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A*etireL This study attempted to determine whether dueangaetie resewace Imaging (MRI), because of Its unique abilityto image the right ventricle, detects abnormalities in patients withright ventricular oudlow tract ventricular tachycardia.

Baefroartsd Right ventricular outflow tract ventricular tachy-cardle scan is the absence of apparent structural heart disease.

MMbse, We compared dare MRI scans in 22 patients withright reurkular outflow tract ventricular tachycardla,16 subjectswithout structural heart disease and 44 patients with othercardlovascdar diseases. Echocardiography was performed In 21paned s with ventricular tachyardle .

Ross . All 22 patients with ventricular tachyardia had nor-mal left ventricular function and no evidence of coronary arterydisease- awe MRI revealed right ventricular structural and wallmouton abnormalit es more often in patients with ventriculartaehyardia (211"%] of 22) than in normal subjects (2 1112.51%]

Idiopathic ventricular tachycardia occurs in the absence ofapparent structural heart disease . Although it may occur ineither ventricle, idiopathic ventricular tachycardia most oftenoriginates in the right ventricular outflow tract (1) . Because itis frequently associated with exercise, right ventricular outflowtract ventricular tachycardia is often described as exercise-induced, or catecholamine-sensitive ventricular tachycardia(2-16). The right ventricular origin of right ventricular outflowtract ventricular tachycardia results in a left bundle branchblock ORS complex configuration and an inferior mean QRScomplex vector on the surface 12-lead electrocardiogram(ECG) (17) .

From the Division of Cardiology . University Hospitals of Cleveland, CaseWestern Reserve University . Cleveland, Ohio. This study was supported in partby a Cardiovascular Research Award from the Bayer Fund Foundation, NewYork, New York; Grants ROI-HL-384t and HL-22484 from the NationalHeart, Lung, and Blood institute, National Institutes of Health, Bethesda,Maryland a Research Initiative Award from the American Heart Association,Northeast Ohio Affiliate; and a grant from the Wuliger Foundation, Cleveland,Ohio.

Manuscript received Apr11 12, 1993; revised manuscript received April 15,1994, accepted April 21, 1994 .

Dr. Mark D. Carlson, Division of Cardiology,University Hospitals of Cleveland, 2(Y74 Abington Road, Cleveland, Ohio 44106 .

01994 by the American College of Cardiology

JACC Vol . 24, No. 3September 1994:720-7

Right Ventricular Outflow Tract Ventricular Tachycardia: Detection ofPreviously Unrecognized Anatomic Abnormalities Using CineMagnetic Resonance Imaging

MARK D. CARLSON, MD, MA, RICHARD D. WHITE, MD, RICHARD G. TROHMAN, MD,

LEE P. ADLER, MD, LEE A. BIBLO, MD, KENNETH A. MERKATZ, MD,

ALBERT L. WALDO, MD

Cleveland, Ohio

of 16, p < 0.0101) or patients without arrhythmia (17 [39%] of 44,p < 0.0001) . The abnormalities in patients with ventriculartachycardia (fixed focal wall thinning, excavation, decreased sys .tolk thickening) were located in the right ventricular outflowtract, whereas those in patients without arrhythmia were confinedto the free wall Clot MRI demonstrated abnormalities in patientswith ventricular tachycardia more often than did echocardiogra-phy (21 [9596] of 22 vs. 2 [9%] of 21, respectively, p < 0.0001) .

Condasions. Right ventricular outflow tract ventricular tachy-cardia was associated with focal structural and wall motionabnormalities of the right ventricular outflow tract that weredetected more often by doe MRI than by other imaging modalitiesand were not present in patients without arrhythmia or in normalsubjects.

