(Circulation. 1997;95:2155-2161.)
© 1997 American Heart Association, Inc.
Articles |
Subendocardial and Intramural Temperature Response During Radiofrequency Catheter Ablation in Chronic Myocardial Infarction and Normal Myocardium
From the Hospital of the Westfälische Wilhelms-University, Department of Cardiology and Angiology and Institute for Arteriosclerosis Research, Münster, Germany.
Correspondence to Hans Kottkamp, MD, Westfälische Wilhelms-Universität Münster, Medizinische Klinik und Poliklinik, Innere Medizin C (Kardiologie und Angiologie), D-48129 Münster, Germany.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background The ability of radiofrequency energy to extend across scar tissue is unknown. We investigated the effects of radiofrequency catheter ablation on intramural temperature in experimental chronic myocardial infarction.
Methods and Results Myocardial infarction was induced in eight dogs by a transcatheter coronary artery occlusion-reperfusion technique. The dogs were reanesthetized after 15 to 24 days. Four additional dogs served as controls. The freshly excised preparations were cut and placed in a saline bath at 37°C. Temperature-guided energy applications with a preselected catheter tip temperature of 80°C were performed for 60 seconds with a 7F ablation catheter. Thermoelements were inserted into the ventricular muscle at depths of 2.5 to 3.0 mm ("subendocardial") and 5.5 to 6.0 mm ("intramural"). Surviving muscle fibers were interspersed among the transmural scar tissue. The maximal temperatures did not differ significantly between normal hearts and chronic infarctions at the subendocardial (64.5±6.4°C versus 66.7±6.6°C) or intramural thermoelement (51.9±5.7°C versus 52.3±5.7°C). The myocardial temperature rise was slow, and steady-state temperatures had not been reached after 60 seconds. The intramural temperatures in chronic infarctions measured 49.0±4.3°C after 40 seconds of energy delivery and were still below the critical tissue temperature of 50°C that is necessary to induce permanent myocardial damage.
Conclusions Temperature-guided radiofrequency ablation in a dog model of chronic myocardial infarction may induce tissue temperatures >50°C at a depth of 5.5 to 6.0 mm. The intramural temperature rise was slow, indicating that long energy applications might be necessary if the arrhythmogenic substrate is subepicardial.
Key Words: ablation • catheter ablation • myocardial infarction • tachycardia
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The applicability of RF catheter ablation as a nonpharmacological treatment modality for patients with VT is currently under intensive investigation. A high degree of success has been reported when bundle-branch reentrant tachycardia1 and so-called idiopathic VT2 3 4 5 6 7 were targeted for ablation. Recently, the feasibility of RF current application for ablation of VT in patients with chronic myocardial infarction or dilated cardiomyopathy has been demonstrated.8 9 10 11 12 However, several features in patients with structural heart disease may limit the applicability of catheter ablation. These include hemodynamic or electrically unstable VT, multiple reentrant circuits, and endocardial thrombotic material overlying the target area. Furthermore, some VTs in patients with structural heart disease may not be amenable to endocardial catheter ablation because critical parts of the reentrant circuits may be located not only subendocardially but also in intramural or even subepicardial layers.13 14 15 Therefore, the limited success rate of RF catheter ablation techniques for the treatment of VTs in patients with structural heart disease might also be related to the limited lesion size created by application of RF energy. In addition, the ability of RF energy to extend across dense fibrotic scar tissue and to permanently damage strands of surviving muscle fibers that are surrounded by scar tissue and are responsible for the maintenance of VT is unknown.
