Table of Contents
Dedication
Title page
Copyright page
List of Contributors
Preface
Acknowledgments
About the Companion Website
About the Enhanced Edition
CHAPTER 1: Biophysical Principles and Properties of Cryoablation
Background
Thermodynamics of the cryoablation system
Mechanisms of injury
Lesion characteristics
Factors affecting cryoablation efficacy
Conclusion
CHAPTER 2: Catheter Cryoablation for Pediatric Arrhythmias
Introduction
Cryoablation in immature myocardium – animal studies
Transcatheter cryoablation technique for the treatment of tachyarrhythmias in pediatrics
Outcomes of cryoablation in pediatrics
Cryoablation for other substrates
Cryoablation in congenital heart disease
Practice trends in pediatric cryoablation
CHAPTER 3: Atrioventricular Nodal Reentrant Tachycardia: What Have We Learned from Radiofrequency Catheter Ablation?
Introduction
Basis of catheter ablation for AVNRT
Techniques of radiofrequency catheter ablation
Safety and efficacy of RFCA
Lessons learned from RFCA
Conclusion
Acknowledgements
CHAPTER 4: Catheter Cryoablation for Atrioventricular Nodal Reentrant Tachycardia
Atrioventricular block after radiofrequency catheter ablation for atrioventricular nodal reentrant tachycardia
Is cryoablation free of the complication of permanent inadvertent AVB in the treatment of AVNRT?
Other advantages of using cryoablation to treat AVNRT
Recurrence rates: The Achilles' Heel of cryoablation in treating AVNRT
Procedural techniques of cryoablation for AVNRT
Strategies to decrease the recurrence rate after cryoablation for AVNRT
Conclusions
CHAPTER 5: Cryoballoon Pulmonary Vein Isolation for Atrial Fibrillation
Introduction
Function of the Arctic Front cryoballoon
Ablation of the pulmonary vein antrum – technique
Significance of measuring the proximal balloon temperature
Factors determining lesion size and homogeneity
Confirming adequate balloon occlusion
Impact of pulmonary vein anatomy
Impact of balloon characteristics
Imaging
Special isolation techniques
Confirming isolation
Monitoring pulmonary vein signals
Risk of phrenic nerve palsy
Other adverse events
Anticoagulation
Results of cryoballoon ablation
Outlook and future development
Acknowledgments
CHAPTER 6: Prevention of Phrenic Nerve Palsy during Cryoballoon Ablation for Atrial Fibrillation
Introduction
Anatomy
Mechanisms of phrenic nerve injury
Pacing the phrenic nerve
Monitoring of the phrenic nerve function
Recommendations
See it, hear it, feel it, and measure it
What to do when phrenic nerve injury occurs
Summary
CHAPTER 7: Linear Isthmus Ablation for Atrial Flutter: Catheter Cryoablation versus Radiofrequency Catheter Ablation
Introduction
Atrial flutter terminology
Pathophysiologic mechanisms of AFL
Electrocardiogram diagnosis of AFL
Mapping of AFL
Radiofrequency catheter ablation of AFL
Procedure endpoints for ablation of AFL
Outcomes of radiofrequency catheter ablation of typical AFL
Cryocatheter ablation of typical AFL
Summary
CHAPTER 8: Catheter Cryoablation for the Treatment of Accessory Pathways
Performance of RFCA of APs
Uncommon complications of RFCA for APs
Potential advantages of using cryoablation instead of RFCA in the treatment of APs
Procedural techniques of cryoablation for accessory pathways
Performance of catheter cryoablation of APs
Conclusions
CHAPTER 9: Catheter Cryoablation for the Treatment of Ventricular Arrhythmias
Introduction
History of cryoablation
Cryoablation technology
Conclusions
CHAPTER 10: Catheter Cryoablation for the Treatment of Miscellaneous Arrhythmias
Electrophysiological characteristics and anatomical locations of focal atrial tachycardia
Efficacy and safety of radiofrequency catheter ablation of FAT
Catheter cryoablation treatment for “high-risk” FAT
Radiofrequency and cryothermal ablation for inappropriate sinus tachycardia
Radiofrequency and cryothermal ablation for atrioventricular nodal ablation in atrial fibrillation
Conclusions
Index
To my wife, Lillian, and my little daughter, Nam Nam, for bringing me a new page of life.
