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J Thorac Cardiovasc Surg 1994;108:855-861
© 1994 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

Balloon electric shock ablation—A surgical technique for treatment of ventricular tachycardia: Influence of endocardial scar on depth of ablation achieved

Lynda L. Mickleborough, MDa, Shunichi Mizuno, MDa, Akihiko Usui, MDa, Greg Wilson, MDb, Donna McComb, MScb, Gordon Gray, BSca


Toronto, Ontario, Canada

Supported by the Canadian Heart Foundation, the Heart and Stroke Foundation of Ontario, and the Cardiovascular Research Fund, University of Toronto.

Received for publication Nov. 23, 1993. Accepted for publication May 10, 1994. Address for reprints: Lynda L. Mickleborough, MD, EN 13 - 217, 200 Elizabeth St., Toronto, Ontario M5G 2C4 Canada.

Abstract

Balloon electric shock ablation is a surgical technique that has been used for treatment of ventricular tachycardia. However, little is known about the energy requirements and precise electrode array best suited to achieve effective ablation of the target area while limiting injury to the surrounding myocardium. This study was designed to determine the effects of endocardial scar (often present at the "site of origin" of clinical ventricular tachycardia) on depth of ablation resulting from balloon electric shock ablation. A chronic canine model of endocardial scar (3.9 ± 0.6 mm thick) was developed with the use of balloon electric shock ablation techniques. We compared depth of ablation achieved with balloon electric shock ablation with low-energy shocks (22 J per bead) in normal dogs versus those with chronic endocardial scar. No difference was found in depth of ablation in normal dogs and in the scar model (7.2 ± 1.2 mm versus 6.2 ± 1.0 mm). Depth of injury expressed as a percentage of wall thickness was not different in the two groups (61% ± 11% versus 57% ± 3%). We conclude that the presence of endocardial scar does not influence depth of injury resulting from balloon electric shock ablation. This data provides guidance for clinical application of the technique as a "closed heart" surgical approach for control of ventricular tachycardia. The data are also discussed in relation to energy levels currently used for direct current catheter ablation in patients with ventricular tachycardia. (J THORACCARDIOVASCSURG1994;108:855-61)

Map-directed operations offer a potential cure for patients with ventricular tachycardia (VT).Go 1 Most surgical candidates have extensive coronary artery disease and a history of previous infarction. Preoperative ventricular function is often significantly compromised, but only 50% of patients have a clear-cut area of transmural scar or resectable aneurysm.Go Go 2-4 Most arrhythmias associated with ischemic heart disease appear to arise from the subendocardium. With standard approaches for intraoperative endocardial mapping and surgical ablation, a ventriculotomy incision is required to obtain access to the inner layers of the heart. The ventriculotomy, and scarring associated with its healing, may contribute to perioperative mortality and postoperative morbidity.Go Go 5,6

We have described a surgical technique that we call balloon electric shock ablation (BESA),Go 7 which can be used to control arrhythmogenic foci in patients with VT. With this method, sequential shocks are delivered to a grid of electrodes on a balloon that is introduced into the intact ventricle across the mitral valve. We have previously shown in normal dog hearts that a predictable area of endocardium can be ablated with this technique.Go 8 We have also reported on possible detrimental effects of the technique on mitral valve function if shocks of sufficient energy are directly applied to the mitral valve apparatus.Go 9

In the clinical application of this technique, it would be important to use the lowest possible energy that results in the desired depth of ablation in the target area while, at the same time, limiting injury to the surrounding myocardium. Because the site of VT origin in patients with coronary artery disease usually corresponds to an area of scar mixed with viable muscle,Go Go 10,11 this study was designed to determine the effects of previous endocardial scarring on depth of ablation achieved with BESA.

METHODS

Creation of model with a layer of endocardial scar
Description of balloon apparatus for shock delivery
A latex double-layered balloon was covered with expandable mesh. Forty-six silver bead electrodes were attached to Teflon-insulated 36-gauge stainless steel wires and sutured to the balloon in a specific pattern at 0.5 cm intervals (Fig. 1, A). The area covered by the electrodes was designed to correspond to the anteroapical portion of the left ventricle including the septum. The wires were attached to a connector which allows an electric shock to be delivered to each bead.



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  		Fig. 1. A, Balloon electrode array used for creation of model of diffuse endocardial scar. B, Indication of electrodes used at the second procedure to produce ablation within the area of previous scar.