The tissue effects of RF energy application are induced primarily by conversion of electrical energy into heat that dissipates into the area in the vicinity of the catheter tip electrode–tissue interface, where current density is high and electrical conductivity low. The extent of tissue coagulation induced by RF current is governed by multiple variables that dynamically influence each other.16 17 18 19 20 Current, voltage, and energy failed to predict lesion size when RF energy was delivered in the beating heart, whereas catheter tip temperature was demonstrated to improve the prediction of lesion size in vivo.21 The myocardial temperature in normal hearts decreases with increasing distance from the ablation electrode in a hyperbolic form,22 23 whereas the myocardial temperature response in structural heart disease is unknown. In the present study, the effects of RF catheter ablation in chronic myocardial infarction were investigated in vitro 15 to 24 days after experimental myocardial infarction in dogs by use of thermoelements placed within the subendocardial and intramural ventricular scar tissue. The results in scar tissue were compared with results obtained in normal LV myocardium.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Animal Preparations
Twelve adult mongrel dogs were anesthetized as previously described.24 Myocardial infarction was induced in 8 dogs by a percutaneous transcatheter coronary artery occlusion-reperfusion technique. An 8F guiding catheter (Judkins, 3.5-cm curve) was placed via the right femoral artery into the left main coronary artery. The angioplasty balloon catheter (balloon diameter, 2.5 to 3.5 mm) was advanced into the LAD, and the LAD was completely occluded by inflation of the balloon distal to the first diagonal branch. Complete LAD occlusion was verified by coronary arteriography. After 2 to 3 hours, reperfusion was allowed and reflow verified by coronary arteriography.24 One dog died suddenly within 24 hours after the procedure. Seven dogs with infarctions were reanesthetized after 15 to 24 days. Four dogs that did not undergo the occlusion-reperfusion procedure served as a control group. The chest was opened through a left lateral thoracotomy, the animals were killed, and the hearts were removed. The infarcted area of the anterior wall of the LV was identified by its hypokinetic aspect and palpable stiffness. The freshly excised preparations of the infarcted LV myocardium were cut and placed in a bath with saline solution at 37°C with the endocardial side up. The ablation procedures were performed within the first hour after the hearts were removed from the animals.
All procedures for animal care and experimentation followed the guidelines of the American Physiological Society and the German Law for Animal Protection. The experimental design had been approved by the Institutional Ethics Committee for Animal Experimentation.
RF Catheter Ablation
RF alternating current was administered with a continuous
sinusoidal unmodulated waveform of 500 kHz (HAT 200S, Dr Osypka GmbH).
Energy was delivered in a unipolar mode between the 4-mm tip electrode
of a 7F ablation catheter (Cerablate, Dr Osypka GmbH) and a 10x16-cm
external backplate electrode that was placed beneath the bath (Fig 1
). The ablation catheter had a thermistor embedded
centrally in the distal part of the tip electrode for continuous
monitoring of catheter tip temperature. Temperature-guided energy
applications were performed with a preselected catheter tip temperature
of 80°C. Pulse duration was 60 seconds. Power, impedance, and
catheter tip temperature were continuously monitored during the energy
applications.
|
Temperature Measurements
For myocardial temperature measurements, custom-made
ferrum-constantan thermoelements with a diameter of 0.7 mm were
used. Before each experiment, the thermoelements were calibrated
(measurement range, 0°C to 100°C; accuracy, 0.5°C). For
protection against electrical interference with temperature
recordings during RF current application, the thermoelements
were coated with a synthetic resin. The thermal probes were inserted
into the ventricular muscle at two depths, 2.5 to 3.0
mm and 5.5 to 6.0 mm, from the endocardial surface, and the tips
of the thermoelements were placed directly beneath the tip electrode of
the ablation catheter (Fig 1
). Throughout this article, the
thermoelements at a depth of 2.5 to 3.0 mm will be labeled
subendocardial and at a depth of 5.5 to 6.0 mm intramural.
Histology
The preparations were fixed in a 4% formalin solution after
ablation. For each RF-induced lesion, multiple sections at 10 µm
were taken perpendicular to the endocardial surface for light
microscopic analysis. The van Gieson technique was used for
staining that contrasts connective tissue from myocardial fibers within
the infarcted scar.
Statistical Analysis
Data are expressed as mean±SD. Statistical evaluation comparing
the parameters of RF energy application, catheter tip
temperature, myocardial temperature, and depths of intramural
thermoelement placement in the two groups of chronic myocardial
infarction and normal myocardium was performed with
Student's t test. Values of P<.05 were
considered significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Myocardial Infarctions
In all 7 dogs that survived the occlusion-reperfusion procedure and were investigated after 15 to 25 days, the infarctions extended to the subepicardium, but surviving subendocardial, intramural, and subepicardial strands of muscle fibers were interspersed among the fibrotic scar tissue (Fig 2
). For analysis of
temperature response to RF energy application, only those infarcts were
selected in which >50% of the tissue from the endocardial surface to
the myocardial thermoelements was composed of fibrotic scar tissue.
