E-Book, Englisch, 450 Seiten
Seiler Collateral Circulation of the Heart
1. Auflage 2009
ISBN: 978-1-84882-342-6
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark
E-Book, Englisch, 450 Seiten
ISBN: 978-1-84882-342-6
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark
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.
Autoren/Hrsg.
Weitere Infos & Material
1;Preface;6
2;Acknowledgments;8
3;Contents;9
4;Chapter 1 Relevance of the Human Coronary Collateral Circulation;13
4.1;1.1 Historical Aspects;13
4.1.1;1.1.1 Introduction;13
4.1.2;1.1.2 First Observations of Collateral Vessels;15
4.1.3;1.1.3 Post-mortem Assessment;20
4.1.3.1;1.1.3.1 Imaging Techniques;21
4.1.3.2;1.1.3.2 Coronary Collateral Vessels in Neonates;27
4.1.3.3;1.1.3.3 Pathoanatomic Studies by Fulton;28
4.1.4;1.1.4 In Vivo Assessment;32
4.1.4.1;1.1.4.1 First Clinico-pathological Associations;32
4.1.4.2;1.1.4.2 First In Vivo Coronary Angiographic Studies;33
4.1.4.3;1.1.4.3 Direct Haemodynamic Collateral Measurements During Bypass Surgery;34
4.1.4.4;1.1.4.4 Direct Haemodynamic Collateral Measurements During Angioplasty;36
4.1.4.5;1.1.4.5 Functional Collaterals in the Absence of Coronary Atherosclerosis;37
4.2;1.2 Interspecies Differences;39
4.2.1;1.2.1 Introduction;39
4.2.2;1.2.2 Pig Versus Dog as a Model for the Human Coronary Collateral Circulation;40
4.2.3;1.2.3 Extensive Interspecies Comparison of the Coronary Collateral Circulation;45
4.3;1.3 Individual Relevance;47
4.3.1;1.3.1 Introduction;47
4.3.2;1.3.2 Collaterals and Transcoronary Ablation of Septal Hypertrophy;48
4.3.3;1.3.3 Coronary Collateral Steal;51
4.3.4;1.3.4 Risk of Coronary Restenosis and Collateral Flow;52
4.3.5;1.3.5 Beneficial Effect of Collaterals on Myocardial Salvage;53
4.4;1.4 Collective Prognostic Relevance;58
4.4.1;1.4.1 Introduction;59
4.4.2;1.4.2 Endpoints for Defining Prognosis and Assessment of Collateral Flow;59
4.4.2.1;1.4.2.1 Surrogate Endpoints;60
4.4.2.2;1.4.2.2 Clinical Endpoints;63
4.4.3;1.4.3 Acute Coronary Artery Disease and Clinical Events in Relation to Collaterals;64
4.4.3.1;1.4.3.1 Studies in the Pre-angioplasty Era;64
4.4.3.2;1.4.3.2 Studies in Patients Undergoing Primary PCI;66
4.4.4;1.4.4 Chronic Coronary Artery Disease and Clinical Events in Relation to Collaterals;68
4.4.4.1;1.4.4.1 Angiographic Collateral Grading;68
4.4.4.2;1.4.4.2 Quantitative Collateral Assessment;71
4.5;Abbreviations;75
4.6;References;76
5;Chapter 2 Assessment of the Human Coronary Collateral Circulation;83
5.1;2.1 Theoretical Aspects in the Assessment of the Coronary Collateral Circulation;83
5.1.1;2.1.1 Introduction;84
5.1.2;2.1.2 Coronary Blood Flow Measurements in the Animal Model;84
5.1.3;2.1.3 Structural Design and Function of the Coronary Circulation;85
