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Surgery and Ablative Therapy for Ventricular Tachycardia
ORIGINAL ARTICLE
Original Article
Surgery and Ablative Therapy for Ventricular Tachycardia David L. Ross, FRACP ∗ Department of Cardiology, Westmead Hospital and University of Sydney, Westmead 2145, Australia
In the absence of acute ischaemia, ventricular tachycardia (VT) is the most common arrhythmia leading to cardiac arrest and death. This paper will describe the history of research into VT and the therapies that evolved. The contributions of John Uther and other members of the Department of Cardiology at Westmead Hospital will be outlined and placed into perspective. (Heart, Lung and Circulation 2007;16:214–221) © 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Ventricular tachycardia; Surgery; Ablation; History
Background
I
started research into VT in 1976, now 30 years ago, in the Department of Cardiology at Royal Melbourne Hospital. The head of department was Graeme Sloman and my supervisor was Jitu Vohra, both pioneers in cardiology, electrophysiology and pacing in Australia. At that time little was known about VT. Hein Wellens in the Netherlands had described inducibility of VT by programmed stimulation1,2 and Roworth Spurrell and colleagues reported surgical interventions based on presumed circuits utilising the bundle branches of the Purkinje system.3 In retrospect, these interpretations were erroneous for the most common forms of VT based on old myocardial infarction but VT circuits reentering via the bundle branches were later shown to be a rare cause of VT in cardiomyopathies. At Royal Melbourne Hospital in 1976 we began performing electrophysiological studies for diagnostic purposes in patients with broad complex tachycardias.4 This was done with much trepidation using what now seem to be very conservative stimulation protocols. The safety of such provocative testing was not known but we thought we had the facilities and staff to handle likely complications. Many cardiologists were very critical of this sort of work. However, time and extensive clinical experience over several decades in large numbers of patients has proven the safety of such an approach. In the mid 1970s there was little clinical benefit to the patient since the only treatments were Type 1 antiarrhythmic drugs such as quinidine, procainamide and disopyramide. In our initial studies we noted that multiple morphologies of VT were often present in the same patient.5 Available online 18 April 2007 ∗
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Although this aspect was novel at the time we made our observations, a series of important papers on VT were then published by Mark Josephson in the USA including one describing the same phenomenon.6–9 Near the end of the 1970s, data were reported showing that antiarrhythmic drugs that inhibited induction of VT at electrophysiological studies predicted a good clinical response to long term oral treatment with the tested drug.10–12 This was the first time that electrophysiological studies achieved an important role in treatment of clinical VT. Concurrently, surgery for VT was shown to be useful for patients with refractory VT.13–17 Uther recruited me to join him at Westmead Hospital, the brand new university teaching hospital built in 1978 at Parramatta in Sydney’s western suburbs. This was considered to be in the nether reaches of Sydney by those who worked in the other teaching hospitals clustered near the city centre. However, even at that time, Parramatta was the demographic centre of Sydney, and the new teaching hospital provided an invaluable resource to the under serviced half of the population who lived west of Parramatta. When I returned in 1982 after training overseas with Wellens in Maastricht and Jay Mason, Roger Winkle and Jerry Griffin at Stanford, there were few electrophysiologists in Australia: Uther in Sydney, Vohra in Melbourne and Andrew Tonkin in Adelaide. Geoff Cope in Perth had trained in electrophysiology but became one of the Australian pioneers in the new field of angioplasty. Kevin Hellestrand studied electrophysiology with John Camm in London and returned to Royal North Shore Hospital in the early 1980s. After a short period of observation with John Gallagher and Will Sealy at Duke University, North Carolina, USA, Uther and cardiac surgeon Douglas Baird began surgery for supraventricular tachycardia (SVT) and VT at Royal Prince Alfred Hospital in the early 1970s. They amassed
© 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2007.03.002
the third largest series in the world and achieved results comparable with the best international centres. Uther was then appointed as the foundation head of Cardiology at the new Westmead Hospital and the majority of the arrhythmia work followed him to Westmead. I considered it a privilege to join him and David Johnson, the Foundation Head of Cardiac Surgery, at Westmead. They were at the forefront of surgical treatment for arrhythmias in Australia at that time.
Surgery for Ventricular Tachycardia Surgery for VT began with resection of left ventricular (LV) aneurysms. However, VT often recurred. With time it became clear that VT circuits usually involved surviving bundles of myocardium at the margins of the aneurysm rather than dead tissue in the centre. The usual method for resecting aneurysms retained scar tissue at the margins to provide firm support for the suture line closing the ventricle. Thus, the arrhythmogenic tissue often remained and led to further arrhythmias.14,18 Other methods were then developed, predominantly map guided subendocardial resection pioneered by Josephson, Alden Harken, and Leonard Horowitz at Philadelphia.13,15,17 This method was based on the idea that reentrant VT circuits usually involved the subendocardium. Activation mapping during VT indicated the area to be resected. Endocardial resection retained the mid and outer walls and minimised compromise of left ventricular systolic function yet permitted resection over a wide area. Other surgical methods included encircling endocardial ventriculotomy19 and right ventricular disconnection20 conceived by the creative Gerard Guiraudon in Paris and later London, Ontario, Canada. The former method involved making a transmural endocardial incision around the margins of the aneurysm. This included the arrhythmogenic border zone and was therefore an improvement but involved compromise of adjacent normal myocardium. Right ventricular (RV) disconnection was designed for ventricular tachycardias due to RV dysplasia. Since RV dysplasia is a multifocal disease, there are usually multiple arrhythmia circuits. Disconnection was therefore an attractive concept. However, complete electrical disconnection of the free wall of the right ventricle was sometimes difficult to achieve. It also caused mechanical isolation of the lateral right ventricle which often had adverse haemodynamic consequences.21,22 Furthermore, the dysplasia often involved the septum which was not disconnected and provided the substrate for continued arrhythmia. All the above methods were reported to have modest success rates but had a significant mortality. Since there was no other alternative to failed antiarrhythmic drug treatment in those days, surgery for VT had an important role in refractory patients.
Surgery for VT at Westmead Hospital Uther, Baird and Johnson developed their modifications of international methods for surgical ablation of VT. Uther
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with Roly Hilder, the biomedical engineer at Royal Prince Alfred Hospital, built an innovative mapping system. These were the early days of computing and digital equipment. Mapping during arrhythmias was difficult because of the fast heart rates. Most systems printed out electrograms on paper at fast paper speeds and the timings of the signals were measured by hand. This made mapping very slow and inefficient. Mapping had to be done on cardiopulmonary bypass because tachycardias under general anaesthesia in this group of patients usually caused haemodynamic collapse. Since most patients with ventricular tachycardia had poor ventricular function, anything that prolonged cardiopulmonary bypass and the duration of the operation was most undesirable. The Hilder-Uther mapping system allowed capture of individual cycles, frozen display of the signals on a Tektronix oscilloscope and automated, real time read out of the activation time. This system was probably the best in the world at that time. It permitted reasonably rapid maps of the heart using a roving hand held electrode. When Uther moved to Westmead from Royal Prince Alfred Hospital, the mapping machine was rebuilt and named the Wing Chanoscope by wags in the Biomedical Engineering Department after the engineer who built it. This system was the size of a small fridge and could be transported with only moderate difficulty. In the first year at Westmead there was no cardiac surgery on site and the operations were performed at Royal North Shore Hospital. The mapping gear was transported in the back of a car to North Shore for the surgery. It was also transported to the Camperdown Children’s Hospital for paediatric cases and even to China for arrhythmia surgery. The Westmead innovation in surgery for ventricular tachycardia in ischaemic heart disease was mapping of late potentials to identify arrhythmia substrates and transmural resection of arrhythmogenic myocardium where possible. Late potential mapping was particularly useful in patients in whom ventricular tachycardia could not be induced at surgery (not an uncommon problem) or those who had too many morphologies for complete mapping or those in whom tachycardia rapidly degenerated to fibrillation. This approach arose from Uther’s work with signal averaging. Rob Denniss, in his MD project supervised by Uther, found late potentials at detailed epicardial mapping in dogs and humans after myocardial infarction and reconstructed the underlying histology.23 The areas with late potentials were associated with bundles of surviving myocardium in the underlying scar with slow conduction, one of the pre-requisites for reentry. In the 1980s Westmead performed over 100 operations for VT with a success rate of 83% as assessed by postoperative VT induction studies and a mortality of 15%. This was similar to most international series. The major problem with VT surgery was further destruction of an already poor ventricle leading to the relatively high mortality. Although outcomes in this group of patients were significantly better with surgery than failed medical therapy, better and safer methods were needed.