Overall, 32 of 55 RF applications were selected for temperature
analysis. Thirty-two RF pulses in normal LV
myocardium served as a control group.
|
RF Energy Application Parameters
The impedance did not differ significantly between the RF
applications in normal hearts and chronic infarction (43±7 versus
41±4 
, P=NS). A sudden rise in impedance >10 did
not occur during any energy application in normal or infarcted hearts.
Thus, RF applications could be maintained in each case for 60 seconds.
The mean energy did not differ significantly between the applications
in normal hearts and chronic infarctions (1296±317 versus 1230±448 J,
P=NS). The preset catheter tip temperature of 80°C was
reached during each RF current application in both groups. In addition,
the time until the preselected catheter tip temperature was reached did
not differ significantly between normal hearts and chronic infarctions
(18±3 versus 19±3 seconds, P=NS).
Myocardial Temperatures
The results of the measurements of myocardial temperatures at the
subendocardial and intramural thermoelements are summarized in Fig 3. The depth of thermoelement placement did not differ
significantly between normal hearts and chronic infarctions
(subendocardial thermoelement, 2.8±0.6 versus 2.7±0.5 mm;
intramural thermoelement, 5.8±0.6 versus 5.7±0.7 mm; each
P=NS). The maximal temperatures after 60 seconds did not
differ significantly between normal hearts and chronic infarctions at
the subendocardial thermoelement (64.5±6.4°C versus 66.7±6.6°C,
P=NS) or at the intramural thermoelement (51.9±5.7°C
versus 52.3±5.7°C, P=NS).
|
The myocardial temperature rise in normal hearts and chronic
infarctions was rather slow and did not differ significantly between
the two groups (Figs 3 and 4). Steady-state temperatures
had not been reached after 60 seconds in either group. When the
temperature rise curves were normalized to 100% at 60 seconds of
energy application, the relative temperature rise at the subendocardial
thermoelement in normal hearts and chronic infarction measured 20%
versus 25% after 10 seconds, 46% versus 52% after 20 seconds, 66%
versus 71% after 30 seconds, 81% versus 84% after 40 seconds, and
92% versus 93% after 50 seconds of energy application. The
temperature rise at the intramural thermoelement was slower than at the
subendocardial thermoelement. The normalized relative temperature rise
at the intramural thermoelement in normal hearts and chronic infarction
measured 14% versus 18% after 10 seconds, 32% versus 43% after 20
seconds, 52% versus 62% after 30 seconds, 68% versus 78% after 40
seconds, and 83% versus 91% after 50 seconds of energy
application.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Main Findings
The results of the present study indicate that temperature-guided RF catheter ablation in a dog model of chronic myocardial infarction may induce tissue temperatures >50°C at a depth of 5.5 to 6.0 mm and therefore permanent myocardial tissue effects. The rate of intramural temperature rise and the maximal temperatures in chronic myocardial infarctions after 60 seconds of energy application were similar to those in normal myocardium. The intramural temperature rise, however, was rather slow, and the critical myocardial temperature of 50°C at a depth of 5.5 to 6.0 mm was reached only after
50 seconds,
indicating that long RF energy applications might be necessary if the
arrhythmogenic target substrate is located toward the
subepicardium.
Infarction Model
In the present study, an ischemia-reperfusion
model was used for creation of chronic myocardial infarctions in dogs
instead of permanent coronary artery occlusion. The latter
model is known to produce homogeneous transmural
infarctions with a surviving narrow epicardial border zone. Mapping
studies using this model identified reentrant arrhythmias being
initiated and perpetuated in the epicardial border zone of transmural
infarcts without surviving subendocardial and intramural muscle
fibers.25 26 27 28 On the other hand, reentrant
arrhythmias in the "mottled" infarctions induced by
ischemia/reperfusion also use intramural and/or subendocardial
pathways because adequate reperfusion leads to myocardial
salvage.25 29 30 31 32 In this study, catheter ablation was
performed 15 to 24 days after the occlusion-reperfusion procedure.
Analysis of the structural and
electrophysiological properties in the
epicardial border zone of experimental myocardial infarction indicated
that by 2 weeks, connective tissue had invaded the border zone, which
resulted in separation of the surviving muscle bundles.33
In accordance with this, surviving strands of muscle fibers were
interspersed among fibrotic scar tissue in the present study.
