(Circulation. 1995;92:1159-1168.)
© 1995 American Heart Association, Inc.
Articles |
Radiofrequency Catheter Ablation of Sustained Ventricular Tachycardia in Idiopathic Dilated Cardiomyopathy
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.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background The feasibility of radiofrequency (RF) catheter ablation for the treatment of sustained ventricular tachycardia (VT) in patients with coronary artery disease and remote myocardial infarction has recently been demonstrated. At present, therapeutic options for VT in patients with idiopathic dilated cardiomyopathy (DCM) include antiarrhythmic drugs and implantable cardioverter/defibrillators (ICD). The purpose of the present study was to investigate the feasibility of RF catheter ablation in patients with idiopathic DCM who could not be adequately treated by conventional treatment modalities because of incessant or frequent, recurrent VT.
Methods and Results RF current application for ablation of 9 VTs (mean cycle length, 402±78 ms) was attempted in 8 patients with idiopathic DCM (4 men, 4 women; mean age, 54±6 years; mean left ventricular ejection fraction, 30±9%). Inclusion criteria for ablation were incessant VT (n=4) or frequent, recurrent VT reproducibly inducible with programmed electrical stimulation (n=5). Three patients had suffered aborted sudden cardiac death, and 2 had experienced syncope. Two patients were artificially ventilated and catecholamine dependent for hemodynamic reasons at the time of attempted ablation. Potential target sites for RF current application were identified by detailed endocardial mapping during sinus rhythm, activation and entrainment mapping during VT, and pace mapping. After 7±5 RF pulses (range, 2 to 18 pulses; median, 6 pulses) applied with 32±7 W for 39±9 seconds, 6 of the 9 target VTs (67%) were rendered noninducible (4 of 4 incessant VTs and 2 of 5 chronic recurrent VTs). In 6 patients, VTs with ECG morphologies other than the target VTs were inducible after RF catheter ablation. Seven patients were on antiarrhythmic drugs during the ablation procedure and during the follow-up period of 8±5 months (range, 2 to 17 months). One patient received an ICD before RF ablation, 4 patients after RF ablation, and 1 patient after ablation of an incessant VT and before attempted ablation of frequent, recurrent VTs. One patient underwent heart transplantation 5 months after ablation in end-stage heart failure. There were no acute complications during the mapping and ablation procedure. During the follow-up period, 1 patient had been resuscitated from ventricular fibrillation 6 weeks after ablation and finally died of congestive heart failure 2 weeks later. No further episodes of incessant VT occurred in the patients who had undergone RF current application for ablation of incessant VT. A complete prevention of VT could be achieved in 2 of 8 patients, whereas in 5 patients, VT episodes were stored in the ICD devices during follow-up.
Conclusions The results of the present study indicate that RF current application for ablation of VT in a select group of patients with idiopathic DCM is feasible. The efficacy of RF ablation may be high in patients presenting with incessant VT, whereas the success rate seems to be only moderate in patients with chronic recurrent VT. In all patients, additional treatment options, including antiarrhythmic drugs, ICDs, and/or heart transplantation, were applied after RF ablation, indicating that RF ablation for this indication may be an adjunctive and not a curative treatment option.
Key Words: tachycardia • cardiomyopathy • catheter ablation
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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In 1986, radiofrequency (RF) catheter ablation has been introduced as a curative treatment modality for patients with Wolff-Parkinson-White syndrome.1 Since then, RF catheter ablation has been established as the treatment of first choice for patients with accessory pathways or AV nodal reentrant tachycardia, with success rates approximating 100%.2 3 4 5 Later, the indication for RF catheter ablation has been extended to the treatment of sustained ventricular tachycardia (VT). A high degree of success has been reported when bundle-branch reentrant tachycardia6 and idiopathic VT arising from either the right7 8 or left9 10 11 ventricle have been targeted for ablation.
Recently, the feasibility and safety of RF current application for ablation of VT in patients with chronic myocardial infarction has been investigated.12 13 14 15 16 In most cases, circus movement is the underlying electrophysiological mechanism for monomorphic sustained VT related to remote myocardial infarction. However, in contrast to AV nodal reentrant tachycardia or AV tachycardia incorporating an accessory pathway, the arrhythmogenic substrate of VT in chronic myocardial infarction is less well defined. Intraoperative and endocardial catheter mapping studies have revealed reentrant circuits in a complex three-dimensional structure of normal and abnormal muscle fibers within the border zone of a remote myocardial infarction.17 18 19 Sophisticated endocardial mapping techniques have been elaborated for the identification and localization of critical parts of the reentrant pathways that might be targeted by catheter ablation.12 20 21 22 23 24 However, several features in patients with VT and coronary artery disease may limit the applicability of catheter ablation. These include hemodynamic or electrically unstable VT, multiple reentrant circuits or reentrant pathways not amenable to endocardial catheter ablation, endocardial thrombotic material overlying the target area, and others. At present, therefore, the role of RF application for ablation of VT in patients with chronic myocardial infarction is restricted to a highly select patient cohort.