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Surgery was also performed for medically refractory idiopathic ventricular tachycardias arising in the right ventricular outflow tract. These patients were usually young people with no detectable structural heart disease. A good long-term success rate was achieved but resection of portions of the outflow tract and ventricular septum were required. Surgery was also performed successfully for young children ranging from infants to 10 years in age with refractory incessant ventricular tachycardias. These were due to ‘hamartomas’, now termed histiocytoid cardiomyopathy.
viously mapped patient and found a multitude of potential pathways through the tissue block rather than a few discrete bundles. This suggested that there were not limited, discrete pathways to target similar to an accessory pathway in Wolff–Parkinson–White syndrome but rather a field problem with multiple potential routes of conduction requiring ablation of a region. Complete ablation of all arrhythmogenic areas therefore would often require damage to a large mass of myocardium in patients with already severely compromised LV function.
Cryoablation and LASER for VT Surgery Detailed Catheter Mapping for VT Prior to Surgery One of the main problems with VT surgery was inability to induce all relevant tachycardias at surgery while under general anaesthesia and after handling of the heart. This prevented complete mapping of all arrhythmogenic areas. We therefore attempted detailed catheter mapping at electrophysiological study prior to surgery in an attempt to localise target areas. As part of his PhD at Westmead, Lloyd Davis inserted multiple decapolar electrodes into the ventricles.24 Up to 100 electrodes were inserted using four retrograde aortic catheters (two catheters in each femoral artery), three transeptal transmitral valve catheters, and single catheters in the coronary sinus, RV apex and RV outflow tract. These were procedural tour de forces in patients who often had major comorbidity that made the procedures more difficult. Transeptal procedures were not used in electrophysiology and rarely during cardiology at that time. Some hospitals had used the transeptal approach routinely for cardiac catheterisation of aortic stenosis but most centres had converted to the retrograde aortic approach. Davis reported that multiple morphologies of VT were the rule rather than the exception in the context of previous myocardial infarction (see Table 1).24 Although 74% of patients had multiple morphologies of inducible VT, different morphologies often arose from the same region of the heart. A single arrhythmogenic area was responsible for all arrhythmias in 57%. This suggested that localised ablation should be able to cure a substantial proportion of patients. However, 43% had multiple arrhythmogenic areas which would require ablation of disparate regions of the heart, usually located around the infarct or aneurysm. Davis made a detailed three dimensional (3D) histological reconstruction of an arrhythmogenic area in a post mortem specimen of a preTable 1. Detailed catheter mapping of VT Morphologies per patient: 1 2 3 ≥4 Arrythmogenic areas per patient: 1 2 3 ≥4 N = 23 patients.
6 (26%) 5 (22%) 6 (26%) 6 (26%) 13 (57%) 4 (17%) 5 (22%) 1 (4%)
Two new technologies for arrhythmia surgery came on the scene. Freezing of tissues with a cryoprobe allowed destruction of arrhythmogenic tissue while maintaining structural integrity. It therefore avoided suture lines and patches and minimised destruction of surrounding normal myocardium. Lasers were also used for surgical ablation. Geraldine Hunt, a veterinary surgeon, did her PhD at Westmead in cardiac electrophysiology and surgery. She studied cryoablation in collaboration with Richard Chard, then a surgical registrar and now surgeon at Westmead Children’s and adult hospitals.25 They showed that only superficial lesions were achieved using a conventional nitrous oxide cryoprobe if applied during normothermia as was done in many centres. Much bigger, clinically useful lesions were created if applied during systemic hypothermia. Lasers were more difficult to use because of safety issues but encouraging results were reported in a few institutions.26,27 Late diffuse myocardial dysfunction occurred in some cases, apparently due to refraction and diffusion of the laser beam into surrounding normal myocardium. Lasers tend to be reflected by shiny surfaces and fat and are more difficult to apply effectively from an epicardial approach. The laser approach has not been widely adopted.
Improved Methods for Surgical Mapping of VT Mapping during surgery was traditionally confined to the epicardial or endocardial surfaces. It was clear that many arrhythmias involved mid wall structures. The interventricular septum was often involved and the depth of the culprit tissues was usually unclear. Endocardial mapping usually involved ventriculotomy with consequent further ventricular damage unless there was a discrete fibrotic aneurysm. James Cox’s group at St Louis developed multi-electrode transmural needles for detailed intramural mapping.28–30 Needles were not commercially available. Davis and Vicki Eipper developed our own mapping needles by inserting four fine insulated wires down 21 gauge needles and out side holes at various depths to create a quadripolar mapping needle with a sharp tip. The needle lumen was then filled with acrylic. Longer needles with eight electrodes were also constructed for mapping the septum. They were inserted perpendicular to the heart surface into the anterior and posterior septum and provided nearly complete coverage of the septum. Subsequently, the needles were refined during
the tenure of the Cooperative Research Centre in Cardiac Technology. Westmead Hospital was one of the major participants along with Telectronics Pty Ltd, the CSIRO and other Sydney cardiovascular research centres. Chris Sodhi and Ilija Koevski, supervised by Andrew Madry and Pramesh Kovoor, developed a much better and professional needle system capable of mapping, temperature sensing at each electrode on each needle and capability of simultaneous radiofrequency ablation through multiple intramural electrodes. Each needle took several manhours to build and all were constructed by hand at the hospital. Detailed mapping of an arrhythmogenic area required 60–100 simultaneous needles. Construction of a set of electrodes for a single human case therefore involved several weeks of work. A dedicated needle maker was employed full time. Kovoor developed a sock electrode for global epicardial mapping to guide placement of the intramural needles in the arrhythmogenic areas. One of the major concerns was whether introduction of so many needles into the heart would damage or distort underlying conduction and whether there would be excessive bleeding. Kovoor performed detailed experiments in dogs which showed that bleeding was not a problem, myocardial conduction was not disturbed by the needles and the technique did not impair LV function.31 He also showed that creation of several intramural radiofrequency lesions in a normal ventricle did not create inducible VT.31
RF Ablation via Transmural Needles for Surgical VT Ablation Kovoor at Westmead studied ventricular intramural RF ablation using the Westmead-CRC multi-electrode temperature sensing needles. He showed that individual unipolar lesions were better than bipolar lesions between neighbouring electrodes. Bipolar lesions give two lesions for the one application of current but the electrode with the highest temperature controls the delivery of RF power in a temperature feedback system, leading to a smaller lesion at the cooler electrode. This technique often leaves gaps in lines of ablation. He also determined the appropriate temperature settings for temperature controlled intramural RF ablation.32 Temperatures up to 90◦ and even 100 ◦ C could be used because the absence of the cooling effects of blood flow caused the electrode temperature to reflect accurately surrounding tissue temperature. Steam or gas formation does not occur till tissue temperature reaches or exceeds 100 ◦ C. One of the concerns raised about RF ablation for VT was that scar would diminish RF lesion size because of less conductivity and make ablation less effective. Although some papers found evidence to support this concept, Kovoor studied ventricular intramural RF ablation in and adjacent to scar and found no effect on lesion size or tissue temperature profile around the ablation electrode.33 The contradictory results in other publications probably related to variation in electrode contact or blood cooling since they used surface electrodes for ablation. The Westmead-CRC multi-electrode intramural needles could therefore give relatively detailed transmural
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maps covering the arrhythmogenic area and extending out to adjacent normal muscle. As part of our CRC work, Michael Daly developed a RF splitter which allowed a single RF generator to deliver RF ablation to multiple electrodes simultaneously with individual temperature control and automatic adjustment of power to each electrode. The prototype device delivered RF ablation to four different electrodes but was capable of expansion to more electrodes if a more powerful generator was used. The mapping needles could also be used for temperature controlled RF ablation since each of the four electrodes on each needle had a thermocouple to sense temperature. If the needles were spaced at 5 mm distances in a grid pattern, it was possible to achieve any desired 3D lesion set in the block of tissue encompassed by the electrode array. If a sufficiently powerful generator was used, the desired 3D lesion set could be achieved in a single application of RF. We used the needle grids and RF splitter in a canine model of post infarction VT initially. The system was then used for surgical mapping and ablation of human post infarction VT and RV outflow tract VT in patients with repaired Tetralogy of Fallot who required pulmonary valve replacement for free pulmonary regurgitation. Gratifying results were obtained. However, this technology later lapsed for several reasons: the company that manufactured the programmable control system collapsed, the costs of construction of the needles were high and it was labour intensive to construct a new set of needles for each patient to ensure adequate sterility. The advent of the implantable defibrillator was the final blow.
