Transcatheter Subendocardial Infusion
A Novel Technique for Mapping and Ablation of Ventricular Myocardium
Background Catheter ablation with radiofrequency energy is feasible in a limited subset of patients with ventricular tachycardia. The purpose of this study was to evaluate a technique for mapping and ablation of ventricular myocardium with the use of transcatheter subendocardial infusion.
Methods and Results A needle-tipped deflectable electrode catheter was used to deliver reagents to endocardial target sites. This was equipped with two central lumens to allow sequential administration of mapping and ablation injectants with minimal admixture. The mapping injectant consisted of a mixture of lidocaine, iohexal, and glycerin; the ablation injectant contained ethanol, iohexal, and glycerin. Infusion of the mapping injectant (1 cm3 over 3 or 5 seconds, n=14) produced a stain on fluoroscopy and increased local capture threshold by 61%. No lesions resulted from mapping infusions. Infusion of the ethanol-containing injectant (n=48) produced discrete lesions, with a mean volume ranging from 0.6 to 1.5 cm3. There was a direct relationship between infusion volume, infusion duration, and resultant lesion volume. Fibrosis in a region of healed myocardial infarction did not impair diffusion of the injectant or affect lesion dimensions. Microscopic analysis of chronic lesions showed a sharply demarcated border zone between fibrotic and normal myocardium.
Conclusions Transcatheter subendocardial infusion can be used to reversibly impair local excitability and mark an injection site fluoroscopically. Subendocardial injection of ethanol can predictably ablate a large volume of ventricular myocardium. Additional study of this system in an arrhythmia model will help to define its potential for mapping and ablation of hypotensive ventricular tachycardia.
Radiofrequency catheter ablation is useful for palliation of a small subset of patients with a history of myocardial infarction and ventricular tachycardia.1 2 3 4 5 Most patients with ventricular tachycardia are not candidates for ablation for several reasons. Most episodes of induced ventricular tachycardia produce hypotension, which precludes detailed endocardial mapping. Arrhythmia foci may be multiple and/or deep to a layer of subendocardial fibrosis.6 7 8 The lesions produced by radiofrequency ablation are typically 0.3 to 0.5 cm3 in volume.9 Although this size may be large enough to interrupt a single isthmus of slow conduction, it is insufficient to ablate larger regions of the border zone of potentially arrhythmic tissue surrounding a healed myocardial infarction. Intracoronary infusion of ethanol can produce larger lesions but is technically demanding, difficult to control, and risky.10 11 12 13 14
The purpose of the current study was to evaluate the feasibility of a novel technique for mapping and ablation of ventricular tachycardia. We used a needle-tipped lumen electrode catheter for subendocardial infusion of reagents to reversibly impair excitability, mark the affected area on fluoroscopy, and then create irreversible injury in a controlled fashion by direct intramyocardial injection of ethanol.
Fig 1⇓ shows the subendocardial infusion catheter used in this study. The 7F device had a deflectable shaft and was equipped with tip and ring electrodes 2.5 mm apart. The two lumens in the core communicated with a No. 27 needle protruding 2 mm from the tip of the distal electrode. This double-lumen configuration allowed sequential administration of mapping and ablation injectants with minimal mixing. The mapping injectant consisted of 2% lidocaine, contrast medium (Hypaque 76), and glycerin in a ratio of 2:1:1. The ablation injectant was a mixture of 95% ethanol, contrast, and glycerin in a ratio of 3:1:1. Glycerin was used to increase viscosity to impair diffusion from the injection site. Aliquots of 1, 2, or 3 cm3 of each mixture were injected at 3, 5, or 7 seconds with a high-pressure perfusion pump (Harvard Apparatus No. 44).