The histopathologic and electrophysiological characteristics of sustained VT in idiopathic dilated cardiomyopathy (DCM) are even less well defined when compared with VT related to coronary artery disease. A variety of factors may contribute to the genesis of ventricular tachyarrhythmias in nonischemic DCM. Histopathologic investigations revealed hypertrophy of the ventricular myocytes in all patients with idiopathic DCM.25 The degree of cardiomyopathic changes detected by electron microscopy was found to discriminate between patients with inducible and noninducible VT.25 In addition, there was a tendency toward more interstitial fibrosis and myocyte hypertrophy in the patients with more severe cardiomyopathic changes.25 Although the electrophysiological mechanisms of VT in idiopathic DCM may include automaticity and triggered activity, the established histological correlation between cardiomyopathic changes, myocyte hypertrophy, and interstitial fibrosis on the one hand and the inducibility of VT with critically timed extrastimuli on the other hand may also indicate the susceptibility to reentrant ventricular arrhythmias. The relation between derangements in cellular electrophysiology and clinical function and ultrastructure has also been demonstrated in human atrial myocytes.26 Such derangements included a decrease in the resting membrane potential and the upstroke velocity of the action potential and thereby might provide the substrate for reentrant arrhythmias.
Current therapeutic options for VT in patients with idiopathic DCM include antiarrhythmic drugs, implantable cardioverter/defibrillators (ICDs), and as a last resort, heart transplantation. However, some of these patients suffer from incessant VT refractory to antiarrhythmic drugs or provoked by antiarrhythmic agents. Furthermore, patients with incessant or frequent, recurrent VT may not be adequately treated by the ICD, and emergency heart transplantation is only exceptionally available. Therefore, we investigated the feasibility of RF catheter ablation as a treatment option for VT in patients with idiopathic DCM who could not be adequately treated by conventional treatment modalities.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Selection Criteria
The study group consisted of 8 patients from a total of 115 patients with idiopathic DCM who had been referred to our department for the management of ventricular tachyarrhythmias during the enrollment period of this study. All patients underwent left- and right-sided contrast ventriculography, coronary arteriography, and Doppler echocardiography. Idiopathic DCM was defined as global hypokinesia with a reduced left ventricular ejection fraction. Patients with a history of myocardial infarction, ECG evidence of myocardial infarction, coronary stenosis of >50% diameter, segmental dyskinetic regions, or significant valvular heart disease were excluded from this study. Additional exclusion criteria were hypertensive, pericardial, and congenital heart diseases.
From the total group of 115 patients with idiopathic DCM, 66 presented with documented VT. In 45 of these patients, sustained monomorphic VT had been documented, including 4 patients who had been referred for treatment of incessant VT. The clinically documented sustained VT was inducible with programmed ventricular stimulation in 22 patients. Of the patients with documented VT, 21 presented with recurrent nonsustained VT and symptoms of syncope or presyncope. Of the total group, 49 patients had been resuscitated from ventricular fibrillation. In 5 of these patients, sustained VT had been documented previously.
At present, only very limited information exists describing mapping criteria of VT in DCM; in addition, the diffuse pathophysiological substrate is likely to limit the applicability of catheter ablation techniques in these patients. Therefore, we included only patients with idiopathic DCM and VT who could not be adequately treated by established therapeutic modalities. Selection criteria for RF catheter ablation included incessant VT and frequent, recurrent VT not controlled by antiarrhythmic drugs and/or frequent discharges of an ICD. In the patients with chronic recurrent VT, an additional prerequisite for inclusion was the reproducible inducibility of the clinical VT with programmed electrical stimulation and hemodynamic stability for endocardial catheter mapping during ongoing VT.
Electrophysiological Study and Mapping
Technique
Electrophysiological testing and RF catheter
ablation were performed in the fasting state, after written informed
consent had been obtained. Multipolar catheters were introduced via
sheaths inserted in the femoral vein and placed under fluoroscopic
guidance in the high right atrium, His bundle region, and right
ventricular apex. Stimulation was performed with
rectangular impulses of 2-ms duration at twice diastolic
threshold. The stimulation protocol consisted of programmed
ventricular stimulation from the right
ventricular apex and outflow tract at four different cycle
lengths with up to three premature extrastimuli.16 Atrial
and ventricular stimulation during VT was performed to
exclude bundle-branch reentrant tachycardia. Two patients with
this type of macroreentrant tachycardia were excluded from this
analysis. One of these patients underwent RF catheter ablation
of the right bundle branch, and the other had implantation of an ICD
because rapid VTs other than the bundle-branch reentrant
tachycardia were also inducible during programmed electrical
stimulation.
When the target VT was reproducibly induced and terminated at a given step within the stimulation protocol, programmed stimulation was continued with the following steps of the protocol (ie, with shorter basic cycle lengths and/or additional extrastimuli) to investigate the inducibility of other VT morphologies. Surface ECG leads and endocardial electrograms were displayed and recorded simultaneously at a paper speed of 100 or 200 mm/s. Data were stored on a multichannel tape recorder for further evaluation.