5.1.4;2.1.4 Signs of Developing Tolerance to Myocardial Ischaemia;94
5.2;2.2 Non-invasive Characterization of Collaterals;101
5.2.1;2.2.1 Indicators for the Coronary Collateral Circulation;101
5.2.2;2.2.2 The Surface Lead ECG for Estimation of the Collateral Circulation;102
5.2.2.1;2.2.2.1 Chronic CAD;102
5.2.2.2;2.2.2.2 Acute Myocardial Infarction;106
5.3;2.3 The Coronary Occlusion Model;109
5.3.1;2.3.1 Introduction;110
5.3.2;2.3.2 Natural Occlusion Model;112
5.3.3;2.3.3 Artificial Occlusion Model;116
5.3.3.1;2.3.3.1 Occlusion Site;117
5.3.3.2;2.3.3.2 Occlusion Duration;117
5.3.4;2.3.4 Angina Pectoris and ECG During Coronary Occlusion;118
5.3.4.1;2.3.4.1 Angina Pectoris;118
5.3.4.2;2.3.4.2 ECG Signs of Ischaemia;119
5.3.5;2.3.5 LV Function During Coronary Occlusion;123
5.4;2.4 Angiographic Collateral Assessment;126
5.4.1;2.4.1 Introduction;127
5.4.2;2.4.2 Angiographic Collateral Pathways;128
5.4.3;2.4.3 Qualitative Angiographic Methods;131
5.4.3.1;2.4.3.1 Collateral Flow Grade;132
5.4.3.2;2.4.3.2 Collateral Frame Count;133
5.4.3.3;2.4.3.3 Bifurcation Count;133
5.4.3.4;2.4.3.4 Collateral Length Grade;134
5.4.3.5;2.4.3.5 Collateral Recipient Filling Grade;134
5.4.4;2.4.4 Semiquantitative Angiographic Methods;135
5.4.5;2.4.5 Washout Collaterometry;136
5.5;2.5 Quantitative Coronary Pressure and Doppler Sensor Measurements;161
5.5.1;2.5.1 Introduction;139
5.5.2;2.5.2 Determinants of Distal Coronary Occlusive Pressure;142
5.5.3;2.5.3 Validation of Pressure-Derived Collateral Flow Index;143
5.5.3.1;2.5.3.1 Theoretical Reason for a Difference Between CFIp and CFIv;147
5.5.3.2;2.5.3.2 Influence of LV Diastolic Pressure on CFIp;151
5.5.4;2.5.4 Technical Considerations, Limitations, Pitfalls and Risks of Collateral Flow Index Measurements;154
5.5.4.1;2.5.4.1 Pressure-Derived CFI Measurements;154
5.5.4.2;2.5.4.2 Doppler-Derived CFI Measurements;158
5.5.4.3;2.5.4.3 Influence of Pharmacologically Induced Hyperaemia on CFI Measurements;159
5.5.4.4;2.5.4.4 Safety of CFI Measurements in Normal Coronary Arteries;160
5.6;2.6 Quantitative Collateral Perfusion Measurements;161
5.6.1;2.6.1 Myocardial Contrast Echocardiography for Collateral Perfusion Measurement;161
5.6.2;2.6.2 Relevance of Direct Coronary Pressure-Flow Measurements;165
5.7;Abbreviations;167
5.8;References;168
6;Chapter 3 Pathogenesis of the Human Coronary Collateral Circulation;176
6.1;3.1 Introduction;176
6.2;3.2 Frequency Distribution of Collateral Flow in Humans;179
6.2.1;3.2.1 Introduction;179
6.2.2;3.2.2 Prevalence of Collaterals in the Absence of CAD;180
6.2.3;3.2.3 Prevalence of Collaterals in Non-occlusive CAD;191
6.2.4;3.2.4 Prevalence of Collaterals in Occlusive CAD;195
6.3;3.3 Clinical Determinants of Collateral Flow;199
6.3.1;3.3.1 Introduction;200
