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Eur J Cardiothorac Surg 2001;20:956-960
© 2001 Elsevier Science NL

Effectiveness of two radiofrequency ablation systems in atrial tissue

Ulrich O. von Oppella, Thomas Rauchb, Gerhard Hindricksb, Hans Kottkampb, Friedrich Mohrb

a Department of Cardiothoracic Surgery, University of Cape Town, Cape Town 7925, South Africa
b Herzzentrum, University of Leipzig, Leipzig, Germany

Received 11 June 2001; received in revised form 6 August 2001; accepted 7 August 2001.

Corresponding author. Current address: Cardiac Directorate, University Hospital of Wales, Heath Park, Cardiff, CF14 4XW, UK. Tel.: +27-21-406-6181; fax: +27-21-448-1145
e-mail: uvonopp{at}thoracic.cts.uct.ac.za


    Abstract
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Objective: The efficacy of the left atrial radiofrequency ablation procedure, for the curative treatment of atrial fibrillation, is dependent upon obtaining a confluent transmural line of hyperthermic cellular death. We compare the in vitro effectiveness of obtaining transmural hyperthermic cellular death (>55°C) of both the Osypka single electrode and Boston Scientific Thermaline multi-electrode radiofrequency systems. Methods: Isolated cadaver porcine hearts were used to measure epicardial temperatures either ‘central’ or at the ‘edge’ in relation to an endocardial applied radiofrequency electrode. Reference set point was 70°C, and 4–6-mm thick atrial tissue was used for all applications. ‘Edge’ temperatures with the Boston Scientific unit were measured whilst activating both adjacent electrodes. Results: Boston Scientific: Probe temperature closely approximated the set point. ‘Central’ epicardial temperature was lower than probe temperature until after 40 s application (P<0.05), 55°C was reached at 50 s, maximal mean temperature 63.0±8.9°C was reached at 100 s. Epicardial ‘edge’ temperature remained lower than probe temperature for the entire 120 s (P<0.05). Osypka: Probe temperature tended to overshoot the set point. ‘Central’ epicardial temperature paralleled and occasionally exceeded probe temperature reaching 55°C within 10 s, maximal mean temperature 76.3±12.7°C was reached at 10 s and exceeded the set point thereafter. ‘Edge’ temperature was no different to probe temperature or ‘central’ epicardial temperature. The mean epicardial temperatures produced with a 65°C set point was no different to that with the 70°C set point, except for a lower final temperature at 60 s. Conclusions: The Boston Scientific system (70°C set point) requires a minimum in vitro application of 40 s to transmurally increase 4–6 mm atrial tissue temperature above 55°C, and 120-s duration per application would appear to be a reasonable clinical recommendation. The Osypka system transfers thermal energy more effectively, requiring less than 10 s in vitro to achieve a similar transmural temperature, and a 30-s application can be recommended. However, a tendency to overshoot both probe and set point temperature, suggests that a lower set point of 65°C might be safer and as effective.

Key Words: Heart • Atrium • Atrial fibrillation • Treatment • Radiofrequency • Hyperthermia


    1. Introduction
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
The major risk of atrial fibrillation is the increased risk of stroke [1]. The ideal strategy to treat atrial fibrillation is therefore to convert too and maintain normal sinus rhythm, thereby curing both symptoms, improving hemodynamics and removing the thromboembolic risk. Patients scheduled for cardiac surgery who have a 6–12 month history of chronic atrial fibrillation or recent onset atrial fibrillation associated with mitral valve disease therefore probably warrant an additional procedure to assist in maintaining sinus rhythm if cost-effective, simple and associated with no significant additional morbidity.

The principle of the left atrial radiofrequency procedure is to produce a confluent transmural line of cellular death by raising tissue temperature to greater than 52–55°C thereby [2], similar to a surgical incision, preventing electrical conduction across this line. Resistive heating is the primary mechanism of radiofrequency energy delivery and occurs in the subendocardial tissue where there is high current density, within a millimetre of the electrode–tissue interface [2]. Deeper tissue heating occurs as a result of passive heat conduction from this subendocardial region along a tissue temperature gradient.

