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Collateral Circulation of the Heart (eBook)

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2009 | 2009
XVI, 450 Seiten
Springer London (Verlag)
978-1-84882-342-6 (ISBN)

Lese- und Medienproben

Collateral Circulation of the Heart - Christian Seiler
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The sober explanation for this book is a call by the Springer-Verlag, London, to edit a publication on 'The functional relevance of the collateral circulation' of the heart. Alternatively, it could be 'sold' as the result of my intention to reduce entropy of 18 years of scientific work on the topic of the coronary circulation, which was itself meant to diminish the amount of 'useless' energy. Such a process of reducing disarray in a system with the aim of grasping it better is related to simplification, which carries the risk of introducing error. This can be exemplified by the historic view of angina pectoris, which used to be simplified as being always fatal, thus obscuring for nearly two centuries the view of a 'self-healing' mechanism such as the collateral circulation of the heart. It would be na?¨ve, to assume the present work to be free of erroneous oversimplification, because the very nature of scientific work is related to generating (simple) hypotheses with their subsequent falsification. In that context and bluntly, my primary interest in the field of the collateral circulation was not initiated with a vision of eradicating the consequences of coronary artery disease (CAD) by promoting the growth of natural bypasses. The time for such sizeable ideas had passed in the 1970s with the start of the work by Wolfgang Schaper.
The sober explanation for this book is a call by the Springer-Verlag, London, to edit a publication on 'The functional relevance of the collateral circulation' of the heart. Alternatively, it could be 'sold' as the result of my intention to reduce entropy of 18 years of scientific work on the topic of the coronary circulation, which was itself meant to diminish the amount of 'useless' energy. Such a process of reducing disarray in a system with the aim of grasping it better is related to simplification, which carries the risk of introducing error. This can be exemplified by the historic view of angina pectoris, which used to be simplified as being always fatal, thus obscuring for nearly two centuries the view of a 'self-healing' mechanism such as the collateral circulation of the heart. It would be na?*ve, to assume the present work to be free of erroneous oversimplification, because the very nature of scientific work is related to generating (simple) hypotheses with their subsequent falsification. In that context and bluntly, my primary interest in the field of the collateral circulation was not initiated with a vision of eradicating the consequences of coronary artery disease (CAD) by promoting the growth of natural bypasses. The time for such sizeable ideas had passed in the 1970s with the start of the work by Wolfgang Schaper.

Preface 6
Acknowledgments 8
Contents 9
Chapter 1 Relevance of the Human Coronary Collateral Circulation 13
1.1 Historical Aspects 13
1.1.1 Introduction 13
1.1.2 First Observations of Collateral Vessels 15
1.1.3 Post-mortem Assessment 20