(J Am Coil Cordial 1994;24:720-7)

Although some investigators (1) have suggested that ana-tomic abnormalities of the right ventricle might exist, conven-tional imaging modalities, including echocardiography andright ventricular cine angiography, have not consistently dem-onstrated structural abnormalities in patients with right ven-tricular outflow tract ventricular tachycardia. However, be-cause these modalities do not image the right ventricle well,the absence of observed abnormalities does not exclude thepresence of right ventricular anatomic abnormalities . Severalstudies have demonstrated the use of magnetic resonanceimaging (MRI) in evaluating right ventricular anatomy(18-25). Furthermore, cine MRI allows for viewing rightventricular wall motion (26,27) . Therefore, we hypothesizedthat ventricular tachycardia originating in the right ventricularoutflow tract is typically associated with anatomic or functionalabnormalities, or both, that can be detected by cine MRI .

MethodsThe study included 22 consecutive patients with right

ventricular outflow tract ventricular tachycardia admitted toUniversity Hospitals of Cleveland or the Cleveland ClinicFoundation between October 1988 and January 1992, 16

0735-1097144157 .00

JACC Vol. 24, No . 3September 1994:720-7

normal subjects without structural cardiovascular disease and44 age- and gender-matched control patients who underwentcardiac cine MRI during a similar period to evaluate thoracicaorta disease (17), pulmonary arterial hypertension (16), leftventricular diastolic dysfunction (7), congenital heart disease(2) or ischemic heart disease (2) . Right ventricular outflowtract ventricular tachycardia was defined as ventricular tachy-cardia with a left bundle branch block QRS complex configu-ration and an inferior mean QRS complex vector in theabsence of apparent structural heart disease .

Patients with right ventricular outflow tract ventriculartachycardia underwent several other diagnostic tests, includingtwo-dimensional and M-mode echocardiography (21), exercistolerance test (16), left heart catheterization (17), right ven-tricular angiography (5) and electrophysiologic testing (22) .None of the patients underwent an electrophysiology study oran ablation procedure before the tine MR] scan .

After completion of a cine MR[ scan, each patient withright ventricular outflow tract ventricular tachycardia under-went electrophysiologic study, including programmed electri-cal ventricular stimulation in the absence of antiarrhythmicdrugs. Right ventricular pacing was performed using a 2-mspulse duration at twice the diastolic threshold. The pro-grammed ventricular stimulation protocol included an 8-beatvcntricular paced drive train at two drive train cycle lengths,followed by decremental introduction of up to three extra-stimuli at the right ventricular apex and the right ventricularoutflow tract . If no monomorphic ventricular tachycardia wasinduced, the induction protocol was repeated during intrave-nous isoproterenol infusion . The end point was either repro-ducible induction of sustained monomorphic ventricular tachy-cardia or the completion of the pacing protocol . Sustainedmonomorphic ventricular tachycardia was defined as ventricu-lar tachycardhi of 30 s duration without beat-to-beat QRScomplex configuration variation in any of the 12 surface ECGleads (28) .

When possible, electrical activation mapping of ventriculartachycardia was performed using a steerable quadripolar elec-trode catheter with 2-mm interelectrode spacing (Mansfield/Webster) . During ventricular tachycardia, the catheter tip wasmanipulated to selected sites in the right ventricle and rightventricular outflow tract . Bipolar electrograms were recorded,and the timing of electrical activation at various sites wascompared with the earliest onset of ventricular depolarizationon surface ECG leads 1, II, aVF and V 1 . Right ventricular pacemapping was also performed in these patients . Pacing wasperformed during sinus rhythm at just above the diastolicthreshold and at the spontaneous ventricular tachycardia cyclelength.