Clinical mapping studies revealed that reentrant pathways of VTs may
circulate through subepicardial, intramural, and subendocardial
pathways.13 14 34 In addition, strands of surviving fibers
have been identified subendocardially, intramurally, and
subepicardially in Langendorff-perfused human hearts of patients who
had undergone cardiac transplantation and seem to play a major role in
the arrhythmogenesis in the setting of chronic myocardial
infarction.35 36 Fenoglio et al37
investigated the structure of subendocardial regions in which VTs
originated in patients who had undergone antitachycardia
surgery and found that bundles of apparently viable myocardial fibers
were embedded in fibrous tissue throughout the subendocardial
resections.37
Catheter Tip Temperatures and Intramural Temperatures
In an in vitro study, Blouin et al38 compared the
catheter tip temperature measured within the distal ablation electrode
and the temperature at the electrode-tissue interface. Although the
temperatures within the ablation electrode were consistently
lower than the electrode-tissue interface temperatures, there was a
linear relation between the two temperatures at multiple power
levels.38 In a canine in vivo model,21
catheter tip temperature was found to be a better predictor of lesion
size than power output because catheter tip temperature is a better
indicator of the catheter tip–tissue contact. However, although
catheter tip temperature is a very useful indicator for the catheter
tip–tissue contact quality, it does not directly reflect myocardial
temperature. At the interface between the electrode and the
endocardium, resistive heating occurs only within a small margin of
tissue, whereas the heat is transferred to deeper myocardial tissue by
convection.22 23 39 Therefore, the relatively steep
temperature rise recorded at the catheter tip electrode does not
reflect the temperature rise within the myocardium, because
current density decreases approximately with the square of the distance
from the catheter tip electrode.39 40 Haines and
Watson22 analyzed the myocardial temperature
response during RF energy application in an in vitro model of isolated
perfused and superfused canine right ventricular free wall.
Power output in their study was adjusted to maintain an electrode tip
temperature of 80°C. Tissue temperatures were measured with
thermistor probes that were inserted 2 mm below the endocardial
surface at various distances from the ablation electrode. In their
study, the temperature of the myocardium decreased in a
hyperbolic form, and steady-state temperatures were reached after about
120 seconds.22 The temperature at the margin between
viable and nonviable tissue was about 48°C.22 Wittkampf
et al23 reported on the myocardial temperature response
during RF catheter ablation in a canine in vivo model. In their study,
steady-state myocardial temperatures at distances >3 mm from the
ablation electrode had not yet been reached after 60 seconds of energy
application.23 The results of the present study for
the first time show that temperature-guided RF energy application
induced myocardial temperature rises in chronic myocardial infarction
that were similar to that obtained in normal myocardium. In
the subendocardial depth of 2.5 to 3.0 mm, the critical
temperature of 50°C that is necessary to induce permanent tissue
effects was reached in both groups after 20 seconds. In contrast, in
the intramural depth of 5.5 to 6.0 mm, the critical temperature of
50°C was reached only after 50 seconds. In addition, steady-state
myocardial temperatures after 60 seconds of energy application were not
yet reached in normal myocardium and chronic infarctions at
both depths. Interestingly, no significant differences in temperature
response were observed between normal myocardium and
chronic infarction at either depth. The similar temperature response
profile indicates that no significant differences in the specific
resistances and the specific heat capacities between normal
myocardium and chronically infarcted tissue seem to
exist.
Ablation of VT and the Role of Myocardial Temperature
A high degree of success has been reported when RF catheter
ablation of bundle-branch reentrant tachycardia or
so-called idiopathic VT was attempted.1 2 3 4 5 6 7 In all these
instances, the arrhythmogenic target is located subendocardially and
therefore is relatively easily amenable to catheter ablation. However,
the scenario is much more complicated in VT in patients with remote
myocardial infarction or dilated cardiomyopathy;
accordingly, RF catheter ablation at this time is less effective for
different potential reasons.8 9 10 11 12 On the one hand, the
critical parts of the reentrant circuits in structural heart disease
may be relatively large compared with tiny accessory
atrioventricular pathways, small ectopic foci, or
microreentry circuits; on the other, the ability of RF current to
permanently affect strands of surviving muscle fibers that are
intermingled in fibrotic scar tissue was suggested to be diminished
compared with normal myocardium. In addition, the central
common pathway of the reentrant circuits of VT related to remote
myocardial infarction may be located relatively far away from the
endocardial surface in intramural or subepicardial
areas.13 14 15 34 35 36 However, the results of the present
study indicate that temperature-guided RF energy application may result
in a temperature rise to 50°C in strands of surviving myocytes
that are embedded in fibrotic scar tissue at a depth of 
6 mm.