– NY
This edition first published 2014 © 2014 by John Wiley & Sons, Ltd.
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Library of Congress Cataloging-in-Publication Data
The practice of catheter cryoablation for cardiac arrhythmias / edited by Ngai-Yin Chan.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-118-45183-0 (cloth : alk. paper) – ISBN 978-1-118-45179-3 – ISBN 978-1-118-45180-9 (Mobi) – ISBN 978-1-118-45181-6 (Pdf) – ISBN 978-1-118-45182-3 (ePub) – ISBN 978-1-118-75776-5 – ISBN 978-1-118-75777-2
I. Chan, Ngai-Yin, editor of compilation.
[DNLM: 1. Arrhythmias, Cardiac–surgery. 2. Catheter Ablation–methods. 3. Cryosurgery–methods. WG 330]
RC685.A65
616.1'28–dc23
2013017939
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Cover image: courtesy of the editor
Cover design by Rob Sawkins for Opta Design Ltd.
List of Contributors
Amin Al-Ahmad, MD
Division of Cardiovascular Medicine
Stanford University School of Medicine
Palo Alto, CA
USA
David J. Burkhardt, MD
Texas Cardiac Arrhythmia Institute
St. David's Medical Center
Austin, TX
USA
Ngai-Yin Chan, MBBS, FRCP, FACC, FHRS
Department of Medicine and Geriatrics
Princess Margaret Hospital
Hong Kong
China
Kathryn K. Collins, MD
University of Colorado and
Children's Hospital Colorado
Aurora, CO
USA
Luigi Di Biase, MD, PhD, FHRS
Texas Cardiac Arrhythmia Institute
St. David's Medical Center;
Department of Biomedical Engineering
University of Texas
Austin, TX
USA;
Department of Cardiology
University of Foggia
Foggia
Italy;
Albert Einstein College of Medicine
Montefiore Hospital
New York, NY
USA
Gregory K. Feld, MD
Clinical Cardiac Electrophysiology Program
Division of Cardiology
University of California, San Diego
San Diego, CA;
Sulpizio Family Cardiovascular Center
La Jolla, CA
USA
Jo Jo Hai, MBBS
Cardiology Division
Department of Medicine
Queen Mary Hospital
The University of Hong Kong
Hong Kong
China
Henry H. Hsia, MD
Division of Cardiovascular Medicine
Stanford University School of Medicine
Palo Alto, CA
USA
Marcin Kowalski, MD, FHRS
Department of Clinical Cardiac Electrophysiology
Staten Island University Hospital
Staten Island, NY
USA
Michael R. Lauer, MD
Permanente Medical Group
Cardiac Electrophysiology Laboratory
Kaiser-Permanente Medical Center
San Jose, CA
USA
Andrea Natale, MD, FACC, FHRS
Texas Cardiac Arrhythmia Institute
St. David's Medical Center;
Department of Biomedical Engineering
University of Texas
Austin, TX;
Division of Cardiovascular Medicine
Stanford University School of Medicine
Palo Alto, CA;
Sutter Pacific Medical Center
San Francisco, CA
USA
Pasquale Santangeli, MD
Texas Cardiac Arrhythmia Institute
St. David's Medical Center
Austin, TX
USA;
Department of Cardiology
University of Foggia
Foggia
Italy;
Division of Cardiovascular Medicine
Stanford University School of Medicine
Palo Alto, CA
USA
Navinder Sawhney, MD
Cardiac Electrophysiology Program
Division of Cardiology
University of California, San Diego
San Diego, CA;
Sulpizio Family Cardiovascular Center
La Jolla, CA
USA
Ruey J. Sung, MD
Division of Cardiovascular Medicine (Emeritus)
Stanford University School of Medicine
Stanford, CA
USA
Hung-Fat Tse, MD, PhD
Cardiology Division
Department of Medicine
Queen Mary Hospital
The University of Hong Kong
Hong Kong
China
George F. Van Hare, MD
Division of Pediatric Cardiology
Washington University School of Medicine and
St. Louis Children's Hospital
St. Louis, MO
USA
Jürgen Vogt, MD
Department of Cardiology
Heart and Diabetes Center North Rhine-Westphalia
Ruhr University Bochum
Bad Oeynhausen
Germany
Xue Yan
Department of Biomedical Engineering
Texas Cardiac Arrhythmia Institute
St. David's Medical Center;
University of Texas
Austin, TX
USA
Charlie Young, MD
Permanente Medical Group
Cardiac Electrophysiology Laboratory
Kaiser-Permanente Medical Center
San Jose, CA
USA
Preface
I was trained to use radiofrequency as the energy source in the ablation of various cardiac arrhythmias more than 20 years ago. This time-honored energy source has been shown to perform well in terms of both efficacy and safety profile. It was not until I encountered my first complication of inadvertent permanent atrioventricular block, in a young patient who underwent catheter ablation for atrioventricular nodal reentrant tachycardia, that I recognized we might need an even better source of energy.
