Structures
  • In Review
• Chapter 13. Plaque Toxins and Clinical Coronary Syndromes
  • The Pathogenesis of Angina Pectoris Pain
  • Variant (Prinzmetals) Angina (VA)
  • Sudden Cardiac Death (SCD)
  • Unstable Angina (UA) and Non S-T Segment Elevation Myocardial Infarction (NSTEMI)
  • S-T Elevation Myocardial Infarction (STEMI)
  • Thrombosis versus Plaque Toxins
  • Myocardial Rupture and Thrombolytic Drugs
  • Stunned Myocardium
  • Silent Ischemia (SI)
  • Oral IIB/IIIA Inhibitors
  • Aspirin (ASA), UPs, and Plaque Toxins
  • Conclusions
  • Future Directions
• The Injection Technique
• References
• Abbreviations

Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The author and the publishers have, as far as it is possible, taken care to ensure that the information given in this text is accurate and up-to-date. However, readers are strongly advised to confirm that the information, especially with regard to drug usage, complies with the latest legislation and standards of practice.