Effects of Implantable Defibrillators on VT Surgery Our studies of antiarrhythmic drug therapy for ventricular tachycardia showed disappointing long-term efficacy. Surgery was too risky and not effective enough for more general use. The need for an alternative was filled by Mirowsky and Mower’s development of the implantable defibrillator.34–36 It rapidly became the primary treatment for VT and markedly reduced the need for VT surgery. The other reason for the demise of arrhythmia surgery was the advent of catheter radiofrequency ablation for arrhythmias including VT.
Catheter Ablation for VT The initial method for catheter ablation involved discharge of a defibrillator down a catheter through the distal electrodes abutting the region of interes.37–39 Discharge of a few thousand volts into a catheter electrode caused arcing and gas formation at the tip resulting in a mini explosion, appropriately termed ‘fulguration’ by Guy Fontaine from Paris, one of the pioneers of this technique. Fulguration caused a patchy area of necrosis which was sometimes arrhythmogenic and was not a suitable method for graded ablation due to multiple uncontrolled variables which determined lesion size. It was soon replaced by radiofrequency ablation (RF). Catheter RF ablation was developed by Steven Huang at Tucson, Arizona for creation of complete heart block in
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patients with intractable supraventricular arrhythmias.40 The first RF ablation for cure of a human tachycardia was reported by Martin Borggreffe at Dusseldorf.41 Catheter RF ablation soon proved to be reliably successful for ablation of the AV node, accessory pathways and AV nodal reentrant tachycardia. It was soon applied to VT. However, the problems with catheter ablation of VT were similar to surgery. It was difficult to map multiple morphologies, and the RF lesions were often not deep enough to reach the critical tissues. Roving catheter mapping could not be performed for tachycardias that were poorly tolerated haemodynamically or rapidly degenerated to ventricular fibrillation. Advantages over surgery were that it was usually easier to induce sustained arrhythmias and catheter procedures could be repeated easily.
Improved Methods of Catheter RF Ablation Catheter RF ablation underwent several improvements. The initial method monitored current and power was adjusted manually to obtain currents of 500 mA or more. At higher powers, coagulation and carbonisation formed at the interface between the electrode and the tissue, often leading to a ‘pop’ as gas was formed. When coagulum formed, a high impedance interface occurred leading to a small and ineffective lesion. Temperature monitoring of the catheter tip was then introduced using thermistors or thermocouples with automated temperature feedback control of power delivery.42 This minimised excessive temperatures at the tip and helped prevent coagulum and impedance rises. If there was no temperature rise as power was delivered, it also indicated that the electrode was not in good contact with the tissue. VT ablation often requires ablation of relatively large volumes of tissue or deeper lesions. This was hard or impossible to achieve with standard 4 mm tip electrodes. Larger electrodes up to 8–12 mm in length were tried with high output RF generators.43 Up to 8 mm electrodes did increase lesion size but the largest electrodes did not with commercially available RF generators. This was due to an inadequate power density for the larger surface area electrodes. The next advance was irrigated tip RF ablation developed by Wittkampf and Mittleman and refined by Nakagawa and Jackman.44,45 Cooling of the tip of the electrode by saline irrigation through the catheter at 20–30 ml/min allowed more energy to be delivered without coagulum formation and created substantially larger and deeper lesions. This innovation was an important advancement which improved results substantially. Other technologies studied for catheter ablation included cryoablation, microwave, laser and ultrasound. At present, RF ablation remains the preferred method.
Improved Methods for Catheter Mapping of VT Detailed catheter mapping is difficult to analyse by the roving catheter method, especially for complex or multiple circuits. The use of simultaneous multi-electrode mapping using large numbers of individual catheters was developed at Westmead as described earlier. Substan-
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tial advances in mapping soon followed. The first method used basket catheters with 64 electrodes arrayed on eight splines.46,47 The basket splines were flexible and could be collapsed within a guiding catheter to be passed to the chamber of interest, then protruded beyond the tip to expand the basket automatically to its native spherical shape. It was a little difficult to identify the position of each spline in 3D space on fluoroscopy and each signal needed to be analysed manually to mark local activation. The shape of the basket usually did not match the complex anatomical shapes of the cardiac chambers closely, thus causing several electrodes to fail to make contact with myocardium. Although an advance, significant problems remained with this system. The electroanatomic mapping system then became available. It used three orthogonal microcoils at the catheter tip to pick up electromagnetic signals from three electromagnets of different frequency spaced in a triangular grid under the bed. By using a triangulation method similar to satellite navigation systems, the position of the catheter tip in 3D space could be determined in real time with an accuracy of 1–2 mm.48,49 This information was combined with computerised 3D displays of the activation sequences and electrogram voltages of the mapped surface. The better anatomical information and precise anatomical marking of the sites of lesion delivery greatly facilitates design and accurate delivery of lesion sets. The main defect of this system is the slowness of roving catheter maps which prevent use in poorly tolerated or non-sustained ventricular tachycardias. Another common problem is to miss a change in arrhythmia morphology and continue mapping as if the original arrhythmia was still present. This generates faulty maps. The non-contact multi-electrode mapping system is another 3D system that uses a 64 electrode array deployed in the cavity of the chamber to be mapped. A locator signal is emitted from the roving electrode catheter as it is moved around to various sites in the chamber of interest to delineate its outer margin. The position of the roving electrode in 3D space is determined by a triangulation method using the array signals detected from the roving electrode. A geometry depicting the chamber of interest is then constructed by moving the catheter to cover the endocardial surface of the chamber. Activation signals detected on the intracavitary array are then processed using La Place’s law to derive the potentials at the endocardial surface of the chamber described by the previous geometry. This permits derivation of 3360 virtual endocardial electrograms in real time. The whole chamber can be mapped in a single beat. This technology is especially useful for non-sustained arrhythmias, especially those seen in some RV outflow tract tachycardias or atrial tachycardias. The accuracy of the derived signals compared to actual electrograms recorded from multiple transmural needle electrodes was studied in sheep left ventricles by Aravinda Thiagalingam at Westmead.50 Accuracy decreased exponentially when the area of interest was >4 cm from the centre of the array or at the poles of the array. It was most accurate opposite the equator of the array. The loss of accuracy in a large chamber is a major limitation since many of
the cardiac chambers to be mapped are dilated. The array is also not very directable and tends to go to a limited number of stable sites that may not be close to the area of interest. Other technologies use three orthogonal currents transmitted from skin patches or ultrasound for locating mapping catheters in space to create 3D maps. The orthogonal current method uses an orthogonal X, Y, and Z grid of patches applied to the thorax transmitting 1 mA currents at 30 kHz and a reference intracardiac catheter.51 The position in 3D space can then be computed real time as the catheter is moved. The ultrasound method uses reference ultrasonic crystals applied to the thorax versus a crystal in the catheter tip and follows a similar principle.
Epicardial Mapping and Ablation for VT A recent innovation in RF ablation for ventricular tachycardia was pioneered by Eduardo Sosa and colleagues in Sao Paolo, Brazil.52 Their group has extensive experience treating ventricular tachycardia due to Chagas’ disease, a protozoal infestation of the heart. VT circuits in this condition often involve the epicardium. Endocardial RF ablation is therefore often ineffective. Sosa and colleagues gained access to the pericardial space using a needle introduced via the xiphisternal approach. Surprisingly, this is usually not difficult even though there is only a potential pericardial space filled with minimal fluid. A guide wire and sheath are then inserted and an ablation catheter can be advanced into the pericardial space. This permits detailed epicardial mapping and RF ablation if necessary. Epicardial ablation is particularly useful for cardiomyopathic or arrhythmogenic RV dysplasia VT, and some idiopathic LV and ischaemic VT.
Intramural Catheter RF Ablation for VT Thiagalingam at Westmead developed a catheter which can insert a needle electrode into the myocardium to any desired depth for intramural and epicardial ablation in cases refractory or unsuitable for endocardial ablation. This technique uses an innovative helical screw to fix the outer catheter to the endocardium so the needle can be delivered easily and reliably to the desired depth.53 Since RF lesions created by a needle electrode are relatively narrow, an irrigated tip version was developed which creates larger volume and transmural lesions if required.54,55 These catheter electrodes have been manufactured in prototype form and used in animal models but not yet in human ablation.