For endocardial mapping and ablation, a 7F deflectable quadripolar catheter with a 4-mm-tip electrode was introduced into the right femoral artery and advanced retrogradely via the aortic valve into the left ventricle. In patients in whom the morphology of the clinically documented VT suggested a right ventricular origin, the mapping catheter was inserted into the right femoral vein and advanced to the right ventricle. Bipolar endocardial electrograms obtained via the ablation catheter were recorded at filter band-pass settings between 40 and 500 Hz. The position of the catheter was determined by biplanar fluoroscopy with 30° right anterior oblique and 60° left anterior oblique projections. All patients received a heparin bolus of 5000 U IV followed by an infusion of 1000 U/h during the ablation procedure, which was continued for at least the following 24 hours. The femoral arterial pressure was continuously monitored throughout the mapping and ablation procedure.
In patients with VT and remote myocardial infarction, endocardial mapping techniques have been described that successfully identify and localize critical parts of the underlying reentrant pathways.20 21 22 23 24 We adopted these criteria for mapping of VT in idiopathic DCM because the electrophysiological criteria of the tachycardias of this highly select group of patients also seemed to be compatible with a reentrant mechanism. Additional evidence supporting this hypothesis came from casuistic results of catheter ablation of VT in idiopathic DCM using high-energy DC application reported previously from our institution27 and other groups.28 29 30 Therefore, the following mapping procedure was used for the identification of target sites for RF energy application. During sinus rhythm, detailed endocardial mapping was performed to examine the presence of fragmented or late potentials. Pace mapping was performed at the sites with fragmented or late potentials during sinus rhythm with bipolar stimulation from the distal pair of electrodes of the mapping catheter. During VT, the site of the earliest detectable local endocardial ventricular activation relative to the onset of the QRS complex and the presence of (mid)diastolic activity separated from the local ventricular electrogram by an isoelectric interval were determined. Pacing maneuvers were performed at these sites during ongoing VT at cycle lengths 40 to 100 ms shorter than the VT cycle length to demonstrate concealed entrainment, ie, no change in QRS morphology during entrainment stimulation compared with VT and no dissociation of these potentials from VT. The presence of middiastolic potentials and the presence of concealed entrainment were accepted as primary target site criteria. In the other patients, the earliest detectable local activity during VT was used. In patients in whom no fragmented potentials could be recorded during sinus rhythm or VT, the localization procedure was guided merely by pace mapping.
RF Catheter Ablation Technique
After identification of
appropriate target sites, RF catheter
ablation was performed. RF AC was administered by use of a continuous
sinusoidal unmodulated waveform of 500 kHz (HAT 200S, Dr Osypka GmbH).
Energy was delivered between the tip electrode of the ablation catheter
and a 10x16-cm external backplate electrode. The preselected power
output ranged between 20 and 50 W, and the preselected time ranged from
30 to 90 seconds. Energy delivery was stopped when sudden rises in
impedance occurred. The catheter was then withdrawn and properly
cleaned of adherent coagulated material. Programmed electrical
stimulation using the above-mentioned protocol was repeated if VT
terminated during RF energy application. The end point of the ablation
session was the noninducibility of the target VT by the above-described
protocol after ablation.
Implantable Cardioverter/Defibrillator Therapy
The
indications for implantation of an ICD after RF catheter
ablation were (1) a history of aborted sudden cardiac death and (2)
induction of either the clinically documented VT or a VT with a
different QRS morphology after RF catheter ablation. A transvenous lead
system with or without additional subcutaneous leads was used in all 5
patients in whom an ICD was implanted after RF ablation as well as in
the patient who received an ICD before ablation. ICD discharges were
regarded as appropriate if the patient experienced syncope or if the
tachycardia had a rate of >200 beats per minute. If the
tachycardia cycle length was >300 ms, criteria for sudden
onset and rate stability as well as the morphology of the stored
electrograms in comparison to sinus rhythm were used to identify
inappropriate ICD therapies.
Follow-up
After the ablation session, all patients had
continuous ECG
monitoring for at least 5 days or until ICD implantation.
Echocardiography was performed 1 to 2 days after
the ablation procedure. All patients underwent a control
electrophysiological study using the
above-described protocol after ICD implantation and/or before
discharge. Additionally, a follow-up
electrophysiological test was done after 6 to 12
weeks. Thereafter, the patients were seen at regular 3-month intervals
in the outpatient clinic.
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Results |
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Clinical Characteristics
The clinical characteristics of the patients are summarized in Table 1
. The patient cohort consisted of 8 patients, 4
men and 4 women, with a mean age of 54±6 years (range, 44 to 64
years). The mean left ventricular ejection fraction as
measured by contrast ventriculography was 30±9%. Sustained VT was
documented on a 12-lead surface ECG in all patients. The cycle length
of the target VTs was 402±78 ms (range, 290 to 510 ms). The patients
had received one to four (median, 2) antiarrhythmic drugs before RF
ablation, which had been discontinued because of clinical VT recurrence
or development of drug intolerance. Seven patients were on
antiarrhythmic drugs at the time of attempted RF catheter ablation.