Protocol 1: Acute Effects of Mapping and Ablation Injectants
Ten dogs (weight, 26±5 kg) were used in this phase of the study. The dogs were anesthetized with morphine (4 mg/kg SC) followed by pentobarbital (20 mg/kg IV). After endotracheal intubation, the dogs were mechanically ventilated, and tidal volume was adjusted to maintain arterial pH between 7.35 and 7.45. The surface ECG and arterial pressure were monitored continuously. Long hemostatic sheaths (730 mm in length and 11F in diameter) were introduced into the femoral artery and vein and advanced under fluoroscopic guidance to the level of the right atrium and the left ventricle. The subendocardial infusion catheter was introduced through the long sheaths and placed at two or three widely disparate sites in both the right and left ventricles. The aliquot volume (1, 2, or 3 cm3) and infusion time (3, 5, or 7 seconds) of mapping or ablation injectants used at each site were randomly chosen. The needle-tipped catheter was placed in a stable endocardial position and manipulated so that it was within 45° of perpendicular relative to the endocardial surface. Bipolar endocardial electrograms (bandpass, 3 to 500 Hz) and bipolar pacing capture threshold were determined. The injectant was then delivered during continuous monitoring. Cinefilm recordings of the resultant subendocardial stain were obtained during injection at 2 and 5 minutes after injection. Repeated determination of bipolar pacing capture threshold was made immediately after injection and every 60 seconds for 5 minutes. Local electrograms also were recorded continuously during this period. One hour after the last injection, 2,3,5-triphenyltetrazolium chloride (4% in phosphate buffer to produce a pH of 7.4) was infused to stain viable myocardium and better delineate the extent of the lesions. The dogs were then killed, and the hearts were excised and fixed in 10% formalin. Blocks of tissue encompassing each of the lesions were excised and analyzed as described below.
Protocol 2: Infusion Ablation in Regions of Healed Myocardial Infarction
The effects of chronic scar on the performance of the subendocardial infusion ablation system were assessed in five dogs (weight, 27±1 kg) 3 months after experimental myocardial infarction. The dogs were anesthetized with morphine (4 mg/kg SC) followed by methohexal (7 mg/kg IV). After intubation and mechanical ventilation, anesthesia was maintained with isoflurane. A left coronary guiding catheter was introduced into the femoral artery and advanced to engage the ostium of the left main coronary artery. A 3F balloon angioplasty catheter (balloon dimensions, 2.5×20 mm) was placed in the midportion of the left anterior descending coronary artery distal to the first diagonal branch. Balloon inflation to 8 atm was maintained for 3 hours. Catheters were then removed, and the dogs were allowed to recover.
The dogs underwent infusion ablation 93±4 days after experimental myocardial infarction. Anesthesia and monitoring were as described in protocol 1. A standard quadripolar electrode catheter (Bard Electrophysiology) was introduced into the femoral vein and positioned in the right ventricular apex. Programmed stimulation at drive cycle lengths of 500 and 350 milliseconds was performed with single, double, and triple extrastimuli at both the right ventricular apex and outflow tract. Next, a cine left ventriculogram was performed in both the left and right anterior oblique projections to delineate the hypokinetic and akinetic segments of the anterior wall.
The infusion ablation catheter was introduced into the left ventricle by use of a long sheath as described above. It was placed against the akinetic segment, and pacing capture threshold and the endocardial electrode were recorded. The ablation injectant was mixed with methylene blue (5 drops per 20 cm3) to distinguish between the acute lesion and chronic scarring during pathological examination. Injectant (3 cm3) was infused over 14 seconds. A second ablation infusion was performed in a distant area of the left ventricular endocardium with normal wall motion with the same protocol. After both injections, left ventriculography and programmed right ventricular stimulation were repeated as before. Finally, staining was performed with 2,3,5-triphenyltetrazolium chloride (4%), the dogs were killed, and the hearts were fixed as described above.
Protocol 3: Chronic Effects of Infusion Ablation
The chronic effects of lesions produced by subendocardial infusion were studied in seven dogs (weight, 26±2 kg). Anesthesia, ventilation, and monitoring were as described in protocol 2. Programmed right ventricular stimulation and left ventricular cineangiography were performed before ablation. Each dog then had a single infusion ablation lesion created by use of 3 cm3 injectant delivered over 14 seconds. Lesions were made in either the intraventricular septum (n=4) or the left ventricular free wall (n=3). One hour after injection, repeated programmed stimulation and ventriculography were performed. The dogs were then allowed to recover. Follow-up study was performed 28±4 days after the infusion ablation procedure. The dogs were anesthetized as described in protocol 1. Programmed stimulation and left ventricular angiography were repeated as in the initial study. Finally, 2,3,5-triphenyltetrazolium chloride (4%) was infused, and the dogs were killed. The hearts were excised, and tissue blocks encompassing the lesion were preserved in 10% formalin solution.