Pace Mapping and Entrainment for VT Other techniques for localising VT circuits are pace mapping and entrainment. Pace mapping was first described by Paul Curry and colleagues in London and involves pacing at different sites to achieve the best match between the paced 12 lead ECG and that in VT.56 A good match implies that the pacing catheter is at or near the exit site of the circuit or focus. This technique is useful when no arrhythmia
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is inducible and a 12 lead ECG of tachycardia is available for comparison. It is also useful for non-sustained or poorly tolerated arrhythmias. However, there may be discrepancies of up to 2–4 cm in the sites of best pace match and the actual origin of the tachycardia. Entrainment was first described by Al Waldo and colleagues57,58 and important additional concepts for VT were added by Bill Stevenson.59,60 These dynamic interventions during a sustained tachycardia prove whether the pacing site is in the circuit rather than just inferred from mapping. It is an invaluable diagnostic tool, especially in complex tachycardias. It is especially useful for defining the area of slow conduction in the circuit which is usually the critical area for successful ablation. However, attempts at entrainment may terminate tachycardia or convert it to different morphologies or accelerate the arrhythmia to a haemodynamically unstable rhythm requiring cardioversion.
Substrate Modification for VT Ablation Other approaches to ablation use an anatomical strategy aiming to create lines of ablation at the margins of the infarct or radial lines from the infarct centre.61 These substrate modification strategies are useful when mapping during tachycardia is impossible or limited or the patient is in extremis and needs a quick procedure.
Ablation of VF Triggers Some patients with medically refractory, frequently recurrent ventricular fibrillation have reproducible initiation of each episode by a single morphology of ventricular ectopic beats. Haissaguerre in Bordeaux found that these ectopics usually arose in the Purkinje system.62,63 Ablation of the initiating ectopy often prevented recurrent arrhythmias.
Role of Implantable Defibrillators in Ablative Therapies for VT The implantable defibrillator is an invaluable adjunct to surgical or catheter ablation therapies for VT. The defibrillator provides protection against dangerous recurrent arrhythmias that may not have been ablated successfully and is an unrivalled method for continuous out-ofhospital arrhythmia monitoring. Implanting a defibrillator permits a strategy where only the most frequent or troublesome tachycardias need to be ablated, leaving the device to handle any other residual arrhythmias. This means that heroic and potentially hazardous attempts to completely ablate all inducible tachycardias are not necessary. Complete abolition of all inducible ventricular tachycardias in the context of coronary artery disease and old myocardial infarction is often not possible if a sensitive induction protocol using up to four extrastimuli is used. Many patients presenting for catheter ablation of VT have implantable defibrillators in situ but suffer intermittent storms of VT with recurrent shocks. These patients are often conscious during such shocks leading to major psychological decompensation. Catheter ablation is very
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useful for abolishing the most troublesome morphologies of VT in this context and markedly improves patient well being.
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15.
Conclusions The evolution of ablative therapies for VT has been an exciting journey leading to major improvements in outcomes for our patients. Uther and subsequent members of the Department of Cardiology have made many contributions to this progress. However, there is still much to be done and VT remains a challenging clinical problem.
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rent sustained ventricular tachycardia. J Thorac Cardiovasc Surg 1980;80:527–34. Horowitz LN, Harken AH, Kastor JA, Josephson ME. Ventricular resection guided by epicardial and endocardial mapping for treatment of recurrent ventricular tachycardia. N Engl J Med 1980;302:589–93. Horowitz LN, Harken AH, Josephson ME, Kastor JA. Surgical treatment of ventricular arrhythmias in coronary artery disease. Ann Int Med 1981;95:88–97. Josephson ME, Harken AH, Horowitz LN. Long-term results of endocardial resection for sustained ventricular tachycardia in coronary disease patients. Am Heart J 1982;104:51–7. Mason JW, Stinson EB, Winkle RA, Oyer PE, Griffin JC, Ross DL. Relative efficacy of blind left ventricular aneurysm resection for the treatment of recurrent ventricular tachycardia. Am J Cardiol 1982;49:241–8. Guiraudon G, Fontaine G, Frank R, Escande G, Etievent P, Cabrol C. Encircling endocardial ventriculotomy: a new surgical treatment for life-threatening ventricular tachycardias resistant to medical treatment following myocardial infarction. Ann Thorac Surg 1978;26:438–44. Guiraudon GM, Klein GJ, Gulamhusein SS, Painvin GA, Del Campo C, Gonzales JC, Ko PT. Total disconnection of the right ventricular free wall: surgical treatment of right ventricular tachycardia associated with right ventricular dysplasia. Circulation 1983;67:463–70. Jones DL, Guiraudon GM, Klein GJ. Total disconnection of the right ventricular free wall: physiological consequences in the dog. Am Heart J 1984;107:1169–77. Tang C, Klein GJ, Guiraudon GM, Yeung-Lai-Wah JA, Qi A, Kerr CR. Pacing in right ventricular dysplasia after disconnection surgery. J Cardiovasc Electrophysiol 2000;11: 199–202. Denniss AR, Richards DA, Waywood JA, Yung T, Kam CA, Ross DL, Uther JB. Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction. Circ Res 1989;64:155–66. Davis LM, Cooper M, Johnson DC, Uther JB, Richards DA, Ross DL. Simultaneous 60-electrode mapping of ventricular tachycardia using percutaneous catheters. J Am Coll Cardiol 1994;24:709–19. Hunt GB, Chard RB, Johnson DC, Ross DL. Comparison of early and late dimensions and arrhythmogenicity of cryolesions in the normothermic canine heart. J Thorac Cardiovasc Surg 1989;97:313–8. Moosdorf R, Pfeiffer D, Schneider C, Jung W. Intraoperative laser photocoagulation of ventricular tachycardia. Am Heart J 1994;127:1133–8. Svenson RH, Gallagher JJ, Selle JG, Zimmern SH, Fedor JM, Robicsek F. Neodymium:YAG laser photocoagulation: a successful new map-guided technique for the intraoperative ablation of ventricular tachycardia. Circulation 1987;76:1319–28. Kramer JB, Saffitz JE, Witkowski FX, Corr PB. Intramural reentry as a mechanism of ventricular tachycardia during evolving canine myocardial infarction. Circ Res 1985;56:736–54. Witkowski FX, Corr PB. An automated simultaneous transmural cardiac mapping system. Am J Physiol 1984;247:H661–8. Pogwizd SM, Hoyt RH, Saffitz JE, Corr PB, Cox JL, Cain ME. Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart. Circulation 1992;86:1872–87. Kovoor P, Campbell C, Wallace E, Byth K, Dewsnap B, Eipper V, Uther J, Ross D. Effects of simultaneous insertion of 66 plunge needle electrodes on myocardial activation, function, and structure. Pacing Clin Electrophysiol 2003;26:1979–85.