These antiarrhythmic agents were amiodarone in 3 patients,
D-sotalol in 2, DL-sotalol in 1, and
amidonal in 1. Two patients were artificially ventilated and
catecholamine dependent for hemodynamic
reasons at the time of RF ablation. Three patients had suffered an
aborted sudden cardiac death, and 2 had experienced syncope. In 4
patients, VT was incessant at the time of admission (Table 2).
In 1 of these patients, a previously recurrent VT
had become incessant after oral loading with amiodarone
(patient 3). One patient had had implantation of an ICD 3 months before
RF catheter ablation (patient 6). Five patients had only one surface
ECG QRS morphology documented during spontaneous VT, and 3 had two or
three distinct surface ECG morphologies documented (Table 2).
In the
latter patients, however, a predominant VT morphology existed that was
accepted as target VT.
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Electrophysiological Studies
The electrophysiological
characteristics are
summarized in Table 2
. In the 4 patients presenting with
incessant
VT, no programmed electrical stimulation could be performed to
investigate whether VTs with different morphologies were inducible, and
how many. In the other patients, the clinical target VTs were
reproducibly inducible by programmed stimulation. The induced VTs were
accepted as clinical VTs if they revealed the same bundle-branch block
pattern, frontal axis, and QRS duration and if they did not differ in
cycle length by >50 ms. However, although clinical VTs and induced VTs
were "monomorphic," minor changes in QRS morphologies and cycle
lengths existed in some cases. In 1 patient, no additional VT
morphology was inducible; in 2 patients, 2 other VT morphologies were
inducible; and 1 and 4 other VT morphologies were inducible in 1
patient each. In 7 patients, one ablation session was performed and in
1 patient (patient 7), two sessions. In this patient, an incessant VT
was ablated in the first session, and she later had an ICD implanted.
After implantation, frequent discharges occurred for termination of
recurrent episodes of VT with another ECG morphology, which was then
also targeted by RF ablation. Therefore, 9 distinct clinical VTs were
targeted by RF catheter ablation in 8 patients.
Catheter Mapping and RF Ablation
The ablation sites were in
the left ventricle in 8 VTs and in the
right ventricle in 1 patient (VT1 in patient 7), as summarized in Table
2. Six of the 9 target VTs (67%) were rendered noninducible
after a
mean of 7±5 RF pulses (range, 2 to 18 pulses; median, 6 pulses). The
mean power during RF current application was 32±7 W, and the mean
duration of current application measured 39±9 seconds.
The 4 VTs
that presented as incessant VTs (patients 1 through 3
and VT1 in patient 7) were successfully terminated by application of RF
current and were rendered noninducible in all. At successful ablation
sites, a discrete middiastolic potential was present in
2 patients (patient 3 and VT1 in patient 7), and in two patients, onset
of local ventricular activation preceded the onset of the
QRS complex by 70 and 110 ms (patients 1 and 2, respectively) (Fig
1). Criteria for concealed entrainment were fulfilled in
patient 1 (Fig 2).
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Additionally, 2 of the 5 VTs
presenting as chronic recurrent VTs
were rendered noninducible after RF energy application (patients 5 and
8). The successful target sites for RF current application included
concealed entrainment and presence of a distinct
middiastolic potential (patient 8), whereas in the other
patient (patient 5), no activation or entrainment mapping criterion was
fulfilled, and successful ablation was based solely on pace mapping
(Fig 3). In 2 patients (patients 4 and 6), the targeted
inducible VT could not be terminated by RF application. In one of these
patients (patient 4), mapping for identification of target sites was
based solely on pace mapping, whereas in the other patient (patient 6),
an area of local activation preceding the onset of the QRS complex by
60 ms was identified. In patient 7, who had undergone successful
ablation of an incessant VT in a previous ablation session, the
inducible VT targeted in the second ablation session could not be
ablated. The best site for RF application according to the proposed
criteria showed local ventricular activation preceding the
QRS complex by 80 ms.
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In 2 patients, in whom the target VT was rendered noninducible by RF catheter ablation, no other VTs were inducible (patients 1 and 5). In 4 patients (patients 2, 3, 7, and 8), 1 to 3 VTs with different QRS morphologies were inducible after successful ablation of the target VT at the end of the ablation session.
Early Restudy
After the ablation session, all patients were
continuously
monitored by ECG until ICD implantation or hospital discharge. In all
patients, a control electrophysiological study was
performed 4 to 6 days after the ablation session. During the time
period from the ablation session to the control study, none of the
successfully ablated target VTs recurred. However, patient 1 had 1
episode of nontarget VT and patient 7 had 18 episodes of nonclinical VT
within this time period. In the latter patient, an incessant VT with a
cycle length of 410 ms had been successfully ablated at the basal right
ventricular midseptum. After the initial ablation session
and implantation of an ICD, frequent, recurrent VTs with a slightly
shorter cycle length of 380 ms occurred. In this patient, no VT had
been documented clinically before the incessant VT. In the patients
with inducible VT that could not be successfully ablated (patients 4
and 6 and VT2 in patient 7), no spontaneous VT occurred in 2 patients
(patients 4 and 6), whereas patient 7 had 2 recurrences of the target
VT.