Certainly, catheter cryoablation is not a substitute for radiofrequency ablation. However, in many of the arrhythmic substrates (notably the perinodal area, Koch's triangle, pulmonary vein, coronary sinus, cavotricuspid isthmus, etc.), cryothermy may be considered as the energy source of choice. Unfortunately, there has been a shortage of educational materials in this area. This work thus represents the first book dedicated to the science and practice of catheter cryoablation.
The Practice of Catheter Cryoablation for Cardiac Arrhythmias is purposefully written and organized to update the knowledge base in catheter cryoablation, with the emphasis on “how to perform.” We compare cryothermy with radiofrequency energy source in different arrhythmic substrates, and we have also supplemented the textual content with a companion website (www.chancryoablation.com) providing interactive cases and real case videos for selected chapters. In this enhanced edition you will also find the videos embedded within the book.
I am sure that this book can benefit all those who are interested in better understanding this relatively new technology and the science behind it. More importantly, this book will serve as an indispensable reference for those who would like to adopt catheter cryoablation in treating patients with different cardiac arrhythmias.
Ngai-Yin Chan, MBBS, FRCP, FACC, FHRS
Acknowledgments
This book is the product of the collective effort of many dedicated people. I would like to thank all the contributing authors, who are all prominent leaders in the field of catheter cryoablation and have found time out of their busy schedules to write the various chapters of the book. I also thank my great colleagues Stephen Choy and Johnny Yuen, who were excellent assistants during my cryoablation procedures. Stephen Cheung, an expert radiologist and a good friend of mine, has to be acknowledged for his contribution of the beautiful reconstructed cardiac CT image that is used on the book cover. Lastly, I have to thank Adam Wang and Perry Tang for their technical support in the preparation of the live cryoablation procedures videos for the companion website.
About the Companion Website
This book is accompanied by a companion website:
www.chancryoablation.com
The website includes:
CHAPTER 1
Biophysical Principles and Properties of Cryoablation
More than 4000 years have passed since the first documented medical use of cooling therapy, when the ancient Egyptian Edwin Smith Papyrus described applying cold compresses made up of figs, honey, and grease to battlefield injuries.1 Not until 1947 did Hass and Taylor first describe the creation of myocardial lesions using cold energy generated by carbon dioxide as a refrigerant.2 In contrast to the destructive nature of heat energy, which produces diffuse areas of hemorrhage and necrosis with thrombus formation and aneurysmal dilation, cryoablation involves a unique biophysical process that gives it the distinctive safety and efficacy profile.3 Cryoablation induces cellular damage mainly via disruption of membranous organelles, such that destruction to the gross myocardial architectures is reduced. Furthermore, cryomapping is feasible as lesions created at a less cool temperature (>−30 °C) are reversible. These potential advantages nurtured the extensive clinical applications of cryoablation in the treatment of cardiac arrhythmias, such as atrioventricular nodal reentrant tachycardia, septal accessory pathways, atrial fibrillation, and ventricular tachycardia, where a high degree of precision is desirable.
Heat flows from higher temperature to lower temperature zones. Cryoablation destroys tissue by removing heat from it via a probe that is cooled down to freezing temperatures, which has been made feasible by the invention of refrigerants that permit ultra-effective cooling.
In the 1850s, James Prescott Joule and William Thomson described the temperature change of a gas when it is forced through a valve and allowed to expand in an insulated environment. Above the inversion temperature, gas molecules move faster. When they collide with each other, kinetic energy is temporarily converted into potential energy. The average distance between molecules increases as gas expands. This results in significantly fewer collisions between molecules, thus lowers the stored potential energy. Because the total energy is conserved, there is a parallel increase in the kinetic energy of the gas. Temperature increases.