Pathological and Statistical Analysis
To quantify lesion volume, tissue blocks were cut into 2- to 3-mm-thick slices. The perimeter of the lesion on each side of each slice was traced and digitally scanned. The surface area of each tracing was calculated, and the volume of the lesion was quantified with the following formula:\left(\frac|<|A1|<|+|>|A2|>||<|2|>|T1\right)|<|+|>|\left(\frac|<|A1|<|+|>|A2|>||<|2|>|T2\right)|<|+|>|\left(\frac|<|A1|<|+|>|A2|>||<|2|>|Tn\right)|<|=|>|Vwhere T is the thickness of each slice, A1 is the planimetered lesion surface area on one side of a slice, and A2 is the planimetered lesion surface area on the other side of the slice.
Representative thin sections from each lesion were dehydrated in and imbedded in imparaffin. These were stained with hematoxylin and eosin or Masson's trichrome stain for microscopic examination.
To quantify the relationship between the area of the stain on fluoroscopy and lesion dimensions, cine frames showing maximal contrast density were enlarged, and the perimeter was traced. The image was digitally scanned and the surface area was calculated with the same technique as that applied to measurement of lesion area.
Values are expressed as mean±SD. Pacing capture threshold and ST-segment elevation were compared before and after ablation by use of Student's t test for paired variables. The relationship between the volume and speed of injection and the resultant lesion size was determined by use of the Wilcoxon signed-rank test. The relationship between the surface area of the stain produced on fluoroscopy and the corresponding lesion volume was determined by use of Pearson's correlation coefficient. Values of P≤.05 were considered statistically significant.
The study protocol was approved by the Institutional Animal Care and Use Committee of Emory University in Atlanta, Ga, and was completed in accordance with the NIH Guidelines on the Care and Use of Experimental Animals.
Acute Effects of Subendocardial Infusion
A total of 55 infusions were delivered in 10 dogs (see the Table⇓). Infusion of the mapping injectant containing lidocaine was performed in 14 of 55 infusions (25%), and the ablation injectant containing ethanol was used in 41 (75%). Of the 55 infusions, 28 (51%) were applied in the right ventricle and 27 (49%) in the left ventricle.
Myocardial Effects of the Mapping Injectant
Bipolar electrograms after advancement of the needle into the endocardium showed ST-segment elevation of 6.5±3.5 mV. Capture threshold was 1.3±0.9 mA. Injection of the mapping infusant produced premature ventricular contractions in all cases and nonsustained ventricular tachycardia in 5 of the 14 injections (36%). There was no change in arterial pressure during or after injection. Pacing capture threshold rose after injection and was 1.9±1.1 mA after 3 minutes (P<.05 versus baseline) and 2.1±1.4 mA after 5 minutes.
None of the mapping of infusions produced myocardial necrosis. A small intramural hematoma (0.29 cm3) was noted at the site of one injection.
Effects of Ethanol Infusion
Placement of the needle-tipped infusion ablation catheter against the endocardium resulted in ST-segment elevation of 6.8±4.5 mV. Initial pacing capture threshold was 1.4±0.8 mA, increasing to 1.75±1.0 mA 5 minutes after infusion of the ethanol-containing ablation injectant (P=.04). Premature ventricular contractions were observed during all 41 infusions of the ablation injectant. Nonsustained ventricular tachycardia occurred during 23 of the 41 infusions (57%). Arterial pressure was not affected by infusion ablation, and no arrhythmias were observed after injection. In each case, well-demarcated fluoroscopic stains were seen surrounding the injection site (Fig 2⇓). Catheter orientation relative to the endocardial surface did not appear to affect the size or shape of the stain.
There were discrete, well-demarcated lesions at all 41 sites of subendocardial infusion of the ablation injectant (Fig 3⇓). Infusion volume and speed significantly influenced lesion size (the Table). Mean lesion volume after injection of 2 cm3 was 0.63±0.3 cm3; it was 1.56±0.9 cm3 after injection of 3 cm3 (P<.001). Increasing the speed of injection also increased the lesion volume. A 7-second injection time produced lesions of 0.81±0.5 versus 1.09±0.5 and 1.50±1.3 cm3 for injection times of 5 and 3 seconds, respectively (P<.01).