1.1.3.1 Imaging Techniques 21
1.1.3.2 Coronary Collateral Vessels in Neonates 27
1.1.3.3 Pathoanatomic Studies by Fulton 28
1.1.4 In Vivo Assessment 32
1.1.4.1 First Clinico-pathological Associations 32
1.1.4.2 First In Vivo Coronary Angiographic Studies 33
1.1.4.3 Direct Haemodynamic Collateral Measurements During Bypass Surgery 34
1.1.4.4 Direct Haemodynamic Collateral Measurements During Angioplasty 36
1.1.4.5 Functional Collaterals in the Absence of Coronary Atherosclerosis 37
1.2 Interspecies Differences 39
1.2.1 Introduction 39
1.2.2 Pig Versus Dog as a Model for the Human Coronary Collateral Circulation 40
1.2.3 Extensive Interspecies Comparison of the Coronary Collateral Circulation 45
1.3 Individual Relevance 47
1.3.1 Introduction 47
1.3.2 Collaterals and Transcoronary Ablation of Septal Hypertrophy 48
1.3.3 Coronary Collateral Steal 51
1.3.4 Risk of Coronary Restenosis and Collateral Flow 52
1.3.5 Beneficial Effect of Collaterals on Myocardial Salvage 53
1.4 Collective Prognostic Relevance 58
1.4.1 Introduction 59
1.4.2 Endpoints for Defining Prognosis and Assessment of Collateral Flow 59
1.4.2.1 Surrogate Endpoints 60
1.4.2.2 Clinical Endpoints 63
1.4.3 Acute Coronary Artery Disease and Clinical Events in Relation to Collaterals 64
1.4.3.1 Studies in the Pre-angioplasty Era 64
1.4.3.2 Studies in Patients Undergoing Primary PCI 66
1.4.4 Chronic Coronary Artery Disease and Clinical Events in Relation to Collaterals 68
1.4.4.1 Angiographic Collateral Grading 68
1.4.4.2 Quantitative Collateral Assessment 71
Abbreviations 75
References 76
Chapter 2 Assessment of the Human Coronary Collateral Circulation 83
2.1 Theoretical Aspects in the Assessment of the Coronary Collateral Circulation 83
2.1.1 Introduction 84
2.1.2 Coronary Blood Flow Measurements in the Animal Model 84
2.1.3 Structural Design and Function of the Coronary Circulation 85
2.1.4 Signs of Developing Tolerance to Myocardial Ischaemia 94
2.2 Non-invasive Characterization of Collaterals 101
2.2.1 Indicators for the Coronary Collateral Circulation 101
2.2.2 The Surface Lead ECG for Estimation of the Collateral Circulation 102
2.2.2.1 Chronic CAD 102
2.2.2.2 Acute Myocardial Infarction 106
2.3 The Coronary Occlusion Model 109
2.3.1 Introduction 110
2.3.2 Natural Occlusion Model 112
2.3.3 Artificial Occlusion Model 116
2.3.3.1 Occlusion Site 117
2.3.3.2 Occlusion Duration 117
2.3.4 Angina Pectoris and ECG During Coronary Occlusion 118
2.3.4.1 Angina Pectoris 118
2.3.4.2 ECG Signs of Ischaemia 119
2.3.5 LV Function During Coronary Occlusion 123
2.4 Angiographic Collateral Assessment 126
2.4.1 Introduction 127
2.4.2 Angiographic Collateral Pathways 128
2.4.3 Qualitative Angiographic Methods 131
2.4.3.1 Collateral Flow Grade 132
2.4.3.2 Collateral Frame Count 133
2.4.3.3 Bifurcation Count 133
2.4.3.4 Collateral Length Grade 134
2.4.3.5 Collateral Recipient Filling Grade 134
2.4.4 Semiquantitative Angiographic Methods 135
2.4.5 Washout Collaterometry 136
2.5 Quantitative Coronary Pressure and Doppler Sensor Measurements 161
2.5.1 Introduction 139
2.5.2 Determinants of Distal Coronary Occlusive Pressure 142
2.5.3 Validation of Pressure-Derived Collateral Flow Index 143
2.5.3.1 Theoretical Reason for a Difference Between CFIp and CFIv 147
2.5.3.2 Influence of LV Diastolic Pressure on CFIp 151