The left atrial radiofrequency procedure is still in a developmental phase in terms of both the ablation line configuration and mechanism of ensuring a confluent transmural line of cellular death. The ablation line configuration originally described by Melo et al. was to merely isolate the pulmonary veins [3]; however, a number of different ablation line configurations are being used clinically and the ideal configuration has not yet been established. Furthermore, individual radiofrequency generators, probes, and the duration of application for each system used may not be similar, and currently there are no published comparative guidelines when using them. Comparing the efficacy of different techniques is thus complicated by both the effectiveness of obtaining transmural cellular death, a confluent line of ablation lesions that may be operator dependent, as well as the configuration of the ablation lines. Clinically, the transmurality of the radiofrequency ablation lesion is not easily or routinely evaluated and therefore the specific mechanism of failure when it occurs is frequently unknown.

Most radiofrequency temperature studies have used ventricular myocardium and have been performed with catheters designed for ‘closed’ intravascular use. In this study we evaluate the predictability of both the Boston Scientific Thermaline (Boston Scientific, Boston, USA) and Osypka (Grenzach-Wyhlen, Germany) systems to in vitro uniformly raise transmural atrial temperature above 55°C by open endocardial application, the objective being to establish comparative guidelines for the use of these tools, in terms of more consistently obtaining a transmural ablation lesion.


    2. Methods
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
The experimental model used was cadaver porcine hearts, warmed to room temperature, and placed in a galley pot partially filled with saline to which the neutral electrode of the unit being evaluated was fixed. The radiofrequency ablation units evaluated were the Osypka Model HAT 200 S (500 kHz, 50 W maximum) and the Boston Scientific Model ASU 4811. The Boston Scientific unit supplies radiofrequency energy in the range of 450–470 kHz and is capable of delivering up to 150 W. Each controlling unit modulates the energy being delivered to a unipolar electrode by a feedback loop according to both a preselected temperature reference set point and a thermocouple monitored temperature at the point/surface of unipolar electrode application. The reference set point for both units was set at 70°C. The duration of application was 120 s for the Boston Scientific unit and 60 s for the Osypka unit, according to previous clinical experiences and preliminary trials.

The Osypka radiofrequency unit has a single rigid unipolar electrode. This resterilizable stainless steel 2x10-mm probe has a thermocouple incorporated into the central distal tip. In contrast, the Boston Scientific Thermaline probe is a non-reusable flexible probe (approximately 2 mm in diameter) consisting of seven unipolar (a single distal 8-mm, and six 12.5-mm) electrodes separated by 2-mm intervals in which two thermocouples are incorporated at the edge of each electrode. Any single or multiple combination of electrodes in the Thermaline probe can be selected for activation and are individually monitored.

The respective hand-held electrode was placed on the opened endocardial surface of either the right or left atrium, not in contact with saline, and a thermocouple (Voltcraft; -40 to 1200°C) placed on the corresponding epicardial surface, either ‘central’ or at the ‘edge’ in relation to the position of the radiofrequency electrode. Contact pressure was sufficient to cause an indentation of the endocardial surface by the electrode and maintained by hand, similar to the clinical situation and not specifically controlled. A fresh section of atrial tissue of between 4 and 6 mm in thickness was used for each measurement. When evaluating the Thermaline probe, only a single electrode (electrode no. 4) was activated for ‘central’ epicardial measurements. However, two adjacent electrodes (electrode nos. 4 and 5) were activated for ‘edge’ temperature measurements in between these two electrodes, in order to simulate the clinical situation when a linear ablation line would be made with more than one electrode.

Six measurements were made with each probe, three epicardial ‘central’ measurements and three ‘edge’ measurements.

The measurements with the Osypka system were repeated using a reference set point of both 65 and 60°C.

2.1. Statistics
Statistical analysis was done with Statistica 5.1 for Windows, 1998 (StatSoft Inc., Tulsa, OK, USA). Means±standard deviations are provided and comparisons between groups was by analysis of variance. Statistical significance was assumed at P<0.05.


    3. Results
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
The mean temperatures measured by the thermocouple in the Boston Scientific Thermaline probe adjacent to the activated electrode consistently approximated the selected set point of 70°C (range 65–72°C; Fig. 1). However, the epicardial temperature measured ‘centrally’ remained statistically lower than that of the probe for the first 40 s of application, and only reached 55°C after 40 s of application; 37.33±0.58, 46.67±4.73, 51.67±7.37, 54.67±8.14°C. The highest ‘centrally’ measured individual epicardial temperature was 73°C, and the mean temperatures from 50–120 s were 57.67±10.79, 59.67±11.59, 59.67±10.79, 61.67±9.29, 62.33±9.45, 63.0±8.89, 63.0±8.72, 62.0±9.64°C, respectively. The epicardial ‘edge’ temperature followed a similar trend, but remained significantly lower than the endocardial probe temperature for the entire 120 s duration of application (Fig. 1).