During the control electrophysiological study, none
of the successfully ablated VTs were inducible. However, as at the end
of the ablation session, nonclinical VTs (1 to 3 VT morphologies) were
still inducible in 4 of 6 patients. In all patients not successfully
treated, the target VTs as well as nonclinical VTs were inducible
(Table 2).
The 2 patients who did not undergo ICD implantation (patients 2 and 8) and the patient who had received an ICD before ablation (patient 6) developed no VTs until hospital discharge. In the patients successfully ablated who received an ICD after ablation, no VT episodes were stored by the device in 2 patients (patients 3 and 5) until hospital discharge, whereas 2 patients had ICD therapies (patients 1 and 7, after the first ablation session).
Echocardiograms performed after the ablation session did not reveal any new abnormalities compared with the preablation echocardiograms. There were no acute complications during the mapping and ablation procedures in this patient cohort.
Follow-up
The mean follow-up period of this patient cohort
was 8±5 months
(range, 2 to 17 months). Seven of the 8 patients were on antiarrhythmic
drugs in the follow-up period, including DL-sotalol,
D-sotalol, and amiodarone (Table 1). No further
episodes of incessant VT occurred during the follow-up period in the
patients who had undergone RF current application for ablation of
incessant VT (patients 1 through 3 and 7). One patient (patient 2) had
been resuscitated from ventricular fibrillation 6 weeks
after the ablation session and finally died 2 weeks later of end-stage
congestive heart failure. The patient had refused to undergo ICD
implantation; thus, no stored data about VT recurrence preceding
ventricular fibrillation were available. One patient
(patient 1) underwent heart transplantation 5 months after ablation in
end-stage heart failure and is alive during a total follow-up of 22
months. Electrophysiological control study was
performed in the remaining 6 patients 6 to 12 weeks after ablation.
During this electrophysiological study, none of the
successfully ablated target VTs were inducible. However, nonclinical
VTs were inducible in all patients.
The data from the memory of the ICD devices were analyzed in 6 patients. One of the patients in whom the target VT was successfully ablated did not develop a VT episode during long-term follow-up (patient 5), whereas in 2 patients (patients 1 and 3), 6 and 5 VT episodes, respectively, were stored in the devices. Analysis of the data revealed that all episodes were correctly recognized by the device, and ICD therapy was adequate and successful in all instances. Patient 8, in whom the target VT was successfully ablated and who rejected ICD implantation, did not experience any VT episode or clinical symptoms compatible with VT during a follow-up of 5 months.
In all patients who had unsuccessful ablation and ICD implantation (patients 4, 6, and 7, after the second ablation session), 29, 5, and 3 VT episodes, respectively, were stored in the devices during follow-up. In the patient who experienced 29 VT episodes (patient 4), a cluster of discharges had occurred during hypokalemia.
Thus, overall, no further episode of incessant VT occurred during the follow-up period, and a complete prevention of VT could be achieved in 2 of 8 patients (25%).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Main Findings
The results of the present study indicate that RF current application for ablation of VT in a highly select group of patients with idiopathic DCM is feasible. Potential target sites for RF current application were identified by concealed entrainment and activation mapping during ongoing VT as well as by pace mapping in those patients in whom no fragmented potentials could be recorded during sinus rhythm or VT. The efficacy of RF ablation may be high in patients presenting with incessant VT, whereas the success rate seems to be only moderate in patients with chronic recurrent VT. Overall, 6 of the 9 target VTs (67%) were rendered noninducible after RF current application. In all patients, additional treatment options, including antiarrhythmic drugs, ICDs, and/or heart transplantation, were applied after RF ablation, indicating that RF current application for ablation of VT in patients with idiopathic DCM may be an adjunctive and not a curative treatment option.
Ventricular Tachyarrhythmias in
Idiopathic DCM
In recent studies, sudden cardiac death has been
reported to
account for 20% to 70% of the total mortality in patients with heart
failure.31 32 33 In about 60% of patients
with idiopathic
DCM, complex ventricular ectopy and nonsustained VT
occur.34 The prognostic significance of
ventricular arrhythmias detected by long-term ECG
recording is controversial.34 35 With increasing
degrees of heart failure, there is a concomitant increase in
spontaneous complex ventricular arrhythmias.
However, the percentage of patients who die suddenly, presumably from
arrhythmic causes, varies and is considerably higher in patients with
early stages of heart failure than in those with advanced
stages.35 The mechanisms and precise
electrophysiological characteristics of
ventricular tachyarrhythmias in patients with
idiopathic DCM are unknown; in addition, several factors may generate
ventricular arrhythmias in idiopathic DCM. These
include neurohumoral activation, fibrosis leading to uncoupling of
cells, ventricular hypertrophy, increase in
cytosolic calcium, subendocardial ischemia, electrolyte
disturbances, and others. Therefore, the causes of sudden
cardiac death in idiopathic DCM may be multifactorial. On the other
hand, the role of tachyarrhythmias may be overestimated.