Each subject underwent a cardiac MR1 scan using commer-cially available MRI systems (1 .5-T GBS2 or SP63 SiemensMagnetom, Erlangen, Germany In = 201 or General ElectricSigna In = 2]) . Each MRI scan was initiated with at least astatic "black-blood" series (standard spin-echo) in the transaxialorientation . Most of each examination focused on the acquisitionof dynamic "bright-blood" image loops of parallel sections of the

CARLSON ET AL. 721RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA

cardiac chambers. Such "cine MRI" scanning involved a standardgradient-echo sequence (fast imaging with steady state precession[FISP], gradient-recalled acquisition in the steady state [GRASS]or Spoiled-GRASS) using a low flip-angle (30°), gradient-refocused echoes with a short echo delay time (TE) (TE = I I to13 ms), first-order (i.e ., velocity) flow compensation, a shortrepetition time (slice repetition time = 23 to 26 ms X2 to 3 slicesper acquisition) and prospective or retrospective ECG gating forreferencing the image data to the cardiac cycle (29). Cine MRIwas performed in all cases in the transaxial orientation withadjacent slices of the cardiac chambers, including the entire rightventricle, represented by 8- to 10-mm thick (interstice gap 0% to10%) dynamic image loops consisting of images of 12 to 24 phasesof the entire cardiac cycle, with two or three anatomic levels whenscanned simultaneously. The image matrix (128 x 256) andnumber of averages (two to three acquisitions) were kept rela-tively constant for all patients, so that total scanning time varied,largely dependent on each patient's heart rate . The typical scantime for a complete cine MR[ series ranged from 15 to 30 min .Ultimately, the cine MR] image loops were interpreted byconsensus by two observers unaware of the subject's diagnosis.Each image loop representing a separate slice was examined bythese observers for anatomic or functional abnormalities, or both .Abnormalities were classified by location and type .

Statistics. Comparisons of test results (cine MRI vs . echo-cardiography) in patients with right ventricular outflow tractventricular tachycardia were made using Student I test forpaired results. Comparisons of cine MRI scan results betweenpatients with and without right ventricular outflow tract ven-tricular tachycardia were made using the chi-square test . Dataare expressed as mean value ± I SE .

ResultsDemographics . There were 14 men and 8 women with right

ventricular outflow tract ventricular tachycardia in the study .The control patients without right ventricular outflow tractincluded 28 men and 16 women. The 16 subjects with normalhearts included 12 men and 4 women . In each patient withright ventricular outflow tract ventricular tachycardia, thearrhythmia exhibited a left bundle branch block QRS complexconfiguration and an inferior mean QRS complex axis . Sixteenpatients with right ventricular outflow tract ventricular tachy-cardia presented with palpitation, and six presented withsyncope. Mean ages of the patients with and without rightventricular outflow tract ventricular tachycardia were 42 ± 3and 42 ± 2 years, respectively (p = NS) ; mean age of the 16subjects with normal hearts was 25 ± 2 years .

Nonsustained ventricular tachycardia occurred during exer-cise in 8 (50%) of the 16 patients with right ventricular outflowtract ventricular tachycardia who underwent an exercise toler-ance test . Ventricular tachycardia associated with exercise wasdocumented by 24-h Holter ambulatory ECG monitoring in 13patients .

Electrophysiologic testing. Ventricular tachycardia oc-curred during electrophysiologic studies in 18 patients . Sus-

722 CARLSON ET ALRIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA

tained ventricular tachycardia was induced by programmedventricular stimulation in 11 patients and occurred spontane-ously in 1 . Nonsustained ventricular tachycardia occurred in sixpatients . In four patients, ventricular tachycardia was inducedonly during intravenous administration of isoproterenol. Meanventricular tachycardia cycle length was 322 ± 10 ms . Trans-catheter sequential site activation mapping of ventriculartachycardia was performed in 10 patients, and in each patientthe earliest site of ventricular electrical activation duringventricular tachycardia was found in the right ventricularoutflow tract near the site of abnormalities noted on the cineMRI. In each patient, pace mapping from the right ventricularoutflow tract mimicked the 12-lead surface ECG ventriculartachycardia QRS complex configuration .

Assessment of the left ventricle. All 22 patients with rightventricular outflow tract ventricular tachycardia had normalleft ventricular systolic function by echocardiogram, left ven-tricular angiogram, or tine MRI scan. None of the patientswho underwent coronary arteriography had hemodynamicallysignificant coronary artery disease. None of the patients whounderwent a treadmill exercise tolerance test had ischcmicECG rcpolarization abnormalities associated with exercise .