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Fig. 1. Means and standard deviations of endocardial temperature produced by the Boston Scientific Thermaline probe and corresponding epicardial temperature measured either ‘central’ to the probe or at the ‘edge’ between two active electrodes (reference set point 70°C). *P<0.005, §P<0.05 versus probe temperature; comparisons of ‘edge’ temperatures are placed to the left of the marker, comparisons of ‘central’ temperatures are placed to right of the marker. The probe temperature means were combined into one group for display purposes. The solid line at 55°C corresponds to the temperature at which cellular death is assumed to occur.

 
The mean endocardial measured probe temperatures of the Osypka system tended to overshoot the set point of 70°C system; range 61–76°C (Fig. 2). The measured epicardial ‘central’ temperature paralleled the probe temperatures closely, with epicardial mean temperatures reaching 55°C within 10 s of application (60.33±11.02°C at 10 s; Fig. 2). The highest individual epicardial ‘central’ temperature produced by the Osypka system was 86°C, and tended to exceed probe temperature after 10 s of application; 76.33±12.66, 72.67±8.39, 71.33±7.37, 72.67±8.39, 72.67±5.51°C, respectively (Fig. 2). All mean epicardial ‘centrally’ measured temperatures from 20 to 60 s of application exceeded the 70°C set point. Epicardial ‘edge’ temperatures were no different to either the endocardial probe or ‘central’ epicardial temperature (Fig. 2).



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Fig. 2. Means and standard deviations of endocardial temperature produced by the Osypka probe and corresponding epicardial temperature measured either ‘central’ to the probe or at the ‘edge’ of the electrode (reference set point 70°C). The probe temperature means were combined into one group for display purposes. The solid line at 55°C corresponds to the temperature at which cellular death is assumed to occur.

 
The Osypka system measured an endocardial probe temperature that varied more than the Boston Scientific, with a higher measured mean temperature at both 20 and 30 s (72.83±2.48 and 73.17±2.86°C, respectively; Fig. 3). The overall mean epicardial tissue temperatures produced by the Osypka system were significantly higher than those produced by the Boston Scientific system at all time intervals (10–60 s), despite the same 70°C temperature set point for both units (Fig. 3).



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Fig. 3. Means and standard deviations of endocardial temperature produced by the Boston Scientific Thermaline probe (BS) or Osypka probe and corresponding mean epicardial temperature (combined ‘central’ and ‘edge’ temperatures) during application (reference set point 70°C). *P<0.01, §P<0.05 versus alternative probe or epicardial temperature. The solid line at 55°C corresponds to the temperature at which cellular death is assumed to occur.

 
The mean epicardial temperature (both ‘edge’ and ‘central’ temperatures) produced by the Osypka system with the reference set point at 65°C was no different to that at 70 °C, except for a lower final temperature at 60 s (P<0.01; Fig. 4). However, when the reference set point was lowered to 60°C, epicardial temperature reached 55°C later only after 20 s of application and was lower than that produced with the 65°C reference set point at both the 30- and 40-s interval (P<0.005).



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Fig. 4. Means and standard deviations of epicardial temperature (combined ‘central’ and ‘edge’ temperatures), measured during application of the endocardial applied Osypka probe with the reference set point at either 60, 65 or 70°C. The solid line at 55°C corresponds to the temperature at which cellular death is assumed to occur. *P<0.005, §P<0.01 versus epicardial temperature with Osypka 65°C reference set point.

 

    4. Discussion
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Factors that increase electrode-tissue interface temperature increase the temperature gradient and therefore lesion size. These include radiofrequency power delivery or generator temperature set point, electrode size, minimal convective heat loss around the ablation electrode, and possibly pulsed radiofrequency energy delivery [2]. In our study we selected the same temperature set point of 70°C for both systems, and activated the ablation electrodes in an ‘open’ atrium, similar to the surgical setting. We have shown that the Boston Scientific Thermaline system controls and maintains its probe temperature at the selected 70°C set point with a lower tendency to overshoot than the Osypka system, presumably due to a higher temperature sampling rate and therefore tighter control. However, a high enough epicardial temperature and therefore a transmural lesion required at least a 40-s application in 4–6-mm thick atrial wall with the Boston Scientific probe. Mean epicardial temperature after 120 s application, although higher than 55°C, remained lower than the measured endocardial probe temperature.