Luu and coworkers36 reported on the diverse mechanisms of
cardiac arrest in 20 patients with advanced heart failure hospitalized
for cardiac transplantation. In 62% of the patients, severe
bradycardia or electromechanical dissociation were recorded at
the time of cardiac arrest, and only 38% were due to
ventricular tachyarrhythmias. Interestingly, in
all 6 patients with idiopathic DCM, sinus bradycardia,
atrioventricular block, or electromechanical
dissociation was observed at the time of cardiac
arrest.36
Pathophysiology of VT in Idiopathic DCM
Idiopathic DCM is a
well-recognized disease characterized by
dilatation of both ventricles and by clinical manifestation of
congestive heart failure and serious ventricular
arrhythmias. The histopathologic characteristics of idiopathic
DCM leading to sustained VT are poorly understood. Roberts and
coworkers37 reported an analysis of cardiac
necropsy findings in 152 patients with idiopathic DCM. In this study,
grossly visible scars were found in 14% of the patients.
Interestingly, the scars involved the left ventricular free
wall in all 22 patients and the ventricular septum in 20
patients, whereas the right ventricular free wall was
involved in only 4 patients. Multiple areas of replacement fibrosis
were present in 57% of sections of the left ventricle, compared
with 35% of sections of the right ventricle.37
Additionally, extensive subendocardial scarring was found in 33% of
left ventricular sections and in only 16% of right
ventricular sections. Unfortunately, no pathological
correlation to the incidence of sustained VT was provided in their
study. However, in accordance with the above findings, the "site of
origin" of the VTs in the present study was found in the left
ventricle in 8 VTs and in the right ventricle in only 1 VT. Lo and
coworkers25 described histopathologic and
electrophysiological correlations in 25 patients
with idiopathic DCM and sustained ventricular
tachyarrhythmias using endomyocardial
biopsies. In their study, the degree of cardiomyopathic
changes analyzed by electron microscopy, including myofibrillar
degeneration, myocyte hypertrophy, and others, was a strong
discriminant for the inducibility versus noninducibility of sustained
monomorphic VT. Additionally, patients with more severe
cardiomyopathic changes had more
interstitial fibrosis than those with less severe
cardiomyopathic changes.25
The structural and electrophysiological changes in the arrhythmogenic epicardial border zone of canine myocardial infarcts during infarct healing were analyzed in detail by Gardner et al38 and Ursell et al.39 Fractionated electrograms were recorded in regions with nonuniform anisotropic characteristics, ie, wide separation of myocardial fibers caused by invaded connective tissue.38 39 DeBakker and coworkers40 investigated the role of the arrangement of surviving cardiac fibers in infarcted Langendorff-perfused human hearts of patients who had undergone heart transplantation. Using epicardial and endocardial mapping as well as histological examination, they found surviving continuous myocardial tracts traversing infarcted tissue and bridging the site of latest activation of one cycle and earliest activation of the next cycle. The mechanisms of sustained monomorphic VT in idiopathic DCM are less well understood than in the setting of chronic myocardial infarction. A high degree of interstitial fibrosis, which was observed in patients with idiopathic DCM and inducible VT,25 is accompanied by a decrease in electrical coupling between adjacent myocytes. This may in turn lead to slowing in conduction and susceptibility to reentrant arrhythmias. Additionally, several electrophysiological properties, including inducibility of VT with critically timed extrastimuli and entrainment mapping, may be indicative of a reentrant mechanism of a subgroup of tachycardias in idiopathic DCM. In these patients, endocardial scarring, interstitial fibrosis, and other histopathologic characteristics may therefore constitute a "final pathological common pathway" for the occurrence of sustained monomorphic VT in patients with DCM and chronic myocardial infarction. Late potentials detected by signal averaging of the surface ECG are considered to represent markers for the presence of an arrhythmogenic substrate in patients with coronary artery disease.41 Mancini and coworkers42 recently reported on the prognostic value of an abnormal signal-averaged ECG in patients with nonischemic congestive cardiomyopathy. In their prospective study, none of the 66 patients with a normal signal-averaged ECG died suddenly or had sustained ventricular arrhythmias, whereas of the 20 patients with an abnormal signal-averaged ECG, 4 patients had sustained VT and 5 patients died suddenly. However, in comparison with patients with remote myocardial infarction, programmed electrical stimulation is less reliable in the induction of sustained monomorphic VT in patients with idiopathic DCM and clinically documented tachyarrhythmias.43 44 45 Bundle-branch reentrant tachycardia constitutes another entity of VT in patients with idiopathic DCM. The surface ECG during bundle-branch reentrant tachycardia in many cases shows a left bundle-branch block pattern and a left superior axis. During tachycardia, intracardiac recordings reveal a His bundle potential preceding the QRS complex, and changes in the tachycardia cycle length are preceded by changes in the HH intervals. Catheter ablation of the right bundle branch for curative treatment of