 
Determination of appropriate shock energy to create contiguous endocarkial scar.
From previous experiments, we know that shocks of 100 J delivered through beads in a 1 cm grid cause transmural scarring in the apical region of a normal dog heart (depth of injury 9 to 11 mm).Go 8 We also know that delivery of 100 J shocks to beads with a closer spacing (0.5 cm) will result in injury up to 16 mm in depth in the region of the papillary muscle.Go 9 The depth of injury depends on energy delivered and spacing between the beads. From previous experience we also know that other factors, such as type of defibrillator used, size of animal, and position of back plate relative to the heart, can influence depth of injury achieved with BESA (unpublished data, 1991). We experimented with decreasing energy levels and a 0.5 cm electrode grid applied to the anteroapical region of the left ventricle including the septum in dogs of a standard size (30 to 35 kg) with the back plate (anode) in a standard position. A Tektronix storage oscilloscope (Tektronix Inc., Beaverton, Ore.) monitored the voltage and current wave forms during delivery of the shocks. In this preparation by using shocks of decreasing energy (75, 50, 35, 30, 26, 22, and 20 J), we determined that shocks of 22 J per bead were needed to create a contiguous layer of endocardial scar in the chronic preparation (Fig. 2).



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  		Fig. 2. Transverse section of dog heart showing thin layer of endocardial scar. The specimen has been stained with tetrazolium to increase contrast between mature scar and viable myocardium. ANT, Anterior; POST., posterior.

 
Operative procedures
Eight adult mongrel dogs (30 to 35 kg) underwent a right thoracotomy and were supported on cardiopulmonary bypass at 37° C. An incision was made in the left atrium, and the balloon apparatus was passed across the mitral valve. The electrode array was positioned so that, after balloon inflation, the beads were in contact with the anteroapical area of the left ventricle including the septum. In this way we avoided injuring the papillary muscles and their attachments during shock delivery. A series of 22 J shocks (synchronous with the R wave) were delivered to each electrode with a Space Labs defibrillator (model 4045; Space Labs, Inc. Redmond, Wash.) which provides a damped sinusoidal discharge. The bead electrodes served as the cathode and a standard cautery pad (15 x 25 cm2) applied to the right hind leg served as the anode. VT or ventricular fibrillation commonly occurred after shock delivery. Delivery of the next shock often interrupted the arrhythmia. If ventricular fibrillation persisted, defibrillation was performed with internal paddles (20 W · sec). After delivery of all shocks the balloon was deflated and removed. Bypass support was continued for 20 to 30 minutes (total pump time 60 to 70 minutes). Air was removed from the left side of the heart and the left atrial incision was closed. The dogs were weaned from bypass and decannulated. After closure of the thoracotomy incision, they were allowed to recover under careful hemodynamic monitoring.

All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH publication No. 86-23, revised 1985).

Measurement of depth of acute injury
Three animals were killed 24 hours later. The hearts were excised and sliced in a breadloaf fashion at 5 mm intervals. The region of acute BESA injury was identified by staining with tetrazolium red (2, 3, 5-triphenyl tetrazolium chloride; BDH Chemicals, Toronto, Ontario, Canada) at 37° C according to the method of Lie and colleagues.Go 12 Areas of interest were blocked (four blocks per dog), fixed in 10% buffered formaldehyde, dehydrated, and imbedded in paraffin. Sections of 5 µm thickness were cut from each block, stained with hematoxylin-phloxine-saffron stain, and examined by light microscopy. The depth of acute injury was determined in multiple blocks in each animal. Injury was also recorded as a percentage of wall thickness in each section.

BESA procedure
In five controls (normal hearts) and in five dogs with chronic endocardial scar (6 to 8 weeks after the initial procedure), BESA was performed. The dogs underwent a left thoracotomy, and the balloon apparatus was inserted as previously described. After balloon inflation, shocks of 22 J were delivered to 14 of the bead electrodes in the center of the grid as indicated in Fig. 1, B, so as to result in acute injury within the area of previous scar formation. Operative techniques have already been described in the section on the scar model. The dogs survived with close hemodynamic monitoring for 24 hours and then were killed.

Pathologic studies
The hearts were excised and sliced in a breadloaf fashion. The region of acute BESA injury was localized by tetrazolium staining and transmural left ventricular tissue blocks were taken from the area of interest (average 40 blocks per dog). Tissue blocks were processed and sections stained as previously described. Depth of injury (chronic scar, if present, plus superimposed acute injury) was determined in multiple blocks in each animal (Fig. 3). Injury was also recorded as percentage of wall thickness in each section. In two dogs, tissue was taken from the area of acute injury, as defined by tetrazolium staining, and immediately placed in a fixative solution of 2% glutaraldehyde in phosphate buffer (0.1 mol/L, pH 7.4). After at least 2 hours of fixation, the tissue samples were rinsed repeatedly in phosphate buffer and postfixed in 1% osmium tetroxide solution for 1 hour. Postfixation was followed by dehydration in graded alcohols and propylene oxide and then embedding in Epon-araldite epoxy resin. Thin sections of samples were mounted on copper grids and stained with uranyl acetate and lead citrate. Sections were viewed and photographed with a Philips 201 electron microscope (Philips N.V., Einthoven, The Netherlands).



