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Inflammatory Atherosclerosis
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Inflammatory Atherosclerosis
Richard J.
Frink
Sacramento,
2002
© 2002 Richard J. Frink
atherosclerosis
Table of Contents
Book Information
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
Copyright © 2002 Richard J. Frink
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