Melo and co-workers originally reported using the Osypka HAT 200S for 30 s [4]. and then the Boston Scientific multi-electrode unipolar probe at 70°C for 60 s [3], and currently report the maintenance of sinus rhythm in approximately 75% of patients with atrial diameters of less than 5.0 cm, but only in 25% of patients with atrial dimensions of more than 5.5 cm (J. Melo et al., personal communication). Hemmer and co-workers report a 3-month success rate of 75% in patients with chronic atrial fibrillation and mitral valve disease using the Boston Scientific system with a 70°C set point and 120 s duration per application [5]. These are better results than our experience in a limited series of patients at the University of Cape Town using the Boston Scientific probe for 60 s per application, albeit with similar ablation line configurations. In this study we have also shown that the epicardial temperature measured in-between two active electrodes (epicardial ‘edge’ temperature with the Boston Scientific unit) closely approximates the ‘central’ measured temperature, suggesting that the multi-electrode configuration of the Boston Scientific probe will produce a confluent linear ablation lesion provided the duration of application is sufficient to produce transmural cellular death. Tissue temperatures of greater than 55°C result in denaturation of cellular proteins and cellular death [2]; however, the required duration of hyperthermia is not exactly known. In the in vivo clinical situation, the macro- and microcirculation would act as a heat sink and conduct heat away from the area, and therefore when extrapolating these in vitro measurements to the in vivo situation one could expect a potential reduction in transmural heat transmission. Hence, increasing the duration of application required to obtain the desired epicardial temperature by 2–3-fold would be appropriate in the clinical in vivo situation, provided this did not result in excessively high temperatures predisposing to perforation. Extrapolation of our results to the in vivo situation suggest that the Boston Scientific system should be used with a set point of at least 70°C and for a duration of at least 2–3 times that required to reach 55°C in vitro. Excessive epicardial temperatures were not obtained in our study at 120 s, and measured epicardial temperature at 120 s had plateaued and were no different to that at 80 s. Hence, clinical experience and extrapolation of our experimental in vitro observations support a 120 s duration of application with this probe as a useful safe guideline.

In contrast, the Osypka system (set point 70°C) appears to transfer energy and therefore heat more rapidly into the tissue as evidenced by epicardial temperatures being greater than 55°C within 10 s of application, and approximating probe temperature. This also suggests that the depth of the more rapid resistive tissue heating is greater with the Osypka system compared to the Boston Scientific system where slower time-dependent conductive heating is important. The earlier study by Kottkamp and co-workers (4 mm tip catheter electrode, 500 kHz Osypka HAT 200S set for 80°C) required approximately 20 s for subendocardial ventricular tissue at a depth of 2.5–3.0 mm to reach 50°C, and approximately 50 s for 5.5–6.0-mm deep tissue to reach these temperatures [6]. Other studies have required between 60 and 120 s to reach steady-state temperatures at myocardial depths of 2–3 mm [7,8]. Our observations of an even more rapid temperature rise with the Osypka unit is probably because we used a larger 10-mm electrode, which utilizes greater radiofrequency power and creates larger lesions [2]. However, thinner walled atrial tissue may also have a different distribution of current density and therefore temperature response compared to ventricular tissue.

The tendency for some individual epicardial temperatures to exceed probe temperature with the Osypka system, which was not observed with the Boston Scientific system, also suggests more effective energy transfer into the tissue, possibly because of the higher frequency used by the Osypka system, 560 as opposed to 460 Hz. The electrode size of both the Osypka and Boston Scientific single electrode were similar, albeit of different design. Overshoot of both the probe and epicardial temperature with the Osypka system, in terms of the selected set point, is a concern in terms of safety and rapidity of feedback control. Excessive tissue temperature could result in necrotic perforation.