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  		Fig. 3. Tissue block from endocardial scar animal who underwent subsequent BESA (stained with tetrazolium) showing inner layer of chronic scar with superimposed layer of acute injury.

 
Statistical analysis
Depth of injury and percentage of wall thickness are summarized as mean ± standard deviation in the text and GoTable I. Differences between two experimental groups were evaluated by t test.


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  		Table I.
 
RESULTS

As previously reported during BESA shock delivery, we obtained a consistent peak voltage and current within each animal. In all cases the wave form was smooth without any breaks. At energy use higher than 22 J per bead, almost transmural injury was identified by tetrazolium staining after 24 hours. With shocks of 20 J, the endocardial injury at 24 hours was patchy and nonconfluent. With shocks of 22 J per bead, the depth of acute injury as assessed by tetrazolium staining in multiple blocks from two animals after 24 hours was 7.3 ± 1.1 mm or 63% ± 12% of wall thickness. Light microscopy of the acute injury showed extensive contraction band necrosis, nuclear pyknosis, and extravasation of red cells into the myocardium. Coronary arteries within the ablated area appeared to be well preserved. Electron microscopic examination showed, in addition to the obvious contraction bands, dehiscence of intercalated disks and changes in the mitochondria, which were swollen and contained numerous electron dense inclusion bodies (Fig. 4).



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  		Fig. 4. Electron micrograph at a magnification of 4355x taken from area of acute BESA injury showing prominent contraction bands and electron dense mitochondrial inclusion bodies.

 
When the animals survived for 6 to 8 weeks (chronic scar model), the average depth of mature scar was only 3.9 ± 0.6 mm (GoTable I). Expressed as a percentage of wall thickness, the scar constituted 30% ± 5%. On light microscopy the mature scar was composed of hypocellular, dense, collagen-rich connective tissue in which intramural coronary arteries were trapped but no viable myocardium was present. At the periphery a loosely organized connective tissue matrix was found containing microvasculature but not myocytes, with a sharp transition to structurally normal myocardium. When comparing the depth of BESA ablation in normal dogs versus the scar model, no significant difference was found in depth of acute injury 7.2 ± 1.2 mm versus 6.2 ± 1.0 mm (GoTable I). Depth of injury expressed as percentage of wall thickness was also not different in the two groups: 61% ± 11% in controls versus 57% ± 3% in the scar model (not significant by t test).

DISCUSSION

In these experiments we have shown that balloon delivery of shocks of relatively low energy (22 J per bead) results in acute injury of a significant depth of myocardium in the normal dog heart and in hearts with previous endocardial scar (depth 7.3 ± 1 mm and 6.2 ± 1.0 mm, respectively). The acute injury is characterized by contraction band necrosis, nuclear pyknosis, swelling of mitochondria, and dehiscence of intercalated disks. Extravasation of red cells into the myocardium is present, but the coronary arteries within the lesion appear relatively well preserved. These morphologic changes are similar to those previously described in association with electric injury associated with catheter ablation or defibrillation.Go Go 13-15

In the chronic phase of the experiments, acute electrical injury is replaced by chronic scar. This scar has been compared with that resulting from myocardial infarction caused by coronary occlusion in human beings. After coronary occlusion the endocardium is intact, whereas after balloon electric shock ablation, with electric energy applied directly to the endocardium, endocardial fibrosis occurs. After coronary occlusion, usually a thin band of myocardium 5 or 10 cells thick escapes ischemic injury caused by nourishment by diffusion from the ventricular cavity. After BESA, this inner rim of the myocardium is destroyed and replaced by scar. The thickness of the scar with BESA is more uniform than that usually seen with a subendocardial infarction as a result of coronary disease, presumably because the zone of lethal electric injury to the myocardium is more uniform than the area at risk in patients, which is made up of multiple microvascular territories of the end circulation supplied by the occluded coronary artery. Some fatty infiltration was seen in the BESA scars in this study, which is similar to scarring seen in transmural infarcts from coronary artery occlusion. Such fatty infiltrates are not commonly seen with subendocardial infarcts. BESA results in necrosis of up to 60% to 70% of the wall thickness and more closely approximates a transmural infarct in this respect. Finally, after BESA in some dogs, we have observed focal areas of cartilaginous metaplasia in the endocardial scar. This nonspecific reaction to injury is common in the dog but unusual in human beings.