There was transmural involvement in 23 of the 41 lesions. There was no significant difference in lesion dimensions or volume between right and left ventricular injections.
Microscopic examination of the lesions revealed coagulation necrosis with hemorrhage. There was a narrow border zone of viable myocytes with mild hemorrhage and neutrophilic infiltration.
Ablation in Regions of Healed Myocardial Infarction
Programmed right ventricular stimulation 3 months after myocardial infarction was notable for the absence of inducible sustained ventricular tachycardia before and after subendocardial infusion of ethanol. Ventricular fibrillation was produced by triple extrastimulation in 2 of 3 dogs before the ablation procedure. One of these had ventricular fibrillation induced again after the subendocardial infusion ablation.
The ST-segment elevation and pacing capture threshold measured at the injection sites were comparable to those seen in protocol 1 (4.9±3.7 mV and 0.89±0.28 mA). As with the acute study, there was no change in arterial pressure during or after infusion of ethanol. Left ventricular ejection fraction was 60±8% before and 56±15% after infusion ablation (P=NS).
Premature ventricular complexes were observed during 7 of 7 ablation infusions; nonsustained ventricular tachycardia was seen in 3 of 7 (43%). One injection into a region of chronic infarction was followed by ventricular tachycardia at a cycle length of 440 milliseconds. The tachycardia terminated spontaneously after 45 seconds.
Lesion depth, width, and volume were comparable to those observed in protocol 1 (12±3 mm, 21±7 mm, and 1.1±0.1 cm3, respectively). There were no significant differences in lesion dimensions between lesions produced in zones of chronic infarction and control lesions made at distant, noninfarcted sites.
Microscopic analysis showed a substrate of fibrosis, collagen formation, and residual round-cell infiltration in the regions of infarction. The acute lesions produced by ethanol injection (and delineated by methylene blue staining) appeared similar to those seen in protocol 1. There was coagulation necrosis of the remaining viable myocytes and hemorrhage. As before, there was an abrupt transition between necrotic and uninvolved tissue.
Long-term Effects of Infusion Ablation
A single lesion was made in the left ventricle of seven dogs (28±4 days before death). The magnitude of initial ST-segment elevation and the pacing capture threshold were similar to those seen in protocols 1 and 2 (3.9±0.8 mV and 0.63±0.19 mA). As before, the capture threshold rose by 67% after infusion of the ablation injectant (0.63±0.19 to 0.94±0.83 mA).
The mean maximal surface area of the fluoroscopic stains resulting from infusion of the ablation injection was 159±83 mm2. As with the previous infusions, all seven injections produced premature ventricular complexes and nonsustained ventricular tachycardia in 4 of 7 injections. In one dog, sinus tachycardia at a rate of 150 bpm was observed for 2 minutes after infusion ablation. Programmed right ventricular stimulation was performed immediately before and after infusion ablation and again at the time of death 1 month later. Sustained ventricular tachycardia was not induced in any of the 21 electrophysiology studies. Ventricular fibrillation was induced with triple extrastimulation at the time of late restudy in one dog.
The mean left ventricular ejection fraction was 65±5% at baseline. There was no significant change in left ventricular ejection fraction measured immediately after infusion ablation or again 1 month after ablation (65±7% and 64±7%, respectively; P=NS).
Discrete endocardial lesions were readily apparent on gross inspection 1 month after ablation (Fig 4⇓). Mean lesion volume 1 month after ablation was 0.58±0.31 cm3. There was a significant positive correlation between the size of the fluoroscopic stain produced at the time of the infusion ablation and the lesion volume seen 1 month later (r=.6, P<.001). Mean maximal lesion depth was 11±4 mm, and 4 of the 7 lesions (57%) were transmural. Maximal lesion width ranged from 11 to 33 mm, with a mean of 21±8 mm. Microscopic examination showed regions of dense fibrosis with mild to moderate chronic inflammatory cell infiltration. There also were regions of cartilage formation with ectopic calcification. The border zone between fibrotic and normal myocardium was quite distinct (Fig 5⇓).