Importantly, the borderline temperature of 50°C that results in
permanent tissue injury may be obtained only after 60 seconds of energy
application or even later. When RF catheter ablation of accessory
pathways is attempted, energy applications often are terminated after
15 to 30 seconds when no apparent success is achieved. The results of
the present study indicate that this clinical practice cannot be
recommended in general when ablation of VT is attempted in patients
with structural heart disease, because endocardial mapping cannot
distinguish between a subendocardial or more intramural site of
low-amplitude, fractionated electrograms obtained in the vicinity of or
within the reentrant circuit. Premature termination of an RF pulse
after 15 or even 30 seconds may thus mislead the electrophysiologist in
such a way that the target site is inadequately interpreted. Instead,
the desired effect of RF ablation, ie, termination of VT, might have
occurred after an adequately prolonged time of energy application with
the resulting increase in tissue penetration. Therefore, the results of
the present study suggest that energy applications should be
continued for 
60 seconds, provided that
electrophysiological mapping criteria
indicated a close proximity to critical parts of the reentry circuit
and a stable catheter position was obtained.
Modifications of the conventional RF ablation equipment or new technologies may improve the results of catheter ablation techniques when lesion depths of >5 to 6 mm are required. Langberg et al41 reported on the results of temperature-guided RF catheter ablation with various tip electrodes in a canine in vivo model. When RF energy was titrated to reach the preselected catheter tip temperature of 80°C, the 60-second pulses resulted in lesion depths of 11 mm when 8-mm tip electrodes were used, compared with lesion depths of 6 mm with the conventional 4-mm tip electrodes.41 Nakagawa et al42 compared the in vivo tissue temperature profile and lesion geometry for RF ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation. These investigators found that saline irrigation enabled the delivery of higher power levels, which resulted in larger lesions with depths of 9.9 mm compared with 6.1 mm by the conventional temperature control mode. However, with this technique, tissue temperatures at a depth of 3.5 mm measured 94.7±9.1°C and thus clearly exceeded the catheter tip temperature. Thus, the significance of monitoring catheter tip temperature to control the lesion-producing process and the maximally achieved temperatures is lost because the catheter tip is permanently cooled with the saline irrigation.
Old myocardial infarcts or aneurysms often are thinned and may measure only 3 to 5 mm in depth, but the strands of surviving myocardial fibers that may serve as critical parts of reentrant circuits may be relatively broad.43 Bartlett et al43 reported on the histological evolution of RF lesions in an old myocardial infarct of a patient who died shortly after catheter ablation of VT. These investigators demonstrated that some RF lesions extended 3.5 mm deep into superficial epicardial strips of myocardium. Furthermore, the lesions reported by Bartlett et al43 were induced by power-controlled energy application, whereas temperature-guided power output might have added to the controllability of lesion formation. The ability to produce lesions in areas in which surviving myocardial fibers are surrounded by fibrous scar tissue is confirmed by our standardized in vitro study. However, Bartlett et al reported that the RF lesions were not sufficiently wide to destroy the broad sheets of surviving myocytes in the reentry circuit. Therefore, in some institutions, RF energy is applied to four adjacent sites to enlarge the lesion when an RF pulse terminates VT.8 Wittkampf et al23 reported that a second identical pulse at the same site resulted in only minor higher myocardial temperatures in an in vivo canine model.
Study Limitations
In the present study, RF energy–induced tissue temperatures
were compared in vitro between normal LV myocardium and
chronic myocardial infarction in canine hearts. The conductivity of
saline is significantly higher than that of blood. Thus, measurements
of impedance and energy cannot be compared with the clinical situation.
