(Circulation. 1997;96:2633-2640.)
© 1997 American Heart Association, Inc.
Articles |
Significance of Morphological Abnormalities Detected by MRI in Patients Undergoing Successful Ablation of Right Ventricular Outflow Tract Tachycardia
From the 2nd Department of Internal Medicine, Division of Cardiology, University of Vienna, Austria.
Correspondence to S. Globits, MD, 2nd Department of Internal Medicine, Division of Cardiology, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
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Abstract |
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Background MRI can demonstrate subtle morphological changes of the right ventricle in patients with idiopathic right ventricular outflow tract tachycardia (RVOT). The present study examines the incidence and significance of right ventricular (RV) abnormalities detected by MRI with respect to the site of successful radiofrequency catheter ablation of the clinical tachycardia.
Methods and Results The study population comprised 20 patients (mean age, 40±12 years) undergoing elimination of recurrent RVOT by radiofrequency catheter ablation. MRI studies were performed before ablation to assess RV volumes and function, as well as structural abnormalities of the RV myocardium. Ten healthy age- and sex-matched subjects served as control subjects. The successful ablation sites, as documented by radiographs of the catheter position, were compared with MRI findings. Patients with RVOT showed no difference in respect to RV volumes and ejection fractions compared with control subjects. Whereas RV abnormalities were limited to prominent fatty deposits of the right atrioventricular groove extending into the inlet portion of the RV wall in 2 of 10 control subjects, MRI studies demonstrated morphological changes of the RV free wall in 13 (65%) of 20 patients with RVOT, including presence of fatty tissue (n=5), wall thinning (n=9), and dyskinetic wall segments (n=4). Eight of these patients had additional fat deposits, thinning, or a saccular aneurysm in the RV outflow tract, corresponding with the ablation site in 6 patients.
Conclusions In RVOT, structural abnormalities of the right ventricle can be detected in a substantial number of patients despite normal RV volumes and global function. MRI abnormalities within the RV outflow tract are significantly associated with the origin of tachycardia.
Key Words: catheter ablation • magnetic resonance imaging • tachycardia
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Introduction |
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In contrast to ARVD, which is characterized by diffuse or localized RV dilatation and presence of fatty tissue predisposing to ventricular tachycardia and sudden cardiac death, idiopathic RVOT is considered a benign entity with nonischemic, often exercise-induced paroxysmal monomorphic tachycardia.1 2 3 As previously shown, this tachycardia can be successfully eliminated by catheter ablation.4 5 6 7 8 Standard diagnostic measures fail to detect a morphological substrate for the arrhythmia, although histological abnormalities including various degrees of fibrosis, infiltration by adipose tissue, and abnormal myocytes have been found in some patients.9
MRI provides accurate information about RV anatomy and function.10 11 12 13 In addition, deposits of fat can be readily identified on T1-weighted spin echo images as areas of bright signal intensity.14 15 16 A recently published study on patients with RVOT showed the ability of MRI to demonstrate subtle structural abnormalities of the right ventricle more often than other imaging techniques, such as echocardiography and angiography.17
Thus, the purpose of this prospective study was to compare morphological abnormalities detected by MRI with the site of successful ablation of the clinical tachycardia in patients with RVOT.
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Methods |
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Patients
Twenty consecutive patients (7 men and 13 women; mean age, 40±12 years) with recurrent episodes of symptomatic RVOT, defined as monomorphic left bundle-branch block configuration and inferior axis, were included in the present study. Demographic patient data are shown in Table 1
. Patient symptoms during
tachycardia included palpitations (n=17), dizziness (n=4),
near syncope or syncope (n=6), and chest pain (n=1). Twelve patients
had daily episodes of tachycardia, 7 experienced
tachycardia at least once a week, and
tachycardia occurred at least once a month in 1 patient.
Physical examination, chest roentgenogram, and a standard 12-lead ECG
were normal in all patients. In particular, none of the patients showed
ventricular postexcitation waves ("epsilon waves") or
delayed ventricular activation in the precordial leads
suggestive of the presence of ARVD.18 All patients had
baseline and predischarge transthoracic
echocardiography, including two-dimensional,
M-mode, and Doppler echocardiography, on a
routine basis. None of the patients had a
transesophageal echocardiogram. On the basis of
qualitative assessment of two-dimensional echocardiograms, RV function
was normal in all patients, as was RV size measured from M-mode
tracings in the parasternal short-axis view. Before RF catheter
ablation, all patients had an MRI scan. Ten healthy subjects (6 men and
4 women; mean age, 37±8 years) with a normal 12-lead ECG and without a
history of arrhythmias were also examined by MRI to serve as a
control group.