2.5.4 Technical Considerations, Limitations, Pitfalls and Risks of Collateral Flow Index Measurements 154
2.5.4.1 Pressure-Derived CFI Measurements 154
2.5.4.2 Doppler-Derived CFI Measurements 158
2.5.4.3 Influence of Pharmacologically Induced Hyperaemia on CFI Measurements 159
2.5.4.4 Safety of CFI Measurements in Normal Coronary Arteries 160
2.6 Quantitative Collateral Perfusion Measurements 161
2.6.1 Myocardial Contrast Echocardiography for Collateral Perfusion Measurement 161
2.6.2 Relevance of Direct Coronary Pressure-Flow Measurements 165
Abbreviations 167
References 168
Chapter 3 Pathogenesis of the Human Coronary Collateral Circulation 176
3.1 Introduction 176
3.2 Frequency Distribution of Collateral Flow in Humans 179
3.2.1 Introduction 179
3.2.2 Prevalence of Collaterals in the Absence of CAD 180
3.2.3 Prevalence of Collaterals in Non-occlusive CAD 191
3.2.4 Prevalence of Collaterals in Occlusive CAD 195
3.3 Clinical Determinants of Collateral Flow 199
3.3.1 Introduction 200
3.3.2 Determinants of Preformed Coronary Collaterals 202
3.3.2.1 Gestational Age and Maternal Age at Birth 205
3.3.2.2 Congenital Heart Disease 205
3.3.2.3 Racial Differences 205
3.3.2.4 Anaemia 205
3.3.2.5 Non-atherosclerotic Heart Diseases 206
3.3.2.6 In Vivo Obtained Determinants of Preformed Coronary Collaterals 207
3.3.3 Determinants of Collateral Function in CAD 207
3.3.3.1 Severity of CAD, Duration of Angina Pectoris and Ischaemic Area at Risk 207
3.3.3.2 Age 211
3.3.3.3 Gender 212
3.3.3.4 Cardiovascular Risk Factors 212
3.3.3.5 Heart Rate 215
3.3.3.6 Cardiovascular Medication 215
3.4 Cellular Determinants of Collateral Flow 216
3.4.1 Introduction 217
3.4.2 Trigger of Arteriogenesis 217
3.4.3 Endothelial Activation 220
3.4.4 The Role of Monocytes 224
3.4.4.1 Acute Coronary Syndrome 225
3.4.4.2 Chronic Stable CAD 228
3.4.5 The Role of Lymphocytes 230
3.4.6 The Role of Stem and Progenitor Cells 230
3.5 Genetic Determinants of Collateral Flow 232
3.5.1 Introduction 232
3.5.2 Evidence from Experimental Studies 233
3.5.3 Genetic Markers of Human Coronary Collaterals 235
Abbreviations 237
References 239
Chapter 4 Pathophysiology of the Human Coronary Collateral Circulation 245
4.1 Introduction 245
4.2 Fluid Shear Stress and Vasomotor Function 245
4.2.1 Introduction 246
4.2.2 Limited and Adaptive Arterial Wall Shear Stress 247
4.2.2.1 Theoretical Considerations 247
4.2.2.2 Fluid Shear Stress and Endothelial Damage 250
4.2.2.3 Limited Shear Stress Control in the Human Epicardial Coronary Circulation 251
4.2.3 Flow-Mediated Vascular Function in ‘Native’ and Collateral Arteries 252
4.2.3.1 Flow-Mediated Vascular Function in ‘Native’ Arteries 252
4.2.3.2 Flow-Mediated Vascular Function in Coronary Collateral Arteries 255
4.2.3.3 Isometric Physical Exercise and Coronary Collateral Function 256
4.2.3.4 Adenosine and Flow-Mediated Coronary Vascular Function 259
4.3 Vascular Resistance Distribution and the Collateral Network 265
4.3.1 Introduction 265
4.3.2 Redistribution of Blood due to Altering Microvascular Resistances 266
4.3.2.1 Biophysical Mechanisms 266
4.3.2.2 Evidence for the Occurrence of Coronary Steal 270
4.3.2.3 Conditions for Coronary Steal 271
4.3.3 ‘Redistribution’ of Blood due to Altering Macrovascular Resistances 275
4.3.3.1 Recanalization of CTO 276
4.3.3.2 Revascularization of Stenotic Lesions 279