Summary of Main Findings
This study evaluated the feasibility of mapping and ablation of ventricular target sites with a novel transcatheter infusion ablation system. Percutaneous subendocardial injection of a mixture of lidocaine, iohexal, and glycerin marked the affected area by producing a well-demarcated fluoroscopic stain surrounding the site. In addition, it increased pacing capture thresholds by an average of 61%, suggesting significant impairment of local excitability. Infusion of an ablation injectant consisting of ethanol, iohexal, and glycerin produced discrete lesions with sharply demarcated borders. Lesion volume could be controlled by adjustment of infusion rate and volume. Lesion formation could be monitored by observation of the fluoroscopic stain, which correlated with resultant lesion volume. Lesions were large, with a mean volume of >1.5 cm3 when 3 cm3 infusant was used. Fibrosis in a region of healed myocardial infarction did not appear to impair diffusion of the infusant or lesion dimensions. Infusion ablation appeared to be safe, without effects on overall left ventricular function or new arrhythmias.
Comparison With Previous Studies
Ethanol infusion into the coronary arterial circulation has been used experimentally and clinically to ablate the AV junction and ventricular tachycardia.10 11 12 13 15 16 A number of problems have been identified with this approach, all related to difficulties with delivery of the ablative agent to the target tissue. Inability to identify or cannulate the target artery occurs in ≈20% of patients having AV junctional ablation and more than half of those being treated for ventricular tachycardia. Even in those patients with initial success, the recurrence rate is 20% to 50%.10 12 14 Moreover, myocardial infarction and death have been a disturbingly frequent complication of intracoronary ethanol infusion, presumably caused by reflux of ethanol from a distal to a larger, more proximal coronary artery.12 17 18
Endocardial injection of ethanol and radiographic contrast appears safer and more controllable than intracoronary infusion. In the present study, lesion formation was confined to the area surrounding the injection site, and there was no change in overall left ventricular function after ablation.
Two preliminary reports have described the use of endocardial injection of ethanol for ablation of ventricular myocardium. As with the current study, the procedure was without complications or change in overall left ventricular function. Weissmuller et al19 used an injection of 1 to 2 mL ethanol to create ventricular lesions in a swine model. Mean lesion depth was 0.15 cm, and the volume was 0.06 cm3. Lesions produced in the present study were >10 times larger. This difference may be the result of rapid high-pressure injection and the use of glycerin to impair diffusion from the injection site. Lu et al20 used 0.5 to 1 mL ethanol to create endocardial lesions in dogs. Lesion diameter was 3±5 mm. Again, the smaller lesions may be the result of differences in the composition of the ablation infusant and the speed of injection. Intracardiac ethanol injection has also been investigated as a means to ablate accessory AV pathways. Creswell and coworkers21 injected 10 mL ethanol directly into the left AV groove in eight open-chest dogs. Histological examination 6 to 12 weeks later revealed fibrosis of the groove and adjacent epicardial muscle.
High-voltage direct-current shocks and radiofrequency current have been used experimentally and clinically for catheter ablation of ventricular tachycardia.1 2 3 4 5 22 23 Although direct-current ablation can produce lesions comparable in size to those seen with infusion ablation, it has a number of drawbacks, including barotrauma, which may result in life-threatening arrhythmias and electromechanical dissociation.24 25 26
Radiofrequency catheter ablation is safer than direct-current shocks and has been proved useful for treatment of idiopathic ventricular tachycardia; bundle-branch reentry tachycardia; and inducible, hemodynamically tolerated ventricular tachycardia in patients with coronary disease.2 4 5 23 27 Most patients who have ventricular tachycardia associated with hemodynamic collapse are not candidates for radiofrequency ablation because of the need to perform detailed endocardial mapping before application of energy. The utility of conventional radiofrequency catheter ablation also is limited by the size of the lesions produced, typically in the range of 0.2 to 0.4 cm3.9 Larger lesions have been created experimentally with elongated distal electrodes and porous-tipped catheters28 29 although the volume of necrosis is still somewhat smaller than that reported in the present study.