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MRI Technique and Measurements
In all patients, MRI was performed 1 to 5 days before the
electrophysiological study with the use of
a 1.0T MRI system (Philips GyroScan NT 10) with prospective ECG gating.
After acquisition of a triple-stack (coronal, sagittal, and axial
planes) scout series, the imaging protocol included a dynamic
horizontal long-axis (coronal-sagittal double angulation)
multislice-multiphase spin echo sequence (repetition time, 600 to 850
ms; time to echo, 27 ms) with seven to eight slices encompassing the
entire heart (slice thickness, 10 mm; interslice gap, 1.0 mm;
scan resolution, 128x256 pixels, interpolated to 256x256 pixels for
reconstruction), as well as axial and sagittal multislice turbo spin
echo images (time to echo, 11 ms).
From the dynamic multislice-multiphase spin echo sequence, volume measurements were performed by two independent observers. Using a cardiac software package (Philips), we calculated RV end-diastolic, end-systolic, and stroke volumes (in milliliters) by summing the areas for each slice (calculated by manual edge detection) multiplied by the slice thickness and corrected for the interslice gap. All volumes were indexed to body surface area (in milliliters per meter squared). The volume method has been validated previously in our laboratory and by other working groups.19 20 21 In the present study, the interobserver variability for RV volume quantification was 5.8%. Ejection fraction (in percent) was calculated by use of the formula SV/EDVx100, where SV is stroke volume and EDV is end-diastolic volume. Measurement of RV wall thickness of a basal and an apical wall segment was performed on a midventricular slice at end diastole. Focal or general wall thinning was defined as a value <1 SD of the mean value (3±0.5 mm) of the control group. Furthermore, the multislice-multiphase sequence was analyzed in a cine-loop mode for regional wall-motion abnormalities. The two observers agreed on the presence of dyskinetic RV free-wall segments in three of four patients. Discrepant MRI findings were resolved by consensus reading.
In addition, the turbo spin echo images were assessed by both expert readers for the following RV criteria: general or local aneurysm formation, increase in RV outflow tract diameter (defined as >1 SD of the mean value of the control group [28±4 mm]), and presence and extent of fatty tissue in the myocardium. There was agreement between the two observers on the presence of a small focal aneurysm in the RV outflow tract in one patient. There was agreement between both observers on the presence of fatty tissue in the RV free wall in five of five patients and in the RV outflow tract in four of five patients, respectively. Consensus reading was performed in case of conflicting MRI results. With regard to the MRI studies in healthy control subjects, there was agreement between the two observers in both of the two cases with prominent fatty deposits of the right AV groove extending into the inlet portion of the RV wall.
Morphological abnormalities of the RV outflow tract were compared with the anatomic position of successful ablation, as determined by radiographs taken in the right and left anterior oblique projections.
Electrophysiological Study and RF Catheter
Ablation
Antiarrhythmic medication was discontinued five half-lives
before the invasive study. Informed consent was obtained from all
patients. The patients were studied in a nonsedated, fasting state.
Four multielectrode catheters (Webster-Cordis) were inserted
percutaneously into the right and left femoral veins
and advanced under fluoroscopic guidance to the right atrial appendage,
His bundle region, and RV apex. One catheter was used for RV mapping.
In all patients, ventricular endocardial mapping and
ablation were performed with the use of a 7F deflectable quadripolar
electrode (2 mm interelectrode spacing) catheter with a 4-mm-tip
electrode. Digitized recordings (Bard Electrophysiology) were
stored in a dedicated computer system for further analysis.
Measurements were made from the computer screen at a speed sweep of
200 mm/s.