4.4 Stimuli for Lowering Coronary Collateral Resistance 281
4.4.1 Introduction 281
4.4.2 Neurohumoral and Pharmacological Stimuli 281
4.4.2.1 Neurohumoral Stimuli 282
4.4.2.2 Pharmacological Stimuli 286
4.4.3 Single and Repetitive Bouts of Myocardial Ischaemia 291
4.4.3.1 Ischaemia Induced Myocardial Hyperaemia 291
4.4.3.2 Repetitive Episodes of Ischaemia and Collateral Recruitment 294
4.5 Extracoronary Physical Determinants of Collateral Flow 296
4.5.1 Introduction 297
4.5.2 LV Preload, Diastolic Coronary Perfusion Pressure and Heart Rate 298
4.5.2.1 LV Preload 298
4.5.2.2 Diastolic Coronary Perfusion Pressure 303
4.5.2.3 Heart Rate 303
4.5.3 LV Contraction 304
4.5.4 LV Afterload 306
Abbreviations 307
References 307
Chapter 5 Therapeutic Promotion of the Human Coronary Collateral Circulation 314
5.1 Introduction 314
5.2 Angiogenic Therapy 316
5.2.1 Angiogenesis 317
5.2.2 Angiogenic Protein and Gene Delivery 319
5.2.2.1 Fibroblast Growth Factors 320
5.2.2.2 Vascular Endothelial Growth Factors 327
5.2.3 Other Pharmacological Substances with Potential Angiogenic Activity 336
5.2.3.1 Heparin 336
5.2.3.2 Dipyridamole 337
5.2.3.3 Nitric Oxide 339
5.2.3.4 Sildenafil 340
5.3 Arteriogenic Therapy 341
5.3.1 Arteriogenesis 342
5.3.1.1 Mechanisms of Arteriogenesis 344
5.3.2 Arteriogenic Substances 349
5.3.2.1 Monocyte Chemoattractant Protein-1 349
5.3.2.2 Colony-Stimulating Factors 352
5.3.2.3 Transforming Growth Factor beta1 362
5.3.2.4 Fibroblast Growth Factors 363
5.3.2.5 Statins 364
5.4 Cell-Based Promotion of the Collateral Circulation 365
5.4.1 Introduction 366
5.4.2 Vasculogenesis 366
5.4.3 Cell-Based Therapy of Myocardial Ischaemia in Humans 369
5.5 Physical Promotion of the Collateral Circulation 373
5.5.1 Introduction 374
5.5.2 Recurrent Increase in Cardiac Output 376
5.5.2.1 Native Epicardial Coronary Artery Remodelling and Exercise 376
5.5.2.2 Exercise and Functional Changes of Coronary Anastomoses Without CAD 378
5.5.2.3 Exercise and Functional Changes of Collaterals with Coronary Obstructions 380
5.5.2.4 Exercise and Functional Changes of Collaterals in Human CAD 384
5.5.3 Prolongation of Diastole 390
5.5.4 Diastolic Perfusion Pressure Augmentation 393
5.5.5 Coronary Back Pressure Augmentation 395
5.6 Issues of Neovascularization to be Resolved 397
5.6.1 Introduction 398
5.6.2 Arteriogenesis Versus Atherogenesis 398
5.6.3 Neovascularization and Tumour Growth 399
5.6.4 Growth Factor Delivery Mode 400
Abbreviations 402
References 403
Index 418

Erscheint lt. Verlag 12.6.2009
Zusatzinfo XVI, 450 p. 321 illus., 120 illus. in color.
Verlagsort London
Sprache englisch
Themenwelt Medizin / Pharmazie Gesundheitswesen
Medizin / Pharmazie Medizinische Fachgebiete Allgemeinmedizin
Medizinische Fachgebiete Chirurgie Herz- / Thorax- / Gefäßchirurgie
Medizinische Fachgebiete Innere Medizin Kardiologie / Angiologie
Medizin / Pharmazie Medizinische Fachgebiete Radiologie / Bildgebende Verfahren
Studium 1. Studienabschnitt (Vorklinik) Biochemie / Molekularbiologie
Schlagworte Angina pectoris • angiogenesis • Cells • Circulation • Collateral Circulation Heart • coronary artery disease • heart • pathophysiology • Physiology
ISBN-10 1-84882-342-8 / 1848823428
ISBN-13 978-1-84882-342-6 / 9781848823426
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