32. Kovoor P, Daly M, Campbell C, Dewsnap B, Eipper V, Uther J, Ross D. Intramural radiofrequency ablation: effects of electrode temperature and length. Pacing Clin Electrophysiol 2004;27:719–25. 33. Kovoor P, Daly MP, Pouliopoulos J, Byth K, Dewsnap BI, Eipper VE, Yung T, Uther JB, Ross DL. Comparison of radiofrequency ablation in normal versus scarred myocardium. J Cardiovasc Electrophysiol 2006;17:80–6. 34. Mirowski M, Mower MM, Langer A, Heilman MS, Schreibman J. A chronically implanted system for automatic defibrillation in active conscious dogs. Experimental model for treatment of sudden death from ventricular fibrillation. Circulation 1978;58:90–4. 35. Mirowski M, Reid PR, Mower MM, Watkins L, Gott VL, Schauble JF, Langer A, Heilman MS, Kolenik SA, Fischell RE, Weisfeldt ML. Termination of malignant ventricular arrhythmias with an implanted automatic defibrillator in human beings. N Engl J Med 1980;303:322–4. 36. Watkins Jr L, Mirowski M, Mower MM, Reid PR, Griffith LS, Vlay SC, Weisfeldt ML, Gott VL. Automatic defibrillation in man. The initial surgical experience. J Thorac Cardiovasc Surg 1981;82:492–500. 37. Gonzalez R, Scheinman M, Bharati S, Lev M. Closed chest permanent atrioventricular block in dogs. Am Heart J 1983;105:461–70. 38. Gonzalez R, Scheinman M, Margaretten W, Rubinstein M. Closed-chest electrode-catheter technique for His bundle ablation in dogs. Am J Physiol 1981;241:H283–7. 39. Scheinman MM, Morady F, Hess DS, Gonzalez R. Catheterinduced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA 1982;248: 851–5. 40. Huang SK, Bharati S, Graham AR, Lev M, Marcus FI, Odell RC. Closed chest catheter desiccation of the atrioventricular junction using radiofrequency energy—a new method of catheter ablation. J Am Coll Cardiol 1987;9:349–58. 41. Borggrefe M, Budde T, Podczeck A, Breithardt G. High frequency alternating current ablation of an accessory pathway in humans. J Am Coll Cardiol 1987;10:576–82. 42. Langberg JJ, Calkins H, el-Atassi R, Borganelli M, Leon A, Kalbfleisch SJ, Morady F. Temperature monitoring during radiofrequency catheter ablation of accessory pathways. Circulation 1992;86:1469–74. 43. Langberg JJ, Gallagher M, Strickberger SA, Amirana O. Temperature-guided radiofrequency catheter ablation with very large distal electrodes. Circulation 1993;88:245–9. 44. Nakagawa H, Yamanashi WS, Pitha JV, Arruda M, Wang X, Ohtomo K, Beckman KJ, McClelland JH, Lazzara R, Jackman WM. Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a salineirrigated electrode versus temperature control in a canine thigh muscle preparation. Circulation 1995;91:2264–73. 45. Mittleman RS, Huang SK, de Guzman WT, Cuenoud H, Wagshal AB, Pires LA. Use of the saline infusion electrode catheter for improved energy delivery and increased lesion size in radiofrequency catheter ablation. Pacing Clin Electrophysiol 1995;18:1022–7. 46. Greenspon AJ, Hsu SS, Datorre S. Successful radiofrequency catheter ablation of sustained ventricular tachycardia postmyocardial infarction in man guided by a multielectrode “basket” catheter. J Cardiovasc Electrophysiol 1997;8:565–70. 47. Eldar M, Ohad DG, Greenspon AJ, Goldberger JJ, Rotstein Z. Percutaneous multielectrode endocardial mapping and ablation of ventricular tachycardia in the swine model. Adv Exp Med Biol 1997;430:313–21.
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48. Shpun S, Gepstein L, Hayam G, Ben-Haim SA. Guidance of radiofrequency endocardial ablation with real-time three-dimensional magnetic navigation system. Circulation 1997;96:2016–21. 49. Gepstein L, Hayam G, Ben-Haim SA. A novel method for nonfluoroscopic catheter-based electroanatomical mapping of the heart. In vitro and in vivo accuracy results. Circulation 1997;95:1611–22. 50. Thiagalingam A, Wallace EM, Boyd AC, Eipper VE, Campbell CR, Byth K, Ross DL, Kovoor P. Noncontact mapping of the left ventricle: insights from validation with transmural contact mapping. Pacing Clin Electrophysiol 2004;27:570–8. 51. Wittkampf FH, Wever EF, Derksen R, Wilde AA, Ramanna H, Hauer RN, Robles de Medina EO. LocaLisa: new technique for real-time 3-dimensional localization of regular intracardiac electrodes. Circulation 1999;99:1312–7. 52. Sosa E, Scanavacca M, d’Avila A, Pilleggi F. A new technique to perform epicardial mapping in the electrophysiology laboratory. J Cardiovasc Electrophysiol 1996;7:531–6. 53. Thiagalingam A, Campbell CR, Boyd A, Ross DL, Kovoor P. Catheter intramural needle radiofrequency ablation creates deeper lesions than irrigated tip catheter ablation. Pacing Clin Electrophysiol 2003;26:2146–50. 54. Thiagalingam A, Pouliopoulos J, Barry MA, Boyd AC, Eipper V, Yung T, Ross DL, Kovoor P. Cooled needle catheter ablation creates deeper and wider lesions than irrigated tip catheter ablation. J Cardiovasc Electrophysiol 2005;16: 508–15. 55. Thiagalingam A, Campbell CR, Boyd AC, Eipper VE, Ross DL, Kovoor P. Cooled intramural needle catheter ablation creates deeper lesions than irrigated tip catheter ablation. Pacing Clin Electrophysiol 2004;27:965–70. 56. Holt PM, Smallpeice C, Deverall PB, Yates AK, Curry PV. Ventricular arrhythmias. A guide to their localisation. Br Heart J 1985;53:417–30. 57. Waldo AL, MacLean WA, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery. Circulation 1977;56:737–45. 58. MacLean WA, Plumb VJ, Waldo AL. Transient entrainment and interruption of ventricular tachycardia. Pacing Clin Electrophysiol 1981;4:358–66. 59. Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, Wiener I. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 1993;88:1647–70. 60. Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH, Friedman PL, Stevenson WG. Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation 2004;110:652–9. 61. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101:1288–96. 62. Haissaguerre M, Shah DC, Jais P, Shoda M, Kautzner J, Arentz T, Kalushe D, Kadish A, Griffith M, Gaita F, Yamane T, Garrigue S, Hocini M, Clementy J. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lancet 2002;359:677–8. 63. Haissaguerre M, Shoda M, Jais P, Nogami A, Shah DC, Kautzner J, Arentz T, Kalushe D, Lamaison D, Griffith M, Cruz F, de Paola A, Gaita F, Hocini M, Garrigue S, Macle L, Weerasooriya R, Clementy J. Mapping and ablation of idiopathic ventricular fibrillation. Circulation 2002;106:962–7.
ORIGINAL ARTICLE
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Original Article
Surgery and Ablative Therapy for Ventricular Tachycardia David L. Ross, FRACP ∗ Department of Cardiology, Westmead Hospital and University of Sydney, Westmead 2145, Australia
In the absence of acute ischaemia, ventricular tachycardia (VT) is the most common arrhythmia leading to cardiac arrest and death. This paper will describe the history of research into VT and the therapies that evolved. The contributions of John Uther and other members of the Department of Cardiology at Westmead Hospital will be outlined and placed into perspective. (Heart, Lung and Circulation 2007;16:214–221) © 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Ventricular tachycardia; Surgery; Ablation; History
Background
I
started research into VT in 1976, now 30 years ago, in the Department of Cardiology at Royal Melbourne Hospital. The head of department was Graeme Sloman and my supervisor was Jitu Vohra, both pioneers in cardiology, electrophysiology and pacing in Australia. At that time little was known about VT. Hein Wellens in the Netherlands had described inducibility of VT by programmed stimulation1,2 and Roworth Spurrell and colleagues reported surgical interventions based on presumed circuits utilising the bundle branches of the Purkinje system.3 In retrospect, these interpretations were erroneous for the most common forms of VT based on old myocardial infarction but VT circuits reentering via the bundle branches were later shown to be a rare cause of VT in cardiomyopathies. At Royal Melbourne Hospital in 1976 we began performing electrophysiological studies for diagnostic purposes in patients with broad complex tachycardias.4 This was done with much trepidation using what now seem to be very conservative stimulation protocols. The safety of such provocative testing was not known but we thought we had the facilities and staff to handle likely complications. Many cardiologists were very critical of this sort of work. However, time and extensive clinical experience over several decades in large numbers of patients has proven the safety of such an approach. In the mid 1970s there was little clinical benefit to the patient since the only treatments were Type 1 antiarrhythmic drugs such as quinidine, procainamide and disopyramide. In our initial studies we noted that multiple morphologies of VT were often present in the same patient.5 Available online 18 April 2007 ∗
Tel.: +61 2 9845 6795; fax: +61 2 9845 8323. E-mail address: [email protected].