Programmed ventricular stimulation at basic drive cycle lengths of 600, 430, and 300 ms with up to three extrastimuli, as well as ventricular burst pacing, was used to induce ventricular tachycardia. In patients in whom ventricular tachycardia was not inducible during baseline, the stimulation protocol was repeated during catecholamine challenge (orciprenaline 0.2 µg · kg-1 · min-1 IV). RV endocardial activation mapping was performed to locate the site of earliest ventricular activity during tachycardia or PVBs with QRS morphology identical to the tachycardia. In addition, during sinus rhythm, 12 ECG leads of the paced beats were compared with the corresponding leads obtained during ventricular tachycardia. The site of earliest activation during tachycardia or during episodes of frequent PVBs with QRS morphology identical to the clinical tachycardia or the pacing site that provided a match in all 12 leads between paced and spontaneous tachycardia QRS complexes was considered a suitable target for ablation.
Catheter ablation was performed by use of a commercially available RF generator (Radionics). Application of energy was immediately terminated in the event of catheter displacement or an impedance rise. Elimination and subsequent noninducibility of tachycardia or complete abolition of PVBs during the application of energy was considered to indicate successful ablation. Subsequently, repeat programmed ventricular stimulation was performed at baseline and, if appropriate, during orciprenaline administration.
For comparison with MRI morphology, the catheter position of the successful application of energy was documented by radiographs taken in the right and left anterior oblique projections. The location of the pulmonary valve was assumed at the level of the right atrial appendage and defined by a significant reduction of the amplitude of the local ventricular signal while the catheter was advanced into the pulmonary artery.
Follow-up
No predischarge electrophysiological
study was performed. All patients underwent postablation
echocardiography, which showed no pathological
findings in any of the patients. The patients were followed up
clinically for a mean period of 7±4 months (range, 1 to 15 months).
All four patients with a short follow-up period of 1 to 2 months
(patients 4, 17, 18, and 19) had daily attacks of palpitation or
dizziness correlating with ventricular
tachycardia on Holter ECG before undergoing the ablation
procedure. All patients received acetylsalicylic
acid (500 mg/d PO) for 6 weeks. Antiarrhythmic drugs were
not prescribed.
Statistical Analysis
All values are expressed as mean±SD. Quantitative MRI results
of patients with RVOT were compared with normal subjects by use of
Student's t test for unpaired results. A value of
P<.05 was considered significant.
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Results |
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Electrophysiological Studies
Table 1
shows the individual data from the
electrophysiological study, mapping, and
ablation procedure. On arrival in the catheter laboratory, 13 patients
had frequent monomorphic PVBs, 2 had nonsustained
ventricular tachycardia with QRS morphology
identical to the clinical tachycardia, and 5 had normal
sinus rhythm. At baseline, programmed ventricular
stimulation produced nonsustained ventricular
tachycardia in 3 patients. During catecholamine
challenge, 2 patients developed frequent PVBs and 2 had spontaneous
sustained ventricular tachycardia (Fig 1). In 2 patients, nonsustained
ventricular tachycardia could be induced by
programmed ventricular stimulation. Mean cycle length
during tachycardia was 356±72 ms (range, 220 to 560
ms).
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RF catheter ablation was successful in all 20 patients. RF current was successfully applied during ventricular tachycardia in 2 patients. Nonsustained VT (5 patients) and frequent PVBs (13 patients) served as the ablation target. Elimination of the arrhythmia required a median of 3 (range, 1 to 12) applications of energy. At sites of successful ablation, RF energy was delivered for a mean duration of 111±39 seconds at 55±5 V, which was not significantly different from the application of RF energy at unsuccessful ablation sites (117±34 seconds at 53±4 V). The earliest local electrical activity was recorded 34±7 ms (range, 25 to 46 ms) before the onset of the QRS complex either during tachycardia or during spontaneous PVBs at the site of successful application of energy. Identical pace match was achieved in 19 of 20 patients. In 1 patient, pace match was present in 10 of 12 ECG surface leads. Successful ablation sites were located in the anteroseptal region of the RV outflow tract close to the pulmonary valve in 16 patients, in the posteroseptal RV outflow tract in 1 patient, anterolaterally in 2 patients, and close to the His bundle in 1 patient.
After the ablation procedure, all patients remained asymptomatic, and 24- to 48-hour continuous ECG monitoring revealed no complex ventricular arrhythmias. During a mean follow-up period of 7±4 months, 19 of 20 patients remained free of tachycardia. One patient experienced recurrence of tachycardia 5 months after ablation, which could be controlled medically. In 6 patients, infrequent PVBs with left bundle-branch block–shaped QRS morphology and inferior axis were documented, but none of these patients had recurrence of tachycardia.