6.3.2;3.3.2 Determinants of Preformed Coronary Collaterals;202
6.3.2.1;3.3.2.1 Gestational Age and Maternal Age at Birth;205
6.3.2.2;3.3.2.2 Congenital Heart Disease;205
6.3.2.3;3.3.2.3 Racial Differences;205
6.3.2.4;3.3.2.4 Anaemia;205
6.3.2.5;3.3.2.5 Non-atherosclerotic Heart Diseases;206
6.3.2.6;3.3.2.6 In Vivo Obtained Determinants of Preformed Coronary Collaterals;207
6.3.3;3.3.3 Determinants of Collateral Function in CAD;207
6.3.3.1;3.3.3.1 Severity of CAD, Duration of Angina Pectoris and Ischaemic Area at Risk;207
6.3.3.2;3.3.3.2 Age;211
6.3.3.3;3.3.3.3 Gender;212
6.3.3.4;3.3.3.4 Cardiovascular Risk Factors;212
6.3.3.5;3.3.3.5 Heart Rate;215
6.3.3.6;3.3.3.6 Cardiovascular Medication;215
6.4;3.4 Cellular Determinants of Collateral Flow;216
6.4.1;3.4.1 Introduction;217
6.4.2;3.4.2 Trigger of Arteriogenesis;217
6.4.3;3.4.3 Endothelial Activation;220
6.4.4;3.4.4 The Role of Monocytes;224
6.4.4.1;3.4.4.1 Acute Coronary Syndrome;225
6.4.4.2;3.4.4.2 Chronic Stable CAD;228
6.4.5;3.4.5 The Role of Lymphocytes;230
6.4.6;3.4.6 The Role of Stem and Progenitor Cells;230
6.5;3.5 Genetic Determinants of Collateral Flow;232
6.5.1;3.5.1 Introduction;232
6.5.2;3.5.2 Evidence from Experimental Studies;233
6.5.3;3.5.3 Genetic Markers of Human Coronary Collaterals;235
6.6;Abbreviations;237
6.7;References;239
7;Chapter 4 Pathophysiology of the Human Coronary Collateral Circulation;245
7.1;4.1 Introduction;245
7.2;4.2 Fluid Shear Stress and Vasomotor Function;245
7.2.1;4.2.1 Introduction;246
7.2.2;4.2.2 Limited and Adaptive Arterial Wall Shear Stress;247
7.2.2.1;4.2.2.1 Theoretical Considerations;247
7.2.2.2;4.2.2.2 Fluid Shear Stress and Endothelial Damage;250
7.2.2.3;4.2.2.3 Limited Shear Stress Control in the Human Epicardial Coronary Circulation;251
7.2.3;4.2.3 Flow-Mediated Vascular Function in ‘Native’ and Collateral Arteries;252
7.2.3.1;4.2.3.1 Flow-Mediated Vascular Function in ‘Native’ Arteries;252
7.2.3.2;4.2.3.2 Flow-Mediated Vascular Function in Coronary Collateral Arteries;255
7.2.3.3;4.2.3.3 Isometric Physical Exercise and Coronary Collateral Function;256
7.2.3.4;4.2.3.4 Adenosine and Flow-Mediated Coronary Vascular Function;259
7.3;4.3 Vascular Resistance Distribution and the Collateral Network;265
7.3.1;4.3.1 Introduction;265
7.3.2;4.3.2 Redistribution of Blood due to Altering Microvascular Resistances;266
7.3.2.1;4.3.2.1 Biophysical Mechanisms;266
7.3.2.2;4.3.2.2 Evidence for the Occurrence of Coronary Steal;270
7.3.2.3;4.3.2.3 Conditions for Coronary Steal;271
7.3.3;4.3.3 ‘Redistribution’ of Blood due to Altering Macrovascular Resistances;275
7.3.3.1;4.3.3.1 Recanalization of CTO;276
7.3.3.2;4.3.3.2 Revascularization of Stenotic Lesions;279
7.4;4.4 Stimuli for Lowering Coronary Collateral Resistance;281
7.4.1;4.4.1 Introduction;281