Although this aspect was novel at the time we made our observations, a series of important papers on VT were then published by Mark Josephson in the USA including one describing the same phenomenon.6–9 Near the end of the 1970s, data were reported showing that antiarrhythmic drugs that inhibited induction of VT at electrophysiological studies predicted a good clinical response to long term oral treatment with the tested drug.10–12 This was the first time that electrophysiological studies achieved an important role in treatment of clinical VT. Concurrently, surgery for VT was shown to be useful for patients with refractory VT.13–17 Uther recruited me to join him at Westmead Hospital, the brand new university teaching hospital built in 1978 at Parramatta in Sydney’s western suburbs. This was considered to be in the nether reaches of Sydney by those who worked in the other teaching hospitals clustered near the city centre. However, even at that time, Parramatta was the demographic centre of Sydney, and the new teaching hospital provided an invaluable resource to the under serviced half of the population who lived west of Parramatta. When I returned in 1982 after training overseas with Wellens in Maastricht and Jay Mason, Roger Winkle and Jerry Griffin at Stanford, there were few electrophysiologists in Australia: Uther in Sydney, Vohra in Melbourne and Andrew Tonkin in Adelaide. Geoff Cope in Perth had trained in electrophysiology but became one of the Australian pioneers in the new field of angioplasty. Kevin Hellestrand studied electrophysiology with John Camm in London and returned to Royal North Shore Hospital in the early 1980s. After a short period of observation with John Gallagher and Will Sealy at Duke University, North Carolina, USA, Uther and cardiac surgeon Douglas Baird began surgery for supraventricular tachycardia (SVT) and VT at Royal Prince Alfred Hospital in the early 1970s. They amassed
© 2007 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2007.03.002
the third largest series in the world and achieved results comparable with the best international centres. Uther was then appointed as the foundation head of Cardiology at the new Westmead Hospital and the majority of the arrhythmia work followed him to Westmead. I considered it a privilege to join him and David Johnson, the Foundation Head of Cardiac Surgery, at Westmead. They were at the forefront of surgical treatment for arrhythmias in Australia at that time.
Surgery for Ventricular Tachycardia Surgery for VT began with resection of left ventricular (LV) aneurysms. However, VT often recurred. With time it became clear that VT circuits usually involved surviving bundles of myocardium at the margins of the aneurysm rather than dead tissue in the centre. The usual method for resecting aneurysms retained scar tissue at the margins to provide firm support for the suture line closing the ventricle. Thus, the arrhythmogenic tissue often remained and led to further arrhythmias.14,18 Other methods were then developed, predominantly map guided subendocardial resection pioneered by Josephson, Alden Harken, and Leonard Horowitz at Philadelphia.13,15,17 This method was based on the idea that reentrant VT circuits usually involved the subendocardium. Activation mapping during VT indicated the area to be resected. Endocardial resection retained the mid and outer walls and minimised compromise of left ventricular systolic function yet permitted resection over a wide area. Other surgical methods included encircling endocardial ventriculotomy19 and right ventricular disconnection20 conceived by the creative Gerard Guiraudon in Paris and later London, Ontario, Canada. The former method involved making a transmural endocardial incision around the margins of the aneurysm. This included the arrhythmogenic border zone and was therefore an improvement but involved compromise of adjacent normal myocardium. Right ventricular (RV) disconnection was designed for ventricular tachycardias due to RV dysplasia. Since RV dysplasia is a multifocal disease, there are usually multiple arrhythmia circuits. Disconnection was therefore an attractive concept. However, complete electrical disconnection of the free wall of the right ventricle was sometimes difficult to achieve. It also caused mechanical isolation of the lateral right ventricle which often had adverse haemodynamic consequences.21,22 Furthermore, the dysplasia often involved the septum which was not disconnected and provided the substrate for continued arrhythmia. All the above methods were reported to have modest success rates but had a significant mortality. Since there was no other alternative to failed antiarrhythmic drug treatment in those days, surgery for VT had an important role in refractory patients.
Surgery for VT at Westmead Hospital Uther, Baird and Johnson developed their modifications of international methods for surgical ablation of VT. Uther
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with Roly Hilder, the biomedical engineer at Royal Prince Alfred Hospital, built an innovative mapping system. These were the early days of computing and digital equipment. Mapping during arrhythmias was difficult because of the fast heart rates. Most systems printed out electrograms on paper at fast paper speeds and the timings of the signals were measured by hand. This made mapping very slow and inefficient. Mapping had to be done on cardiopulmonary bypass because tachycardias under general anaesthesia in this group of patients usually caused haemodynamic collapse. Since most patients with ventricular tachycardia had poor ventricular function, anything that prolonged cardiopulmonary bypass and the duration of the operation was most undesirable. The Hilder-Uther mapping system allowed capture of individual cycles, frozen display of the signals on a Tektronix oscilloscope and automated, real time read out of the activation time. This system was probably the best in the world at that time. It permitted reasonably rapid maps of the heart using a roving hand held electrode. When Uther moved to Westmead from Royal Prince Alfred Hospital, the mapping machine was rebuilt and named the Wing Chanoscope by wags in the Biomedical Engineering Department after the engineer who built it. This system was the size of a small fridge and could be transported with only moderate difficulty. In the first year at Westmead there was no cardiac surgery on site and the operations were performed at Royal North Shore Hospital. The mapping gear was transported in the back of a car to North Shore for the surgery. It was also transported to the Camperdown Children’s Hospital for paediatric cases and even to China for arrhythmia surgery. The Westmead innovation in surgery for ventricular tachycardia in ischaemic heart disease was mapping of late potentials to identify arrhythmia substrates and transmural resection of arrhythmogenic myocardium where possible. Late potential mapping was particularly useful in patients in whom ventricular tachycardia could not be induced at surgery (not an uncommon problem) or those who had too many morphologies for complete mapping or those in whom tachycardia rapidly degenerated to fibrillation. This approach arose from Uther’s work with signal averaging. Rob Denniss, in his MD project supervised by Uther, found late potentials at detailed epicardial mapping in dogs and humans after myocardial infarction and reconstructed the underlying histology.23 The areas with late potentials were associated with bundles of surviving myocardium in the underlying scar with slow conduction, one of the pre-requisites for reentry. In the 1980s Westmead performed over 100 operations for VT with a success rate of 83% as assessed by postoperative VT induction studies and a mortality of 15%. This was similar to most international series. The major problem with VT surgery was further destruction of an already poor ventricle leading to the relatively high mortality. Although outcomes in this group of patients were significantly better with surgery than failed medical therapy, better and safer methods were needed.
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Surgery was also performed for medically refractory idiopathic ventricular tachycardias arising in the right ventricular outflow tract. These patients were usually young people with no detectable structural heart disease. A good long-term success rate was achieved but resection of portions of the outflow tract and ventricular septum were required. Surgery was also performed successfully for young children ranging from infants to 10 years in age with refractory incessant ventricular tachycardias. These were due to ‘hamartomas’, now termed histiocytoid cardiomyopathy.
viously mapped patient and found a multitude of potential pathways through the tissue block rather than a few discrete bundles. This suggested that there were not limited, discrete pathways to target similar to an accessory pathway in Wolff–Parkinson–White syndrome but rather a field problem with multiple potential routes of conduction requiring ablation of a region. Complete ablation of all arrhythmogenic areas therefore would often require damage to a large mass of myocardium in patients with already severely compromised LV function.
Cryoablation and LASER for VT Surgery Detailed Catheter Mapping for VT Prior to Surgery One of the main problems with VT surgery was inability to induce all relevant tachycardias at surgery while under general anaesthesia and after handling of the heart. This prevented complete mapping of all arrhythmogenic areas. We therefore attempted detailed catheter mapping at electrophysiological study prior to surgery in an attempt to localise target areas. As part of his PhD at Westmead, Lloyd Davis inserted multiple decapolar electrodes into the ventricles.24 Up to 100 electrodes were inserted using four retrograde aortic catheters (two catheters in each femoral artery), three transeptal transmitral valve catheters, and single catheters in the coronary sinus, RV apex and RV outflow tract. These were procedural tour de forces in patients who often had major comorbidity that made the procedures more difficult. Transeptal procedures were not used in electrophysiology and rarely during cardiology at that time. Some hospitals had used the transeptal approach routinely for cardiac catheterisation of aortic stenosis but most centres had converted to the retrograde aortic approach. Davis reported that multiple morphologies of VT were the rule rather than the exception in the context of previous myocardial infarction (see Table 1).24 Although 74% of patients had multiple morphologies of inducible VT, different morphologies often arose from the same region of the heart. A single arrhythmogenic area was responsible for all arrhythmias in 57%. This suggested that localised ablation should be able to cure a substantial proportion of patients. However, 43% had multiple arrhythmogenic areas which would require ablation of disparate regions of the heart, usually located around the infarct or aneurysm. Davis made a detailed three dimensional (3D) histological reconstruction of an arrhythmogenic area in a post mortem specimen of a preTable 1. Detailed catheter mapping of VT Morphologies per patient: 1 2 3 ≥4 Arrythmogenic areas per patient: 1 2 3 ≥4 N = 23 patients.