MRI Functional Studies in RVOT Patients Compared With Normal
Subjects
RV volume and ejection fraction measurements of patients with RVOT
showed no significant difference compared with normal subjects (Fig 2).
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Structural Abnormalities by MRI: RVOT Patients Compared With
Normal Subjects
In 7 patients, MRI revealed no pathological findings of the right
ventricle (Fig 3A). In 13 (65%) of 20
patients with RVOT, MRI showed structural abnormalities of the RV free
wall (Table 2), including focal or
general wall thinning in 9 patients (Fig 3B), presence of fatty tissue
in 5 patients (Fig 3C), and dyskinetic wall segments in 4 patients (Fig 3D). Moreover, in 8 of these 13 patients, RV outflow tract pathologies
could be demonstrated, namely, focal presence of fatty tissue in 5
patients (Fig 4), thinning or
circumscribed dilatation in 4 patients, and a small focal
aneurysm in 1 patient (patient 13; Fig 5).
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Two of 10 control subjects showed prominent fatty deposits of the right AV groove extending into the inlet portion of the RV wall. None of the control subjects demonstrated wall thinning, dyskinetic wall segments, or aneurysm.
Structural Abnormalities by MRI Compared With the Successful
Ablation Site
In 6 of 8 patients with MRI abnormalities in the anteroseptal
region of the RV outflow tract, the successful ablation site
corresponded with the location of these abnormalities. Fig 5 shows a
small aneurysm in the anteroseptal region on the MRI study (Fig 5A) in patient 13, which corresponded to the location of the catheter
tip during ablation (Fig 5B and 5C). A subgroup analysis with
regard to the presence or absence, location, and type of RV
abnormalities showed no correlation with the ability to induce
tachycardia either by ventricular stimulation
or catecholamine challenge, as well as the timing of the
electrical target signal at the successful ablation site.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study indicates that structural changes of the RV free wall can be detected in a substantial number of patients with idiopathic RVOT. Moreover, some patients present with morphological abnormalities of the RV outflow tract that are associated with the origin of the clinical tachycardia.
Early reports describe only a small incidence of organic heart disease in patients with RVOT, which is probably due to the limited accuracy of standard noninvasive diagnostic measures.22 In contrast, the combined application of angiography and biopsy, as well as the recent use of MRI, is able to detect morphological abnormalities in a higher percentage of patients.17 23 24 25 26 27 28 However, a direct connection between morphological changes and the origin of tachycardia has not been established. Carlson et al17 performed transcatheter sequential site activation mapping in 10 of 22 patients with RVOT and found the earliest site of ventricular electrical activation during tachycardia in the RV outflow tract near the site of abnormalities shown by cine MRI. On the other hand, malformations of the RV outflow tract are not necessarily specific for the origin of tachycardia, as shown in a recently published case report using transesophageal echocardiography.29
In the present study, the majority of patients with idiopathic RVOT presented with structural changes limited to the RV free wall. These changes included fatty tissue and dyskinetic wall segments, resembling features of ARVD.16 30 31 32 33 34 35 36 37 38 39 40 However, independent of the absence or presence of morphological abnormalities or dyskinetic wall segments of the RV free wall, all patients with RVOT had normal RV volumes and global function, contrasting findings in most patients with ARVD.3 Moreover, despite occasional progression to clinically overt ARVD,18 several long-term follow-up studies in patients with RVOT could not reveal development of structural heart disease over time.16 23 24 28 32 33 41 42 On the other hand, the hypothesis of possible linkage between RVOT and ARVD is supported by rare case reports of sudden cardiac deaths in RVOT patients.39 43 44 45 46 Another similarity between RVOT and ARVD is the fact that the origin of both forms of tachycardia tends to cluster within the RV outflow tract.36
The abnormalities found in the RV outflow tract were heterogeneous and included wall thinning, focal presence of fatty tissue, and a small saccular aneurysm. In most (six of eight) patients, the pathologies correlated with the site of successful ablation, all being located in the anteroseptal region of the RV outflow tract. Despite the morphological heterogeneity of RV outflow tract changes, the clinical behavior of tachycardia, including spontaneous occurrence and response to ventricular stimulation or catecholamine challenge, was not related to the type of abnormality, and furthermore, there was no difference between patients with and without MRI changes. In this regard, it might be noteworthy that the present study group resembles patients of previous reports by Coggins et al8 and Klein et al5 who showed comparable features of RVOT in patients without echocardiographic evidence of structural heart disease. Furthermore, the high success rate of catheter ablation in the present study compares well with previously published data in the same type of patients. This contrasts with ablation results in patients with ARVD, in which, apart from enhanced automaticity, reentry within a widespread area plays a major role as the underlying mechanism of ventricular tachycardia.23 47
Clinical Implications
Only a limited number of previous reports using
echocardiography and angiography describe RV
structural abnormalities,17 23 48 which relates to the
fact that none of the "conventional" imaging modalities can
directly detect adipose tissue replacement in the RV wall. In the
present study, none of the patients had wall abnormalities detected
by echocardiography. Other investigators also found
a low sensitivity of 
25% for echocardiography
in detecting structural abnormalities in patients with
RVOT.49 Because of the proximity of the right ventricle to
the sternum, echocardiography is of limited value
for assessment of the RV free wall.