Assessment of the right ventricle . Echocardiographic andangiographic results. Echocardiography demonstrated rightventricular abnormalities in only two (9%) of the 21 patientswith right ventricular outflow tract ventricular tachycardia whounderwent the test . The echocardiograms of these two patientsdemonstrated right ventricular dilation . Right ventricular an-giography was interpreted as normal in two patients butdemonstrated a dilated, hypokinetic right ventricle in one, mildright ventricle and pulmonary artery enlargement in one andright ventricular outflow tract dyskinesia associated with a rightventricular outflow tract membrane in one (Fig . 1) .

Cine MR1 results in patients with right ventricular outflow tractventricular tachycardia. The cine MRI scan demonstrated rightventricular structural abnormalities in 21 of the 22 patientswith right ventricular outflow tract ventricular tachycardia . Thedifference in detection of right ventricular abnormalities be-tween cine MRI and echocardiography (21195%] of 22 vs. 2]9%] of 21) was significant (p < 0 .0001). The one patient whohad a normal cine MRI scan also had a normal echocardio-gram and a normal right ventricular angiogram .

The vine MRI scan structural abnormalities of the rightventricle included fixed focal wall thinning (distinguishablefrom adjacent regions of the right ventricle with normal thickness)with or without excavations (discrete areas of severely diminishedwall thickness), regionally decreased systolic wall thickening andabnormal wall motion during systole (Fig. 2). Regionally de-creased systolic wall thickening or abnormal wall motion was themost common finding, occurring in 21 patients. These findingswere observed only on the cine MRI scan and not on theechocardiogram or right ventricular angiogran . Fixed focal wallthinning was observed in 14 patients, including 5 with excavations .Fumd wall thinning and excavations were best appreciated on thevine MRI scan image loops but in some cases were observed onthe static MRI scans. In each patient in whom abnormalities were

JACC Vol. 24, No. 3September 1994 :720-7

Figure 1. Right ventricular angiogram in the right anterior obliqueview during diastole in a patient with right ventricular outflow tractventricular tachycardia. A dyskinetic area was noted in the lateral rightventricular outflow tract (arrow) .

detected, the abnormalities were clearly distinguishable fromadjacent regions of the right ventricle with normal wall thicknessand function, often on the same image slice .

Anatomic and functional abnormalities, or both, were ob-served on the cine MRI scan in various parts of the rightventricle but were most prevalent above the crista supraven-tricularis in the anterior and lateral right ventricular outflowtract (20 patients) (Fig . 3). Abnormalities were less prevalentin the right ventricular anterior free wall and the right ventric-ular apex (15 patients) . Abnormalities were near the earliestsite of electrical activity during ventricular tachycardia in the10 patients whose ventricular tachycardia was mapped .

Cine MR1 results in patients without right ventricular outflowtract ventricular tachycardia. Cine MRI demonstrated rightventricular structural abnormalities (hypertrophy and dilation)in 17 (39%) of 44 patients without right ventricular outflowtract ventricular tachycardia . Abnormalities were most com-mon in patients with pulmonary artery hypertension under-going evaluation for lung transplantation (15) but were alsonoted in one patient with aortic dissection and one with dilatedcardiomyopathy. Diffuse right ventricular hypokinesia wasnoted in 13 of the 17 patients with right ventricle hypertrophyor dilation . None of the patients without right ventricularoutflow tract ventricular tachycardia had focal structural orregional right ventricular wall motion abnormalities resem-bling the findings observed in the patients with right ventricularoutflow tract ventricular tachycardia .