In addition, coagulum formation may occur in blood, which leads to
sudden rises in impedance and necessitates termination of energy
application. Thus, the myocardial temperatures obtained in this study
may not be related directly to the beating heart, in which multiple
variables influence the extent of tissue coagulation. Furthermore,
a coronary perfusion model would have been more accurate
because it would have prevented death of the surviving muscle fibers
for a longer period after the hearts were removed from the animals and
would have affected myocardial temperature by cooling. However, the
excised blocks of chronically infarcted tissue were cut into relatively
small pieces to allow proper placement of the thermal probes within the
chronically infarcted tissue and were thus too small for a reperfusion
model. In addition, we measured only myocardial temperatures and not
lesion volumes, which are difficult to identify in fibrotic scar
tissue. Previous studies, however, indicated that 50°C is the
critical temperature that causes permanent tissue
damage.22 44 On the other hand, the present setup was
undertaken to compare the tissue effects of RF energy in a strictly
standardized procedure to allow a comparison between the temperature
response of normal myocardium and chronic infarction.
In the present study, a 15- to 24-day-old chronic myocardial infarction model was chosen. In the clinical setting, myocardial infarctions causing VT may be 10 or 20 years old and are histologically distinct from our experimental model. However, Bartlett et al43 demonstrated that RF-induced lesions extended across dense subendocardial scar tissue into the subepicardium and thus confirmed the ability of RF energy to produce lesions in areas in which surviving myocardial strands are surrounded by very old fibrous scar. However, calcified aneurysms certainly may alter the ability of RF energy to penetrate into intramural or subepicardial regions.43
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was supported by the Deutsche Forschungsgemeinschaft, grant BR 759/1-1 and 1-2, and the Franz Loogen Foundation.
Received June 27, 1996; revision received November 18, 1996; accepted November 25, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Cohen TJ, Chien WW, Lurie KG, Young C, Goldberg HR, Wang YS, Langberg JJ, Lesh MD, Lee MA, Griffin JC, Scheinman MM. Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: results and long-term follow-up. J Am Coll Cardiol. 1991;18:1767-1773. [Abstract]
2.
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.
3.
Wilber DJ, Baerman J, Olshansky B, Kall J, Kopp
D. Adenosine-sensitive ventricular
tachycardia: clinical characteristics and response to
catheter ablation. Circulation. 1993;87:126-134.
4.
Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda
M, Santoro I, Hazlitt HA, Abdalla I, Singh A, Gossinger H, Sweidan R,
Hirao K, Widman L, Pitha JV, Lazzara R, Jackman WM.
Radiofrequency catheter ablation of idiopathic left
ventricular tachycardia guided by a Purkinje
potential. Circulation. 1993;88:2607-2617.
5.
Wen MS, Yeh SJ, Wang CC, Lin FC, Chen IC, Wu D.
Radiofrequency ablation therapy in idiopathic left
ventricular tachycardia with no obvious
structural heart disease. Circulation. 1994;89:1690-1696.
6. Coggins DL, Lee RJ, Sweeney J, Chein WW, Van Hare G, Epstein L, Gonzalez R, Griffin JC, Lesh MD, Scheinman MM. Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol. 1994;23:1333-1341. [Abstract]
7. Kottkamp H, Chen X, Hindricks G, Willems S, Wichter T, Haverkamp W, Breithardt G, Borggrefe M. Idiopathic left ventricular tachycardia: new insights into electrophysiologic characteristics and radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1995;18:1285-1297. [Medline] [Order article via Infotrieve]
8.
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;88:1647-1670.
9.
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. 1993;87:363-372.
10.
Kim YH, Soza-Suarez G, Trouton TG, O'Nunain SS,
Osswald S, McGovern BA, Ruskin JN, Garan H. Treatment of
ventricular tachycardia by
transcatheter radiofrequency ablation in patients with
ischemic heart disease. Circulation. 1994;89:1094-1102.
11. Gonska BD, Cao K, Schaumann A, Dorszewski A, von zur Mühlen F, Kreuzer H. Catheter ablation of ventricular tachycardia in 136 patients with coronary artery disease: results and long-term follow-up. J Am Coll Cardiol. 1994;24:1506-1514. [Abstract]
12.
Kottkamp H, Hindricks G, Chen X, Brunn J, Willems S,
Haverkamp W, Breithardt G, Borggrefe M. Radiofrequency catheter
ablation of sustained ventricular tachycardia
in idiopathic dilated cardiomyopathy.
Circulation. 1995;92:1159-1168.
13.
Kaltenbrunner W, Cardinal R, Dubuc M, Shenasa M, Nadeau
R, Tremblay G, Vermeulen M, Savard P, Pagé PL. Epicardial
and endocardial mapping of ventricular
tachycardia in patients with myocardial infarction: is the
origin of the tachycardia always subendocardially
located? Circulation. 1991;84:1058-1071.