In contrast, gas molecules move slower at temperatures below the inversion point. The effect of collision-associated energy conversion becomes less important. The average distance between molecules increases when the gas is allowed to expand. The intermolecular attractive forces (van der Waals forces) increase, and so does the stored potential energy. As the total energy is conserved, there is a parallel decrease in the kinetic energy of the gas. Temperature decreases.4
In the 1870s, Carl Paul Gottfried von Linde applied the Joule–Thompson effect to develop the first commercial refrigeration machine. In his original design, liquefied air was first cooled down by a series of heat exchangers, followed by rapid expansion through a nozzle into an isolated chamber, such that the gas rapidly cooled down to freezing temperature. The cold air generated was then coupled with a countercurrent heat exchanger, where ambient air was chilled before expansion began. This further lowered the temperature of the compressed air entering the apparatus, and it increased the efficiency of the machine (Figure 1.1).5
Figure 1.1. Schematic representation of the von Linde refrigerator. The direction of air flow is shown by the arrows.
According to the principles of the Joule–Thompson effect, only gases with a high inversion temperature can be used as refrigerants. This is because gases with a low inversion temperature under atmospheric pressure, such as hydrogen and helium, warm up rather than cool down during expansion.6
A cryoprobe is a high-pressure, closed-loop gas expansion system. The cryogen travels along the vacuum's central lumen under pressure to the distal electrode, where it is forced through a throttle and rapidly expands to atmospheric pressure. This causes a dramatic drop in the temperature of the metallic tip, so that the heat of tissue in contact with it is rapidly carried away by conduction and convection. The depressurized gas then returns to the console, where it is restored to the liquid state (Figure 1.2).3,6
Figure 1.2. Schematic diagram to show the design of the cryoablation probe.
The probe temperature varies with the cryogen used. The most widely used cryogens in surgery are liquid nitrogen, which can attain a temperature as low as −196 °C; and argon gas, which can achieve a temperature as low as −186 °C.7 Nevertheless, the complex and bulky delivery systems for these agents limit their utility in percutaneous cardiac procedures. To date, only a nitrous oxide–based cryocatheter is commercially available for use by cardiologists, and its lowest achievable temperature is −89.5 °C.3,7,8
The minimal temperature and maximal cooling rate occur at the tissue in contact with the metal tip. With increasing distance from the tip, the nadir temperature rises, cooling rates decrease, and thawing rates increase. The resultant isotherm map determines the mechanism of injury of those cells lying within each temperature zone, and hence the outcome of the procedure (Figure 1.3).8
Figure 1.3. Isotherm map of the tip of the catheter electrode of a cryoablation probe (marked by the cross). As shown here, different mechanisms of cell injuries occur at different temperatures.
Freezing results in both immediate and delayed damage to the targeted tissue. Immediate effects include hypothermic stress and direct cell injury, while delayed consequences are the results of vascular-mediated injury and apoptotic cell death.5
When the temperature is lowered to below 32 °C, the membranes of the cells and organelles become less fluid, causing ion pumps to lose their transport capabilities. Electrophysiologically, this is reflected by a decrease in the amplitude of action potential, an increase in its duration, and an extension of the repolarization period. As the temperature continues to decline, metabolism slows, ion imbalances occur, intracellular pH lowers, and adenosine triphosphate levels decrease.9 Intracellular calcium accumulation secondary to ion pump inactivity and failure of the sarcoplasmic reticulum reuptake mechanism may lead to further free radical generation and cellular disruption.5 Nevertheless, these effects are entirely transient, provided that the duration of cooling does not exceed a few minutes. The rapidity of recovery is inversely related to the duration of hypothermic exposure.3
Contrasting the transient effect of hypothermia, ice formation is the basis of permanent cell injury. When the tissue approaches freezing temperature, ice formation begins and results in cryoadhesion. It acts as a “heat sink” by which heat is rapidly extracted from the tissue.5 With further lowering of temperature, ice crystals form in both extracellular and intracellular compartments.3,10,11 Water crystallization begins inside the cells (heterogeneous nucleation) at −15 °C, but intracellular ice generally forms (homogeneous nucleation) at temperatures below −40 °C.11 Besides, intracellular ice formation is more likely to occur under rapid cooling and at the sites where cells are tightly packed, as water cannot diffuse fast enough through the cellular membrane to equilibrate the intracellular and extracellular compartments.6,8,10 Intracellular ice compresses and deforms the nuclei and cytoplasmic components, induces pore formation in the plasma membranes, and results in permanent dysfunction of the cellular transport systems and leakage of cellular components.3,6,8,11 All these events lead to irreversible cell damage and ultimately cell death.