6 (26%) 5 (22%) 6 (26%) 6 (26%) 13 (57%) 4 (17%) 5 (22%) 1 (4%)
Two new technologies for arrhythmia surgery came on the scene. Freezing of tissues with a cryoprobe allowed destruction of arrhythmogenic tissue while maintaining structural integrity. It therefore avoided suture lines and patches and minimised destruction of surrounding normal myocardium. Lasers were also used for surgical ablation. Geraldine Hunt, a veterinary surgeon, did her PhD at Westmead in cardiac electrophysiology and surgery. She studied cryoablation in collaboration with Richard Chard, then a surgical registrar and now surgeon at Westmead Children’s and adult hospitals.25 They showed that only superficial lesions were achieved using a conventional nitrous oxide cryoprobe if applied during normothermia as was done in many centres. Much bigger, clinically useful lesions were created if applied during systemic hypothermia. Lasers were more difficult to use because of safety issues but encouraging results were reported in a few institutions.26,27 Late diffuse myocardial dysfunction occurred in some cases, apparently due to refraction and diffusion of the laser beam into surrounding normal myocardium. Lasers tend to be reflected by shiny surfaces and fat and are more difficult to apply effectively from an epicardial approach. The laser approach has not been widely adopted.
Improved Methods for Surgical Mapping of VT Mapping during surgery was traditionally confined to the epicardial or endocardial surfaces. It was clear that many arrhythmias involved mid wall structures. The interventricular septum was often involved and the depth of the culprit tissues was usually unclear. Endocardial mapping usually involved ventriculotomy with consequent further ventricular damage unless there was a discrete fibrotic aneurysm. James Cox’s group at St Louis developed multi-electrode transmural needles for detailed intramural mapping.28–30 Needles were not commercially available. Davis and Vicki Eipper developed our own mapping needles by inserting four fine insulated wires down 21 gauge needles and out side holes at various depths to create a quadripolar mapping needle with a sharp tip. The needle lumen was then filled with acrylic. Longer needles with eight electrodes were also constructed for mapping the septum. They were inserted perpendicular to the heart surface into the anterior and posterior septum and provided nearly complete coverage of the septum. Subsequently, the needles were refined during
the tenure of the Cooperative Research Centre in Cardiac Technology. Westmead Hospital was one of the major participants along with Telectronics Pty Ltd, the CSIRO and other Sydney cardiovascular research centres. Chris Sodhi and Ilija Koevski, supervised by Andrew Madry and Pramesh Kovoor, developed a much better and professional needle system capable of mapping, temperature sensing at each electrode on each needle and capability of simultaneous radiofrequency ablation through multiple intramural electrodes. Each needle took several manhours to build and all were constructed by hand at the hospital. Detailed mapping of an arrhythmogenic area required 60–100 simultaneous needles. Construction of a set of electrodes for a single human case therefore involved several weeks of work. A dedicated needle maker was employed full time. Kovoor developed a sock electrode for global epicardial mapping to guide placement of the intramural needles in the arrhythmogenic areas. One of the major concerns was whether introduction of so many needles into the heart would damage or distort underlying conduction and whether there would be excessive bleeding. Kovoor performed detailed experiments in dogs which showed that bleeding was not a problem, myocardial conduction was not disturbed by the needles and the technique did not impair LV function.31 He also showed that creation of several intramural radiofrequency lesions in a normal ventricle did not create inducible VT.31
RF Ablation via Transmural Needles for Surgical VT Ablation Kovoor at Westmead studied ventricular intramural RF ablation using the Westmead-CRC multi-electrode temperature sensing needles. He showed that individual unipolar lesions were better than bipolar lesions between neighbouring electrodes. Bipolar lesions give two lesions for the one application of current but the electrode with the highest temperature controls the delivery of RF power in a temperature feedback system, leading to a smaller lesion at the cooler electrode. This technique often leaves gaps in lines of ablation. He also determined the appropriate temperature settings for temperature controlled intramural RF ablation.32 Temperatures up to 90◦ and even 100 ◦ C could be used because the absence of the cooling effects of blood flow caused the electrode temperature to reflect accurately surrounding tissue temperature. Steam or gas formation does not occur till tissue temperature reaches or exceeds 100 ◦ C. One of the concerns raised about RF ablation for VT was that scar would diminish RF lesion size because of less conductivity and make ablation less effective. Although some papers found evidence to support this concept, Kovoor studied ventricular intramural RF ablation in and adjacent to scar and found no effect on lesion size or tissue temperature profile around the ablation electrode.33 The contradictory results in other publications probably related to variation in electrode contact or blood cooling since they used surface electrodes for ablation. The Westmead-CRC multi-electrode intramural needles could therefore give relatively detailed transmural
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maps covering the arrhythmogenic area and extending out to adjacent normal muscle. As part of our CRC work, Michael Daly developed a RF splitter which allowed a single RF generator to deliver RF ablation to multiple electrodes simultaneously with individual temperature control and automatic adjustment of power to each electrode. The prototype device delivered RF ablation to four different electrodes but was capable of expansion to more electrodes if a more powerful generator was used. The mapping needles could also be used for temperature controlled RF ablation since each of the four electrodes on each needle had a thermocouple to sense temperature. If the needles were spaced at 5 mm distances in a grid pattern, it was possible to achieve any desired 3D lesion set in the block of tissue encompassed by the electrode array. If a sufficiently powerful generator was used, the desired 3D lesion set could be achieved in a single application of RF. We used the needle grids and RF splitter in a canine model of post infarction VT initially. The system was then used for surgical mapping and ablation of human post infarction VT and RV outflow tract VT in patients with repaired Tetralogy of Fallot who required pulmonary valve replacement for free pulmonary regurgitation. Gratifying results were obtained. However, this technology later lapsed for several reasons: the company that manufactured the programmable control system collapsed, the costs of construction of the needles were high and it was labour intensive to construct a new set of needles for each patient to ensure adequate sterility. The advent of the implantable defibrillator was the final blow.
Effects of Implantable Defibrillators on VT Surgery Our studies of antiarrhythmic drug therapy for ventricular tachycardia showed disappointing long-term efficacy. Surgery was too risky and not effective enough for more general use. The need for an alternative was filled by Mirowsky and Mower’s development of the implantable defibrillator.34–36 It rapidly became the primary treatment for VT and markedly reduced the need for VT surgery. The other reason for the demise of arrhythmia surgery was the advent of catheter radiofrequency ablation for arrhythmias including VT.
Catheter Ablation for VT The initial method for catheter ablation involved discharge of a defibrillator down a catheter through the distal electrodes abutting the region of interes.37–39 Discharge of a few thousand volts into a catheter electrode caused arcing and gas formation at the tip resulting in a mini explosion, appropriately termed ‘fulguration’ by Guy Fontaine from Paris, one of the pioneers of this technique. Fulguration caused a patchy area of necrosis which was sometimes arrhythmogenic and was not a suitable method for graded ablation due to multiple uncontrolled variables which determined lesion size. It was soon replaced by radiofrequency ablation (RF). Catheter RF ablation was developed by Steven Huang at Tucson, Arizona for creation of complete heart block in
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patients with intractable supraventricular arrhythmias.40 The first RF ablation for cure of a human tachycardia was reported by Martin Borggreffe at Dusseldorf.41 Catheter RF ablation soon proved to be reliably successful for ablation of the AV node, accessory pathways and AV nodal reentrant tachycardia. It was soon applied to VT. However, the problems with catheter ablation of VT were similar to surgery. It was difficult to map multiple morphologies, and the RF lesions were often not deep enough to reach the critical tissues. Roving catheter mapping could not be performed for tachycardias that were poorly tolerated haemodynamically or rapidly degenerated to ventricular fibrillation. Advantages over surgery were that it was usually easier to induce sustained arrhythmias and catheter procedures could be repeated easily.
Improved Methods of Catheter RF Ablation Catheter RF ablation underwent several improvements. The initial method monitored current and power was adjusted manually to obtain currents of 500 mA or more. At higher powers, coagulation and carbonisation formed at the interface between the electrode and the tissue, often leading to a ‘pop’ as gas was formed. When coagulum formed, a high impedance interface occurred leading to a small and ineffective lesion. Temperature monitoring of the catheter tip was then introduced using thermistors or thermocouples with automated temperature feedback control of power delivery.42 This minimised excessive temperatures at the tip and helped prevent coagulum and impedance rises. If there was no temperature rise as power was delivered, it also indicated that the electrode was not in good contact with the tissue. VT ablation often requires ablation of relatively large volumes of tissue or deeper lesions. This was hard or impossible to achieve with standard 4 mm tip electrodes. Larger electrodes up to 8–12 mm in length were tried with high output RF generators.43 Up to 8 mm electrodes did increase lesion size but the largest electrodes did not with commercially available RF generators. This was due to an inadequate power density for the larger surface area electrodes. The next advance was irrigated tip RF ablation developed by Wittkampf and Mittleman and refined by Nakagawa and Jackman.44,45 Cooling of the tip of the electrode by saline irrigation through the catheter at 20–30 ml/min allowed more energy to be delivered without coagulum formation and created substantially larger and deeper lesions. This innovation was an important advancement which improved results substantially. Other technologies studied for catheter ablation included cryoablation, microwave, laser and ultrasound. At present, RF ablation remains the preferred method.