14.
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.
15.
Pogwizd SM, Hoyt RH, Saffitz JE, Corr PB, Cox JL, Cain
ME. Reentrant and focal mechanisms underlying
ventricular tachycardia in human heart.
Circulation. 1992;86:1872-1887.
16. Hoyt RH, Huang SK, Marcus FI, Odell RS. Factors influencing trans-catheter radiofrequency ablation of the myocardium. J Appl Cardiol. 1986;1:469-486.
17. Grogan EW, Nellis SH, Subramanian R. Catheter ablation of ventricular endocardium using radiofrequency energy: determinants of lesion volume and shape. J Electrophysiol. 1989;3:243-252.
18.
Wittkampf FHM, Hauer RNW, Robles de Medina EO.
Control of radiofrequency lesion size by power regulation.
Circulation. 1989;80:962-968.
19. Langberg JJ, Lee MA, Chin MC, Rosenqvist M. Radiofrequency catheter ablation: the effect of electrode size on lesion volume in vivo. Pacing Clin Electrophysiol. 1990;13:1242-1248. [Medline] [Order article via Infotrieve]
20. Haines DE. Determinants of lesion size during radiofrequency catheter ablation: the role of electrode-tissue contact pressure and duration of energy delivery. J Cardiovasc Electrophysiol. 1991;2:509-515.
21.
Hindricks G, Haverkamp W, Gülker H, Rissel U,
Budde T, Richter KD, Borggrefe M, Breithardt G. Radiofrequency
coagulation of ventricular myocardium: improved
prediction of lesion size by monitoring catheter tip
temperature. Eur Heart J. 1989;10:972-984.
22. Haines DE, Watson DD. Tissue heating during radiofrequency catheter ablation: a thermodynamic model and observations in isolated perfused and superfused canine right ventricular free wall. Pacing Clin Electrophysiol. 1989;12:962-976. [Medline] [Order article via Infotrieve]
23. Wittkampf FHM, Simmers TA, Hauer RNW, Robles de Medina EO. Myocardial temperature response during radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1995;18:307-317. [Medline] [Order article via Infotrieve]
24. Kottkamp H, Vogt B, Hindricks G, Shenasa M, Haverkamp W, Borggrefe M, Breithardt G. Anisotropic conduction characteristics in ischemia-reperfusion induced chronic myocardial infarction. Basic Res Cardiol. 1994;89:177-191.
25.
Cardinal R, Savard P, Carson DL, Perry JB, Pagé
P. Mapping of ventricular tachycardia
induced by programmed stimulation in canine preparations of myocardial
infarction. Circulation. 1984;70:136-148.
26.
Cardinal R, Vermeulen M, Shenasa M, Roberge F,
Pagé P, Helie F, Savard P. Anisotropic conduction and
functional dissociation of ischemic tissue during reentrant
ventricular tachycardia in canine myocardial
infarction. Circulation. 1988;77:1162-1176.
27.
Dillon SM, Allessie MA, Ursell PC, Wit AL.
Influences of anisotropic tissue structure on reentrant circuits in the
epicardial border zone of subacute canine infarcts.
Circ Res. 1988;63:182-206.
28.
El-Sherif N, Smith RA, Evans K. Canine
ventricular arrhythmias in the late myocardial
infarction period, 8: epicardial mapping of reentrant circuits.
Circ Res. 1981;49:255-265.
29.
Karagueuzian HS, Fenoglio JJ, Weiss MB, Wit AL.
Protracted ventricular tachycardia induced by
premature stimulation of the canine heart after coronary artery
occlusion and reperfusion. Circ Res. 1979;44:833-846.
30.
Kramer JB, Saffitz JE, Witkowski FX, Corr PB.
Intramural reentry as a mechanism of ventricular
tachycardia during evolving canine myocardial
infarction. Circ Res. 1985;56:736-754.
31. Michelson EL, Spear JF, Moore EN. Electrophysiologic and anatomic correlates of sustained ventricular tachyarrhythmias in a model of chronic myocardial infarction. Am J Cardiol. 1980;45:583-590. [Medline] [Order article via Infotrieve]
32. Wit AL, Allessie MA, Bonke FIM, Lammers W, Smeets J, Fenoglio JJ. Electrophysiologic mapping to determine the mechanism of experimental ventricular tachycardia initiated by premature impulses. Am J Cardiol. 1982;49:166-185. [Medline] [Order article via Infotrieve]
33.