bundle-branch reentrant tachycardia has been reported.6 46 However, patients with idiopathic DCM and bundle-branch reentrant tachycardia may also suffer from other ventricular tachyarrhythmias.6 46 In addition to the different types of reentrant arrhythmias, mechanisms of VT in idiopathic DCM may also include abnormal automaticity, triggered activity, and others. Hypertrophy of the ventricular myocytes is a common finding in DCM and leads to prolongation of the action potential duration.47 48 This in turn has been shown to be related to an increased susceptibility to triggered activity resulting from early afterdepolarizations.48 49 Hypokalemia is frequently encountered in patients with DCM and may be related to the use of diuretic agents and/or ß-adrenergic stimulation. Hypokalemia may aggravate the susceptibility of hypertrophied myocardium to early afterdepolarizations and torsade de pointes tachycardias.48 50
Mapping Techniques and RF Catheter Ablation in Idiopathic
DCM
Detailed endocardial mapping techniques have been elaborated for
the identification and localization of critical parts of the reentrant
pathways of VT in chronic myocardial infarction that might be targeted
by catheter
ablation.12 20 21 22 23 24
Conversely, only very
limited information exists describing mapping criteria of VT in DCM; in
addition, the diffuse pathophysiological substrate
is likely to limit the applicability of catheter ablation techniques in
these patients. Therefore, we included only patients with idiopathic
DCM and VT who could not be adequately treated by established
therapeutic modalities. Selection criteria for RF catheter ablation
included incessant VT and frequent, recurrent VT, with the additional
prerequisite for inclusion that the clinical VT had to be reproducibly
inducible with programmed electrical stimulation. Given the
above-described histopathologic characteristics of idiopathic
DCM25 37 together with
electrophysiological properties of the target VTs
in this highly select subgroup, we speculated that it might be possible
to adopt the techniques established for mapping of VT in chronic
myocardial infarction for mapping of VT in idiopathic DCM. Additional
evidence supporting this hypothesis came from casuistic results of
catheter ablation of VT in idiopathic DCM using high-energy DC
application reported previously from our institution27 and
other groups.28 29 30 In these reports,
earliest endocardial
ventricular activation preceding the onset of the QRS
complex by up to 100 ms had been reported as a target site for DC
ablation.29 In the present study, priority was given
to concealed entrainment and middiastolic potentials as
target sites for RF current application. However, earliest detectable
local endocardial ventricular activation and pace mapping
were also accepted as appropriate mapping techniques in those patients
in whom no concealed entrainment or middiastolic potentials
could be recorded. In accordance with this assumption, fragmented
presystolic or (mid)diastolic potentials were recorded
in 7 of 9 target VTs during endocardial catheter mapping. In addition,
pacing from these sites during ongoing VT with cycle lengths shorter
than the VT cycle length resulted in 2 patients in concealed fusion,
indicating that the pacing site was within a reentrant circuit,
although pacing from "dead-end" pathways near the reentrant
circuit could have produced the same QRS morphology.12
Five of these 7 target VTs were rendered noninducible after RF current
application. In 2 patients, however, no fragmented potentials could be
recorded during VT. It may be speculated that critical parts for
the maintenance of these tachycardias were located at
intramural or subepicardial sites. Perlman et al51
reported on abnormal epicardial and endocardial electrograms in
patients with idiopathic DCM. They found that patients in whom no
ventricular tachyarrhythmias or only
ventricular fibrillation was induced had a low incidence of
both epicardial and endocardial abnormal electrograms. In contrast,
patients with inducible VT showed a significantly greater degree of
both epicardial and endocardial abnormal electrograms, with electrogram
abnormalities being equally distributed between epicardial and
endocardial sites.51 In our patients in whom no fragmented
potentials could be recorded, appropriate target sites for ablation
were identified only by pace mapping. With this technique, 1 of the 2
VTs could be successfully ablated. Overall, 67% of the target VTs were
rendered noninducible in the present study, and the success rate
thereby was slightly lower than the results reported recently for
ablation of VT in chronic myocardial infarction, which ranged from 80%
to 84%.13 14 15 Most importantly,
however, all 4 VTs
presenting as incessant VTs were successfully ablated in the
present study. In this life-threatening situation, conventional
treatment options, including the ICD and antiarrhythmic drugs, often
are inappropriate, and antiarrhythmic drugs may even provoke incessant
VTs, as was the case in 1 of our patients. Additionally, in contrast to
patients with remote myocardial infarction and incessant VT,
antitachycardia surgery is not feasible. At present,
emergency heart transplantation constitutes a bailout therapy in this
situation, but it is only rarely available. Therefore, RF current
application for ablation of incessant or frequent, recurrent VT in
patients with idiopathic DCM seems a worthwhile treatment option with a
reasonable benefit-to-risk ratio.