Improved Methods for Catheter Mapping of VT Detailed catheter mapping is difficult to analyse by the roving catheter method, especially for complex or multiple circuits. The use of simultaneous multi-electrode mapping using large numbers of individual catheters was developed at Westmead as described earlier. Substan-
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tial advances in mapping soon followed. The first method used basket catheters with 64 electrodes arrayed on eight splines.46,47 The basket splines were flexible and could be collapsed within a guiding catheter to be passed to the chamber of interest, then protruded beyond the tip to expand the basket automatically to its native spherical shape. It was a little difficult to identify the position of each spline in 3D space on fluoroscopy and each signal needed to be analysed manually to mark local activation. The shape of the basket usually did not match the complex anatomical shapes of the cardiac chambers closely, thus causing several electrodes to fail to make contact with myocardium. Although an advance, significant problems remained with this system. The electroanatomic mapping system then became available. It used three orthogonal microcoils at the catheter tip to pick up electromagnetic signals from three electromagnets of different frequency spaced in a triangular grid under the bed. By using a triangulation method similar to satellite navigation systems, the position of the catheter tip in 3D space could be determined in real time with an accuracy of 1–2 mm.48,49 This information was combined with computerised 3D displays of the activation sequences and electrogram voltages of the mapped surface. The better anatomical information and precise anatomical marking of the sites of lesion delivery greatly facilitates design and accurate delivery of lesion sets. The main defect of this system is the slowness of roving catheter maps which prevent use in poorly tolerated or non-sustained ventricular tachycardias. Another common problem is to miss a change in arrhythmia morphology and continue mapping as if the original arrhythmia was still present. This generates faulty maps. The non-contact multi-electrode mapping system is another 3D system that uses a 64 electrode array deployed in the cavity of the chamber to be mapped. A locator signal is emitted from the roving electrode catheter as it is moved around to various sites in the chamber of interest to delineate its outer margin. The position of the roving electrode in 3D space is determined by a triangulation method using the array signals detected from the roving electrode. A geometry depicting the chamber of interest is then constructed by moving the catheter to cover the endocardial surface of the chamber. Activation signals detected on the intracavitary array are then processed using La Place’s law to derive the potentials at the endocardial surface of the chamber described by the previous geometry. This permits derivation of 3360 virtual endocardial electrograms in real time. The whole chamber can be mapped in a single beat. This technology is especially useful for non-sustained arrhythmias, especially those seen in some RV outflow tract tachycardias or atrial tachycardias. The accuracy of the derived signals compared to actual electrograms recorded from multiple transmural needle electrodes was studied in sheep left ventricles by Aravinda Thiagalingam at Westmead.50 Accuracy decreased exponentially when the area of interest was >4 cm from the centre of the array or at the poles of the array. It was most accurate opposite the equator of the array. The loss of accuracy in a large chamber is a major limitation since many of
the cardiac chambers to be mapped are dilated. The array is also not very directable and tends to go to a limited number of stable sites that may not be close to the area of interest. Other technologies use three orthogonal currents transmitted from skin patches or ultrasound for locating mapping catheters in space to create 3D maps. The orthogonal current method uses an orthogonal X, Y, and Z grid of patches applied to the thorax transmitting 1 mA currents at 30 kHz and a reference intracardiac catheter.51 The position in 3D space can then be computed real time as the catheter is moved. The ultrasound method uses reference ultrasonic crystals applied to the thorax versus a crystal in the catheter tip and follows a similar principle.
Epicardial Mapping and Ablation for VT A recent innovation in RF ablation for ventricular tachycardia was pioneered by Eduardo Sosa and colleagues in Sao Paolo, Brazil.52 Their group has extensive experience treating ventricular tachycardia due to Chagas’ disease, a protozoal infestation of the heart. VT circuits in this condition often involve the epicardium. Endocardial RF ablation is therefore often ineffective. Sosa and colleagues gained access to the pericardial space using a needle introduced via the xiphisternal approach. Surprisingly, this is usually not difficult even though there is only a potential pericardial space filled with minimal fluid. A guide wire and sheath are then inserted and an ablation catheter can be advanced into the pericardial space. This permits detailed epicardial mapping and RF ablation if necessary. Epicardial ablation is particularly useful for cardiomyopathic or arrhythmogenic RV dysplasia VT, and some idiopathic LV and ischaemic VT.
Intramural Catheter RF Ablation for VT Thiagalingam at Westmead developed a catheter which can insert a needle electrode into the myocardium to any desired depth for intramural and epicardial ablation in cases refractory or unsuitable for endocardial ablation. This technique uses an innovative helical screw to fix the outer catheter to the endocardium so the needle can be delivered easily and reliably to the desired depth.53 Since RF lesions created by a needle electrode are relatively narrow, an irrigated tip version was developed which creates larger volume and transmural lesions if required.54,55 These catheter electrodes have been manufactured in prototype form and used in animal models but not yet in human ablation.
Pace Mapping and Entrainment for VT Other techniques for localising VT circuits are pace mapping and entrainment. Pace mapping was first described by Paul Curry and colleagues in London and involves pacing at different sites to achieve the best match between the paced 12 lead ECG and that in VT.56 A good match implies that the pacing catheter is at or near the exit site of the circuit or focus. This technique is useful when no arrhythmia
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is inducible and a 12 lead ECG of tachycardia is available for comparison. It is also useful for non-sustained or poorly tolerated arrhythmias. However, there may be discrepancies of up to 2–4 cm in the sites of best pace match and the actual origin of the tachycardia. Entrainment was first described by Al Waldo and colleagues57,58 and important additional concepts for VT were added by Bill Stevenson.59,60 These dynamic interventions during a sustained tachycardia prove whether the pacing site is in the circuit rather than just inferred from mapping. It is an invaluable diagnostic tool, especially in complex tachycardias. It is especially useful for defining the area of slow conduction in the circuit which is usually the critical area for successful ablation. However, attempts at entrainment may terminate tachycardia or convert it to different morphologies or accelerate the arrhythmia to a haemodynamically unstable rhythm requiring cardioversion.
Substrate Modification for VT Ablation Other approaches to ablation use an anatomical strategy aiming to create lines of ablation at the margins of the infarct or radial lines from the infarct centre.61 These substrate modification strategies are useful when mapping during tachycardia is impossible or limited or the patient is in extremis and needs a quick procedure.
Ablation of VF Triggers Some patients with medically refractory, frequently recurrent ventricular fibrillation have reproducible initiation of each episode by a single morphology of ventricular ectopic beats. Haissaguerre in Bordeaux found that these ectopics usually arose in the Purkinje system.62,63 Ablation of the initiating ectopy often prevented recurrent arrhythmias.
Role of Implantable Defibrillators in Ablative Therapies for VT The implantable defibrillator is an invaluable adjunct to surgical or catheter ablation therapies for VT. The defibrillator provides protection against dangerous recurrent arrhythmias that may not have been ablated successfully and is an unrivalled method for continuous out-ofhospital arrhythmia monitoring. Implanting a defibrillator permits a strategy where only the most frequent or troublesome tachycardias need to be ablated, leaving the device to handle any other residual arrhythmias. This means that heroic and potentially hazardous attempts to completely ablate all inducible tachycardias are not necessary. Complete abolition of all inducible ventricular tachycardias in the context of coronary artery disease and old myocardial infarction is often not possible if a sensitive induction protocol using up to four extrastimuli is used. Many patients presenting for catheter ablation of VT have implantable defibrillators in situ but suffer intermittent storms of VT with recurrent shocks. These patients are often conscious during such shocks leading to major psychological decompensation. Catheter ablation is very
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useful for abolishing the most troublesome morphologies of VT in this context and markedly improves patient well being.
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15.
Conclusions The evolution of ablative therapies for VT has been an exciting journey leading to major improvements in outcomes for our patients. Uther and subsequent members of the Department of Cardiology have made many contributions to this progress. However, there is still much to be done and VT remains a challenging clinical problem.
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