Extracellular ice usually forms under moderate freezing temperatures and slower cooling rates.3,11 The ice crystals sequestrate free water, which increases solute concentration and hence tonicity of the extracellular compartment. Water is withdrawn from the cells along the osmotic gradient, causing cellular dehydration and elevated intracellular solute concentration. As the process continues, these alterations in the internal environment damage intracellular constituents and destabilize the cell membranes. This is termed solution–effect injury.3,6,11
Cells densely packed in a tissue are subjected to shearing forces generated between ice crystals, which can result in mechanical destruction.8,11 However, a previous study has shown that membrane integrity was preserved for up to 2 min after thawing, questioning the actual importance of this theoretical effect.12
During thawing, extracellular ice melts and results in hypotonicity of the extracellular compartment. Water is shifted back to the intracellular space, causing cell swelling and bursting. It also perpetuates the growth of intracellular ice crystals, exacerbating cell destruction and cell death. This process of recrystallization occurs at temperatures between −40 and −15 °C, predominantly from −25 to −20 °C.8,9,11
Cooling results in vasoconstriction, which jeopardizes blood flow to the tissue supplied.11 At −20 to −10 °C, vascular stasis occurs, water crystallizes, and endothelial cell injury ensues.11,13 When the blood flow restores at the thawing phase, platelets aggregate and form thrombi at the sites of endothelial injury, leading to small vessel occlusion.11 The resultant ischemia triggers an influx of vasoactive substances that lead to regional hyperemia and tissue edema, and migration of inflammatory cells that clear up cell debris.4,6,11 The chance of cell survival is minimized, and uniform coagulation necrosis develops.4,6,8
Cells that survive the initial freeze and thaw phases may also die from apoptosis in the next few hours to days.8 This is because cellular injuries, especially damage to the mitochondria, activate caspases, which cleave proteins and cause membrane blebbing, chromatin condensation, genomic fragmentation, and programmed cell death.8,13 This is particularly important at the peripheral zone of ablation, where temperatures and cooling rates achieved are less likely to be immediately lethal to the cells.
A detailed description of the histological effect of cryoablation has been published elsewhere.12 In summary, it can be divided into three phases: the immediate postthaw phase, hemorrhagic and inflammatory phase, and replacement fibrosis phase.
Within 30 min of thawing, the myocytes become swollen and the myofilaments appear stretched. The increase in membrane permeability causes mitochondria to swell, which results in oxidation of the endogenous pyridine nucleotides, membrane lipid peroxidation, and enzymatic hydrolysis. This is followed by progressive loss in myofilament structure and irreversible mitochondrial damage.12
Coagulation necrosis, characterized by hemorrhage, edema, and inflammation, becomes evident at the central part of the lesion within 48 hours after thawing.12 At the peripheral zone, apoptosis progressively increases and becomes apparent in 8 to 12 hours. At 1 week, infiltrates of inflammatory cells, fibrin and collagen stranding, and capillary ingrowth sharply demarcate the periphery of the lesion.12 Endothelial layers remain intact, and thrombus formation is uncommon compared with radiofrequency ablation.14
Necrotic tissue is largely cleared up by the end of the fourth week. The lesion now consists mainly of dense collagen fibers and fat infiltration, with new blood vessels reestablishing at the periphery. Healing continues for 3 months until a small, fibrotic scar with an intact endothelial layer and a well-demarcated boundary is formed (Figure 1.4).
Figure 1.4. Examples of gross (left panel) and histological (right panel) sections show cryoablation lesions after percutaneous cryoablation at the pulmonary vein in a canine. Note the well-demarcated boundary and intact endothelial layer at the site of the cryoablation lesion.