The focal nature of the structural and functional changes in RVOT patients may be one reason for the conflicting results of studies using angiography. In a recent study by Carlson et al,17 2 RVOT patients with normal angiograms had right ventricular outflow tract abnormalities on MRI. On the other hand, Kunze et al50 found RV outflow tract aneurysms by cine angiography in 4 of 11 patients with RVOT.
The anatomic abnormalities in patients with RVOT may predispose for catheter complications, particularly perforation. The fact that RV free-wall abnormalities prevail may explain why RV free-wall perforation has been reported in few instances,51 52 whereas to date, only one case of deadly perforation of the RV outflow tract has been published.8 Wall perforation can occur as a consequence of manipulation and positioning of the ablation catheter, the type of power source used, and anatomic reasons. MRI could help to rule out abnormalities that predispose a patient to catheter-related complications and to help guide the catheter placement in case of RV outflow tract abnormalities.
Electron-beam CT is a relatively new imaging technique that has been proven useful in diagnosing several features of ARVD.53 Compared with MRI, this method is less expensive and allows shorter image acquisition times than conventional spin echo MRI. In addition, image quality of electron-beam CT is not hampered by respiratory or slow-flow artifacts.
The MRI technique used in the present study is relatively time consuming, with imaging times between 30 and 40 minutes and analysis time for functional parameters of 10 minutes. However, with the advent of new technical developments, such as fast gradient echo sequences in breath-hold mode and echo planar imaging (with acquisition times in the millisecond range), the shortcomings of conventional MRI sequences will be overcome and the method will be more competitive.
Study Limitations
Because of arrhythmias during MRI scanning in some
patients, the image quality was not homogeneously good.
Additionally, the currently used MRI technique has a limited spatial
resolution of 5 mm. Therefore, an improved correlation between
anatomic abnormalities and the origin of arrhythmias might be
possible if a more sensitive MR sequence with better image quality
could be applied.
In the present study, none of the patients underwent RV angiography, which has been shown to be helpful in diagnosing RV contraction abnormalities. Carlson et al17 described the results of RV angiography in five patients with RVOT. However, they concluded that MRI might be a more sensitive tool because two patients with normal angiograms had RV outflow tract abnormalities on cine MRI.
None of our patients had RV biopsy. The patchy nature of the disease makes it very likely that a biopsy is nondiagnostic in such patients. On the other hand, negative myocardial biopsy has limited diagnostic value because for reasons of safety, biopsy is usually done in a low septal segment at a distance from the myocardial area that is targeted by RF catheter ablation.
Conclusions
The present study indicates that in patients with
idiopathic RVOT, structural abnormalities of the RV free wall
resembling features of ARVD can be found in a substantial number of
patients despite normal RV function and volumes. Some patients
demonstrate additional morphological changes of the RV outflow tract,
which appear to be associated with the origin of clinical
tachycardia, as documented by successful RF catheter
ablation. However, the presence and type of RV abnormalities as shown
by MRI do not correlate with the
electrophysiological features of the
ventricular tachycardia.
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Selected Abbreviations and Acronyms |
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Received March 18, 1997; revision received May 8, 1997; accepted May 28, 1997.
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