Direct current catheter ablation has been used since 1983 with some success in the treatment of ventricular tachycardia.Go Go 16-24 During catheter ablation, shocks from a standard defibrillator are associated with arcing, which results in intense heat and gas formation. Subsequent collapse of the "vapor globe" gives rise to high energy shock waves which may result in damage of adjacent tissue and, in remote areas of the myocardium, "farfield effects".Go Go 25-30 It is thought that tissue destruction resulting from catheter ablation depends on a complex interaction between barotrauma and thermal phenomena, as well as the biologic effects of electric current. However, voltage is thought to be the main factor responsible for desired tissue damage.Go Go 31,32 Lesion size also depends on type of catheter used, degree of catheter tissue contact maintained during shock delivery,Go 28 the physical characteristics of the energy delivered (voltage wave form, cathodal versus anodal shocks),Go Go 26,27 and position of the back plate relative to the electrode.Go 33

With the catheter technique, even in controlled studies, the depth of ablation achieved has been variable. Using standard USCI catheters (United States Catheter and Instruments Co., Murray Hill, N.J.), Hauer and colleaguesGo 34 reported a lesion depth of 6 to 10 mm when shocks of 30 J were delivered in dogs weighing 14 to 18 kg (back plate positioned on the chest wall). In contrast, Huang and colleagues,Go 35 using similar catheters and back plate configuration, reported lesion depths of only 5.2 mm after catheter delivery of shocks of 100 to 300 J in dogs weighing 22 to 30 kg. These differences in depth of injury may be related to variable electrode contact and loss of energy into the surrounding blood-filled ventricular cavity (arcing).

BESA differs from catheter ablation in the following important respects: (1) because of balloon inflation, close contact is maintained between the electrodes and the endocardium during shock delivery, (2) the silver bead electrodes used on the balloon differ from standard catheter electrodes and are more similar in design to electrodes developed for the National Heart Hospital ablator,Go 36 and (3) arcing has rarely occurred during BESA (lack of breaks in voltage and current wave form obtained during shock delivery).

Our data from these experiments may have implications in interpreting the results of catheter ablation. In clinical practice with the use of catheter techniques for ablation of VT, energy levels of 200 to 400 J have been required to achieve successful ablation.Go Go 16-24 On the basis of depth of injury achieved in animals with catheter ablation and assuming an endocardial site of origin of VT in most patients,Go Go 35-37 clinical success should be expected with shocks of much lower energy. Possible explanations for this discrepancy may include variability in the spacial relationship between ablation site and position of anodal sink or back plate,Go Go Go 34,36,38 variable loss of energy into the surrounding blood-filled cavity related to variability in electrode-tissue contact, and the possibility that efficacy of ablation may be limited by preciseness of mapping techniques. In the past it has been suggested that the high energies needed to achieve effective ablation with the catheter technique could be related to existence of previous scarring in the target area.Go 38 However, our experiments show that with balloon electrodes the presence of previous scar has no effect on depth of electric ablation achieved with defibrillator shocks.

In the chronic phase of our experiment, the area of contraction band necrosis becomes replaced by mature scar. With time, progressive contraction of collagen fibers within the scar reduces the depth of tissue injury from 7.3 ± 1.1 mm to 3.9 ± 0.6 mm. A similar decrease in depth of chronic lesion has been previously reported after catheter ablation with the use of direct current.Go 38 In our study it is noteworthy that the extent of tissue injury, expressed as a percentage of total wall thickness, was 63% ± 12% at 1 day and only 30% ± 5% after 6 to 8 weeks. It appears that surviving myocardium overlying the endocardial infarction hypertrophied to compensate for thinning of the wall, which results from electric ablation.

Our data provide guidelines for the clinical application of BESA as a closed heart surgical procedure for control of VT. When we first used BESA in patients with VT, according to previous experience with catheter ablation, we used high energy shocks (175 J per bead).Go 7 In our more recent experience we have reduced energy of shocks delivered through the balloon electrodes and have obtained cure of VT in patients with energy levels as low as 75 J per bead. Further experience is needed to define the minimal level of energy needed to achieve successful ablation with BESA in patients while minimizing injury to surrounding normal myocardium.

Acknowledgments

We extend our appreciation to Hilary Vincent for the excellent preparation of the manuscript and to Richard Adams, Peter Bertozzi, and the late Erma Minaker for technical assistance. We are grateful to Dr. Jack Butany, Cardiovascular Pathologist at The Toronto Hospital for reviewing the histology from this experimental study in regard to similarities and differences with healing myocardial infarcts from coronary artery disease.

Footnotes

From the Division of Cardiovascular Surgery, The Toronto Hospitala, the Department of Pathology, The Hospital for Sick Childrenb; and the Departments of Surgerya and Pathology,b University of Toronto, Toronto, Ontario, Canada. Back

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