One patient (patient 7) had 18 VT episodes after the initial ablation session and implantation of an ICD. In this patient, an incessant VT with a cycle length of 410 ms had been successfully ablated at the basal right ventricular midseptum. The best site for RF application for ablation of the frequent, recurrent VTs after the initial ablation according to the proposed criteria showed local ventricular activation preceding the QRS complex by 80 ms, which could be recorded at the basal left anterior septum. In this patient, no VT had been documented before the incessant VT. Therefore, the frequent, recurrent VTs, which were found to originate in close proximity to the previously incessant VT, might have been the result of a modification of the arrhythmogenic substrate by RF current application during the initial ablation session leading to a different exit point of the VT. However, a proarrhythmic effect of RF current application cannot be completely excluded. In addition, the role of ICD implantation before the occurrence of frequent, recurrent VTs can be discussed, because the postoperative exacerbation of ventricular tachyarrhythmias has occasionally been reported. Kim and coworkers52 recently analyzed the frequency of ventricular arrhythmias after ICD implantation by thoracotomy versus nonthoracotomy approaches and found that postoperative exacerbation is very rare with nonthoracotomy approaches, which were used for the implantation in the present case.
Clinical and Nonclinical VT in Idiopathic DCM
The role of
so-called nonclinical VTs, ie, VTs of different
morphology in the surface ECG compared with the clinically documented
VTs that are inducible with programmed electrical stimulation but had
not yet been documented clinically, is still a matter of controversy.
Different results have recently been reported for patients with remote
myocardial infarction and VT who underwent RF catheter ablation. In a
study by Morady et al,13 no recurrences of the ablated VTs
were observed in the 11 patients in whom the target VTs were
successfully ablated. Two of 3 patients who had an ICD, however,
experienced discharges from the device in the follow-up period in their
study. Since the rate cutoff of the ICDs was faster than the rate of
the VTs targeted by catheter ablation, Morady et al considered these
discharges not to be recurrences of the target VTs. In another study by
Kim et al,14 5 of 16 patients in whom the target VT was
rendered noninducible after catheter ablation had documented recurrent
VTs. In 3 of these patients, the recurrent VT had a different surface
ECG morphology compared with the previously ablated VT. In addition, a
recurrence of the target VT was observed in 1 of 16 patients in whom
ablation was successful over the short term.14 In
contrast, Stevenson et al12 reported that none of the 10
patients in whom either no monomorphic VT was inducible at restudy 5 to
7 days after ablation or inducible VTs were modified have suffered
recurrences during the follow-up period. Overall, in patients with VT
and remote myocardial infarction, recurrence of VTs with surface ECG
morphologies other than the previously documented VTs, ie, so-called
nonclinical VTs, seems to occur more often than recurrence of acutely
successfully ablated target VTs.
At present, it is the policy of our institution to implant an ICD in all patients with idiopathic DCM and VT who are resuscitated from sudden cardiac death or who experience syncope related to VT regardless of the results of programmed stimulation after attempted RF catheter ablation. Additionally, ICDs are implanted in patients if sustained VTs of any morphology, ie, clinical or so-called nonclinical VTs, are inducible after RF catheter ablation. The rationale of this policy is based on the diffuse nature of pathology in idiopathic DCM, whereas RF current application induces only limited regional changes. Therefore, it seems that no "electrical cure" can be achieved with RF catheter ablation in patients with idiopathic DCM and recurrent VT. Two patients of the present series refused implantation of an ICD. One of these patients (patient 2) was resuscitated from ventricular fibrillation 6 weeks after the ablation session and finally died of end-stage congestive heart failure 2 weeks later. Since the patient refused to undergo ICD implantation, no stored data about VT recurrences were available. However, the occurrence of ventricular fibrillation might have been the result of degeneration from a so-called nonclinical VT, because the previously clinical target VT had been rendered noninducible by RF ablation, whereas two nonclinical VTs still had been inducible after ablation. In the other patient (patient 8), the target VT also was noninducible after ablation, and 3 distinct nonclinical VTs were inducible after ablation. During the follow-up period of 5 months, no VT episodes occurred in this patient.
Study Limitations
The results of the present study are based
on the findings of
RF catheter ablation of 9 VTs in 8 patients. A larger patient cohort is
needed for confirmation of the efficacy and safety of RF catheter
ablation of VT in patients with idiopathic DCM. Additionally, the
patient cohort of this study presents a highly select subset of
patients with idiopathic DCM and ventricular
tachyarrhythmias, since only a very small subgroup who
presented with incessant VT or frequent, recurrent VT that
could be reproducibly induced with programmed electrical stimulation
was selected for RF catheter ablation. Although the results of the
present study are encouraging, they may not be generalized to the
large group of patients with idiopathic DCM who suffer from
ventricular tachyarrhythmias. The limited role
of catheter ablation is also emphasized by the fact that in all
patients, additional treatment modalities, including antiarrhythmic
drugs, ICDs, and/or heart transplantation, were applied after attempted
RF catheter ablation. Nevertheless, the results of the present
study indicate that RF current application for ablation of VT in
patients with idiopathic DCM is feasible and may be a valuable
adjunctive therapy in patients who cannot be adequately treated by
conventional treatment modalities, eg, in patients presenting with
incessant or frequent, recurrent VTs.
Received January 18, 1995; accepted February 25, 1995.
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