Catheter ablation is useful in only a small subset of patients with ventricular tachycardia. Endocardial mapping with activation times or entrainment is impractical in the setting of a hypotensive arrhythmia. Multielectrode arrays deployed on an endocardial basket-shaped catheter are being investigated as a means to rapidly identify target sites.30 Results of the present study suggest that additional investigation of the infusion system for mapping of hypotensive ventricular tachycardia is warranted. Pace mapping with the infusion ablation catheter would allow it to be manipulated to the general region of interest. Infusion of the mapping injectant would mark the site of injection on fluoroscopy and reversibly impair local excitability. If this prevented reinduction of ventricular tachycardia with programmed stimulation, it would suggest that tissue critical to the maintenance of the arrhythmia had been affected and ethanol would be infused. If inducible ventricular tachycardia persisted, the catheter would be moved to an adjacent site and the process repeated. This “stun mapping” approach obviates the need for recording or pacing from prospective target sites during sustained ventricular tachycardia.
Several features of the ethanol-induced lesions produced in the study might prove useful for ablation of ventricular tachycardia. Lesion volume was more than twice that typically produced by radiofrequency energy. Given the relationship between infusion volume and lesion size, it seems likely that even larger lesions could be created with infusions >3 cm3. The ability to safely ablate large areas of endocardial tissue may allow a more regional approach to treatment, akin to operative subendocardial resection. Indeed, infusion ablation targeting a large portion of the arrhythmogenic substrate (identified, for example, by fractionated electrograms) might reduce the risk of future arrhythmias and ablating of the “clinical” ventricular tachycardia.
Previous reports have suggested that fibrosis in the region of healed myocardial infarction can interfere with radiofrequency lesion formation.31 32 Infusion ablation appears to be unaffected by previously infarcted tissue. Moreover, penetration is deeper with infusion ablation than radiofrequency energy, with more than half of the lesions in this study being transmural. Thus, infusion ablation might prove useful for targeting sites in the midmyocardial or subepicardial regions.
This preliminary study of endocardial infusion ablation has several significant limitations. The duration of monitoring after infusion of the mapping (lidocaine-containing) injectant was insufficient to determine the time course of recovery of the capture threshold. Persistent stunning might contribute to the electrophysiological effects of subsequent ethanol infusion at the same site, thereby complicating assessment of lesion adequacy. However, stains produced by infusion of the mapping injectant were no longer visible after 5 minutes, suggesting prompt diffusion of the reagent from the point of injection.
Lesions formed by endocardial injection of ethanol were not directly compared with lesions created with other ablation techniques intended to affect a large volume of myocardium such as laser, microwave, or ultrasound.33 34 35 36 37 However, all these techniques rely on emanation of energy from a small applicator, making it difficult to create large lesions without excessive energy density at the catheter-tissue interface. These constraints do not apply to diffusion of ethanol from an injection site. Results of the present study suggests that large lesions can be created safely without excessive injury at the point of contact.
Results of this preliminary study show that the infusion ablation system can be used to reversibly impair local excitability and mark an injection site on fluoroscopy. Subendocardial injection of ethanol can safely and predictably ablate a large volume of ventricular myocardium. Additional study of this system in an arrhythmia model is needed to define its potential role in the treatment of ventricular tachycardia.
This work was supported by gifts from the Carlyle Fraser Heart Center and EP Technologies, Inc.
- Received September 25, 1995.
- Revision received March 21, 1996.
- Accepted March 26, 1996.
- Copyright © 1996 by American Heart Association
Morady F, Harvey M, Kalbfleisch SJ, El-Atassi R, Calkins H, Langberg JJ. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation.. 1991;87:363-372.
Gonska BD, Brune S, Bethge KP, Kreuzer H. Radiofrequency catheter ablation in recurrent ventricular tachycardia. Eur Heart J.. 1991;12:1257-1265.
Scheinman MM, Laks MM, Di Marco JP, Plumb V. Current role of catheter ablation procedures in patients with cardiac arrhythmias. Circulation.. 1991;83:2146-2153.
Kaltenbrunner W, Cardinal R, Dubuc M, Shensasa M, Nadeau R, Tremblay G, Vermeulen M, Savard P, Page PL. Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction: is the origin of the tachycardia always subendocardially localized? Circulation.. 1991;84:1058-1071.
Littmann L, Svenson RH, Gallagher JJ, Selle JG, Zimmern SH, Fedor JM, Colavita PG. Functional role of the epicardium in postinfarction ventricular tachycardia: observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation. Circulation.. 1991;83:1577-1591.