Kottkamp and co-workers originally reported their clinical use of the Osypka system at a set point of 60–75°C for 20–30 s per application and reported an 86% success rate with this procedure, in patients undergoing combined mitral valve surgery who where previously in chronic atrial fibrillation for at least 1 year prior to surgery, with apparently no major influence of left atrial size [9]. Our results support the use of a slightly lower set point of 65°C with the 10-mm Osypka electrode because of the observed tendency for hyperthermic overshoot. An epicardial temperature of 55°C was reached within 10 s, 25% of the time required by the Boston Scientific system, and extrapolation of our results to the in vivo situation, as previously discussed, would suggest that a recommended clinical duration of application with this probe is 30 s per application.

The limitations of this current study is that 4–6 mm cadaver porcine atrial wall as opposed to living human atrial tissue was used and that a single point, as opposed to an array, epicardial thermocouple was used. Nevertheless, we have shown that the two radiofrequency generators evaluated have different efficiencies of thermal energy transfer into tissue.

In conclusion, the Boston Scientific Thermaline system (set point of 70°C) requires an in vitro application of at least 40 s to elevate epicardial temperature of 4–6 mm tissue to 55°C. In contrast, the Osypka system is more effective in terms of energy transfer, requiring less than 10 s to achieve a similar in vitro epicardial temperature. Extrapolation of our results to the in vivo situation suggests that a 120-s duration of application at a set point of at least 70°C would appear to be a reasonable safe clinical recommendation for the Boston Scientific system. Higher epicardial temperatures, equal to the selected set point, and a tendency to overshoot both epicardial and probe temperatures suggest that both a lower set point of 65°C and a 75% shorter duration of application of 30 s is more appropriate and safer in vivo with the Osypka system. Application times and temperature set points used to achieve transmural radiofrequency ablation lesions differ with different radiofrequency generators and probes.


    Acknowledgments
 
We thank the Medical Research Council of South Africa for their support.


    References
 Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

  1. Wolf P.A., Dawber T.R., Thomas H.E., Jr, Kannel W.B. Epidemiologic assessment of chronic atrial fibrillation and risk of stroke: the Framingham study. Neurology 1978;28:973-977.[Abstract/Free Full Text]
  2. Nath S., Haines D.E. Biophysics and pathology of catheter energy delivery systems. Prog Cardiovasc Dis 1995;37:185-204.[Medline]
  3. Melo J., Adragão P.R., Neves J., Ferreira M., Rebocho M., Teles R., Morgado F. Electrosurgical treatment of atrial fibrillation with a new intraoperative radiofrequency ablation catheter. Thorac Cardiovasc Surg 1999;47:370-372.
  4. Melo J., Adragao P., Neves J., Ferreira M.M., Pinto M.M., Rebocho M.J., Parreira L., Ramos T. Surgery for atrial fibrillation using radiofrequency catheter ablation: assessment of results at one year. Eur J Cardiothorac Surg 1999;15:851-855.[Abstract/Free Full Text]
  5. Hemmer W., Botha C., Ickrath O., Starck C., Paula J., Roser D., Stilz S., Rein J.G. Background and early results of a modified left atrial radiofrequency procedure concomitant to cardiac surgery. Cardiovasc J South Afr 2001;12:19-26.
  6. Kottkamp H., Hindricks G., Horst E., Baal T., Fechtrup C., Breithardt G., Borggrefe M. Subendocardial and intramural temperature response during radiofrequency catheter ablation in chronic myocardial infarction and normal myocardium. Circulation 1997;95:2155-2161.[Abstract/Free Full Text]
  7. Haines D.E., Watson D.D. Tissue heating during radiofrequency catheter ablation: a thermodynamic model and observations in isolated perfused and superperfused canine right ventricular free wall. Pacing Clin Electrophysiol 1989;12:962-976.[Medline]
  8. Wittkampf F.H.M., Simmers T.A., Hauer R.N.W., Roobles de Medina E.O. Myocardial temperature response during radiofrequency catheter ablation. Pacing Clin Electrophysiol 1995;18:307-317.[Medline]
  9. Kottkamp H., Hindricks G., Hammel D., Autschbach R., Mergenthaler J., Borggrefe M., Breithardt G., Mohr F., Scheld H.H. Intraoperative radiofrequency ablation of chronic atrial fibrillation: a left atrial curative approach by elimination of anatomic ‘anchor’ reentrant circuits. J Cardiovasc Electrophysiol 1999;10:772-780.[Medline]



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