7.4.2;4.4.2 Neurohumoral and Pharmacological Stimuli;281
7.4.2.1;4.4.2.1 Neurohumoral Stimuli;282
7.4.2.2;4.4.2.2 Pharmacological Stimuli;286
7.4.3;4.4.3 Single and Repetitive Bouts of Myocardial Ischaemia;291
7.4.3.1;4.4.3.1 Ischaemia Induced Myocardial Hyperaemia;291
7.4.3.2;4.4.3.2 Repetitive Episodes of Ischaemia and Collateral Recruitment;294
7.5;4.5 Extracoronary Physical Determinants of Collateral Flow;296
7.5.1;4.5.1 Introduction;297
7.5.2;4.5.2 LV Preload, Diastolic Coronary Perfusion Pressure and Heart Rate;298
7.5.2.1;4.5.2.1 LV Preload;298
7.5.2.2;4.5.2.2 Diastolic Coronary Perfusion Pressure;303
7.5.2.3;4.5.2.3 Heart Rate;303
7.5.3;4.5.3 LV Contraction;304
7.5.4;4.5.4 LV Afterload;306
7.6;Abbreviations;307
7.7;References;307
8;Chapter 5 Therapeutic Promotion of the Human Coronary Collateral Circulation;314
8.1;5.1 Introduction;314
8.2;5.2 Angiogenic Therapy;316
8.2.1;5.2.1 Angiogenesis;317
8.2.2;5.2.2 Angiogenic Protein and Gene Delivery;319
8.2.2.1;5.2.2.1 Fibroblast Growth Factors;320
8.2.2.2;5.2.2.2 Vascular Endothelial Growth Factors;327
8.2.3;5.2.3 Other Pharmacological Substances with Potential Angiogenic Activity;336
8.2.3.1;5.2.3.1 Heparin;336
8.2.3.2;5.2.3.2 Dipyridamole;337
8.2.3.3;5.2.3.3 Nitric Oxide;339
8.2.3.4;5.2.3.4 Sildenafil;340
8.3;5.3 Arteriogenic Therapy;341
8.3.1;5.3.1 Arteriogenesis;342
8.3.1.1;5.3.1.1 Mechanisms of Arteriogenesis;344
8.3.2;5.3.2 Arteriogenic Substances;349
8.3.2.1;5.3.2.1 Monocyte Chemoattractant Protein-1;349
8.3.2.2;5.3.2.2 Colony-Stimulating Factors;352
8.3.2.3;5.3.2.3 Transforming Growth Factor beta1;362
8.3.2.4;5.3.2.4 Fibroblast Growth Factors;363
8.3.2.5;5.3.2.5 Statins;364
8.4;5.4 Cell-Based Promotion of the Collateral Circulation;365
8.4.1;5.4.1 Introduction;366
8.4.2;5.4.2 Vasculogenesis;366
8.4.3;5.4.3 Cell-Based Therapy of Myocardial Ischaemia in Humans;369
8.5;5.5 Physical Promotion of the Collateral Circulation;373
8.5.1;5.5.1 Introduction;374
8.5.2;5.5.2 Recurrent Increase in Cardiac Output;376
8.5.2.1;5.5.2.1 Native Epicardial Coronary Artery Remodelling and Exercise;376
8.5.2.2;5.5.2.2 Exercise and Functional Changes of Coronary Anastomoses Without CAD;378
8.5.2.3;5.5.2.3 Exercise and Functional Changes of Collaterals with Coronary Obstructions;380
8.5.2.4;5.5.2.4 Exercise and Functional Changes of Collaterals in Human CAD;384
8.5.3;5.5.3 Prolongation of Diastole;390
8.5.4;5.5.4 Diastolic Perfusion Pressure Augmentation;393
8.5.5;5.5.5 Coronary Back Pressure Augmentation;395
8.6;5.6 Issues of Neovascularization to be Resolved;397
8.6.1;5.6.1 Introduction;398
8.6.2;5.6.2 Arteriogenesis Versus Atherogenesis;398
8.6.3;5.6.3 Neovascularization and Tumour Growth;399
8.6.4;5.6.4 Growth Factor Delivery Mode;400
8.7;Abbreviations;402
8.8;References;403
9;Index;418