Kramer JB, Saffitz JE, Witkowsky FX, Corr PB. Intramural reentry as a mechanism of ventricular tachycardia during evolving canine myocardial infarction. Circ Res.. 1985;56:736-754.
Brugada P, de Swart J, Smeets JLRM, Wellens HJJ. Transcoronary chemical ablation of ventricular arrhythmias. Circulation.. 1989;29:475-482.
Wang PJ, Schoen FJ, Aronowitz M, Oakes D, Kim JH, Estes NAM. Myocardial ablation using selective cardiac venous catheterization and ethanol injection. Circulation. 1990;82(suppl III):III-719. Abstract.
Okishige K, Friedman PL. Alcohol ablation for tachycardia therapy. J Cardiovasc Electrophysiol.. 1992;3:354-364.
Weismuller P, Mayer U, Richter P, Heieck F, Kochs M, Hombach V. Chemical ablation by subendocardial injection of ethanol via catheter—preliminary results in the pig heart. Eur Heart J.. 1991;12:1234-1239.
Lu C, Liu X, Jia G, Mao S. Experimental ventricular tachycardia treated by transcatheter intramyocardial chemical ablation. PACE Pacing Clin Electrophysiol. 1994;17(pt II):861. Abstract.
Creswell LL, Rosenbloom M, Pirolo JS, Saffitz JE, Cox JL. Potential ablation of accessory atrioventricular pathways: injection of alcohol into the atrioventricular groove. Ann Thorac Surg. 1994;57(pt 1):203-207.
Lerman BB, Weiss JL, Bulkley BH, Becker LC, Weisfeldt ML. Myocardial injury and induction of arrhythmia by direct current shock delivered via endocardial catheters in dogs. Circulation.. 1984;69:1006-1012.
Evans GT, Scheinman MM, Zipes DP, Benditt D, Breithardt G, Camm AJ, El-Sherif N, Fisher J, Fontaine G, Levy S, Prystowsky E, Josephson M, Morady F, Ruskin J. The percutaneous cardiac mapping and ablation registry: final summary of results. PACE Pacing Clin Electrophysiol.. 1988;11:1621-1626.
Cunningham D, Rowland E, Ahsan A, Richards A. Mechanism and significance of shock wave and gas production during catheter ablation. New Trends Arrhythmias.. 1988;4:885-891.
Davies DW, Nathan AW, Camm AJ. Three deaths after attempted high energy catheter ablation of ventricular tachycardia. Br Heart J.. 1986;55:506-507.
Klein LS, Shih HT, Hackett K, Zipes DP, Miles WM. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation.. 1992;85:1666-1674.
Langberg JJ, Gallagher M, Strickberger S, Amirana O. Temperature-guided radiofrequency catheter ablation using very large distal electrodes. Circulation.. 1993;88:245-249.
Huang SKS, Cuenoud H, Tan de Guzman W. Increase in the lesion size and decrease in the impedance rise with saline infusion electrode catheter for radiofrequency catheter ablation. Circulation. 1989;80(suppl II):II-324. Abstract.
Jenkins KJ, Colan SD, Saul P, Lock JE, Walsh EP. A new catheter for rapid mapping of atrial arrhythmias during percutaneous cardiac catheterization. J Am Coll Cardiol.. 1993;21:418A. Abstract.
Haverkamp W, Hief C, Hammel D, Hindricks G, Scheld HH, Borggrefe M, Breithardt G. Radiofrequency ablation of diseased (arrhythmogenic) human myocardium. J Am Coll Cardiol.. 1992;19:100A. Abstract.
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;76:1319-1328.
Svenson R, Littmann L, Gallagher J, Selle JG, Zimmern SH, Fedor JM, Colavita PG. Termination of ventricular tachycardia with epicardial laser photocoagulation: a clinical comparison with patients undergoing successful endocardial photocoagulation alone. J Am Coll Cardiol.. 1990;15:163-170.
Lee BI, Gottdiener JS, Fletscher RD, Rodriquez ER, Ferrans VJ. Transcatheter ablation: comparison between laser photoablation and electrode shock ablation in the dog. Circulation.. 1985;71:579-586.