Ursell PC, Gardner PI, Albala A, Fenoglio JJ, Wit
AL. Structural and
electrophysiological changes in the
epicardial border zone of canine myocardial infarcts during infarct
healing. Circ Res. 1985;56:436-451.
34.
De Bakker JMT, van Capelle FJL, Janse MJ, Wilde AAM,
Coronel R, Becker AE, Dingemans KP, van Hemel NM, Hauer RNW.
Reentry as a cause of ventricular tachycardia
in patients with chronic ischemic heart disease:
electrophysiologic and anatomic correlation.
Circulation. 1988;77:589-606.
35. De Bakker JMT, Coronel R, Tasseron S, Wilde AAM, Opthof T, Janse MJ, van Capelle FJL, Becker AE, Jambroes G. Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers. J Am Coll Cardiol. 1990;15:1594-1607. [Abstract]
36.
De Bakker JMT, van Capelle FJL, Janse MJ, Tasseron S,
Vermeulen JT, de Jonge N, Lahpor JR. Slow conduction in the
infarcted human heart: `zigzag' course of activation.
Circulation. 1993;88:915-926.
37.
Fenoglio JJ Jr, Duc Pham T, Harken AH, Horowitz LN,
Josephson ME, Wit AL. Recurrent sustained
ventricular tachycardia: structure and
ultrastructure of subendocardial regions in which
tachycardia originates. Circulation. 1983;68:518-533.
38. Blouin LT, Marcus FI, Lampe L. Assessment of effects of a radiofrequency energy field and thermistor location in an electrode catheter on the accuracy of temperature measurement. Pacing Clin Electrophysiol. 1991;14:807-813. [Medline] [Order article via Infotrieve]
39.
Wittkampf FHM. Temperature response in
radiofrequency catheter ablation. Circulation. 1992;86:1648-1650.
40. Kalbfleisch SJ, Langberg JJ. Catheter ablation with radiofrequency energy: biophysical aspects and clinical applications. J Cardiovasc Electrophysiol. 1992;3:173-186.
41.
Langberg JJ, Gallagher M, Strickberger SA, Amirana
O. Temperature-guided radiofrequency catheter ablation with very
large distal electrodes. Circulation. 1993;88:245-249.
42.
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 saline-irrigated electrode versus
temperature control in a canine thigh muscle preparation.
Circulation. 1995;91:2264-2273.
43. Bartlett TG, Mitchell R, Friedman PL, Stevenson WG. Histologic evolution of radiofrequency lesions in an old human myocardial infarct causing ventricular tachycardia. J Cardiovasc Electrophysiol. 1995;6:625-629. [Medline] [Order article via Infotrieve]
44.
Nath S, Lynch C, Whayne JG, Haines DE. Cellular
electrophysiological effects of
hyperthermia on isolated guinea pig papillary muscle.
Circulation. 1993;88:1826-1831.
This article has been cited by other articles:
 |
|
 |
|
  S. P. Thomas, D. J.R. Guy, A. C. Boyd, V. E. Eipper, D. L. Ross, and R. B. Chard Comparison of epicardial and endocardial linear ablation using handheld probes Ann. Thorac. Surg., February 1, 2003; 75(2): 543 - 548. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. O. von Oppell, T. Rauch, G. Hindricks, H. Kottkamp, and F. Mohr Effectiveness of two radiofrequency ablation systems in atrial tissue Eur. J. Cardiothorac. Surg., November 1, 2001; 20(5): 956 - 960. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Erdogan, J. Carlsson, S. Grumbrecht, S. Kostin, B. Schulte, M. Schlapp, J. Neuzner, and H. F. Pitschner Electrochemical potentials during radiofrequency energy delivery: a new method to control catheter ablation of arrhythmias Europace, January 1, 2001; 3(3): 201 - 207. [Abstract] [PDF]
|
|
|
|
 |
|
 H. H. Petersen, X. Chen, A. Pietersen, J. H. Svendsen, and S. Haunso Lesion Dimensions During Temperature-Controlled Radiofrequency Catheter Ablation of Left Ventricular Porcine Myocardium : Impact of Ablation Site, Electrode Size, and Convective Cooling Circulation, January 19, 1999; 99(2): 319 - 325. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||