Thus, cine MRI detected right ventricular structural andwall motion abnormalities more often in patients with right

JACC Vol . 24, No. 3September 1994 :720-7

Figure 2 . Static and cine magnetic resonance imagingscans. A. Dysplastic myocardial changes within theinfundibulum and anterior wall of the right ventricle(static spin-echo and tine gradient-echo ; transaxial)On the "black-blood" spin-echo images . generalizedthinning (arrows) involving the lower infundibulumand extending into the anterior free wall of the rightventricle is noted . B, Dynamic "bright-blood" gradi-ent-echo images (cine) representing phases of thecardiac cycle at the level of the crista supraventricularis(large arrowhead) demonstrate overall dilation of theright ventricle (RV) with anterior wall thinning, in-cluding focal excavation (curved arrow) within thearea of dysplasia. The moderator band (small arrow-head) is shown . A = anterior ; L = left; RA = rightatrium.

ventricular outflow tract ventricular tachycardia than in pa- in patients with right ventricular outflow tract ventriculartients without arrhythmia (21 [95%] of 22 vs . 17 [39%] of 44, tachycardia were qualitatively different from those detected inp < 0.0001). Furthermore, abnormalities detected by tine MRI patients without this arrhythmia . The focal abnormalities

CARLSON ET AL.RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA 723

724 CARLSON E': AL .RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA

observed in 21 of 22 patients with right ventricular outflowtract ventricular tachycardia were not observed in patientswithout this arrhythmia.

One MR1 results in subjects with nominal hearts. Cine MRIwas normal in 14 (87 .S%) of 16 normal subjects. However, cineMRI demonstrated decreased systolic thickening of the rightventricular free wall in two normal subjects. In both patients,the decreased wall thickening was located well below the cristasupraventricularis in the right ventricular free wall .

Thus, cine MRI detected right ventricular structural andwall motion abnormalities more often in patients with rightventricular outflow tract ventricular tachycardia than in normalsubjects (21 [95%] of 22 vs . 2 [12.5%] of 16, p < 0.0001) .Abnormalities noted in normal subjects were confined to theright ventricular free wall, whereas most patients with ventric-ular tachycardia had abnormalities of the right ventricularoutflow tract .

DiscussionThe present study. This was the first study to demonstrate

that right ventricular outflow tract ventricular tachycardia isassociated with myocardial structural and wall motion abnor-malities. Previous reports (1,6,30-35) have claimed that rightventricular outflow tract ventricular tachycardia occurs in theabsence of structural heart disease or that right ventricularabnormalities are present in a minority of such patients .However, in our study, cine MRI demonstrated right ventric-

JACC Vol. 24, No. 3September 1994 :720-7

Figure 3. Cine magnetic resonance imaging . Dysplas-tic infundibulum (cine gradient-echo ; transaxial) . De-spite generalized degradation of image quality due topoor gating from ventricular ectopy, a patulous anddeformed lower infundibulum is demonstrated onimages from two adjacent levels (above to more cra-nial) . From end-diastole (left), to end-systole (right),multiple areas of diminished wall thickening and in-ward motion (white arrows) are revealed proximal anddistal to both the moderator band (curved arrow) andan accessory muscle bundle bridging the anterior andseptal surface of the infundibular cavity (arrowhead) .A = anterior; L = left; LA = left a trium . LV = leftventricle .

ular outflow tract structural abnormalities in 21 (95%) of 22patients with this arrhythmia. Right ventricular structural andwall motion abnormalities were less prevalent in both thecontrol patients with other cardiovascular diseases (17 [39%]of 44, p < 0.001) and the group with normal hearts (2 [12.5%]of 16, p < 0.001) . The abnormalities in patients with ven-tricular tachycardia were qualitatively different from thoseobserved in patients with other cardiovascular diseases . Fur-thermore, in patients with ventricular tachycardia the abnor-malities were in the right ventricular outflow tract, whereasabnormalities observed in two normal subjects (focal de-creased systolic wall thickening) were confined to a single-image slice of the right ventricular free wall . The right ventric-ular free wall is a relatively thin structure, even in normalhearts. The findings of this study suggest that focal decreasedright ventricular wall thickening alone is not associated withright ventricular outflow tract ventricular tachycardia and mustbe accompanied by abnormalities in the right ventricularoutflow tract .

In this study the cine MRI scan often revealed right ventricularoutflow tract abnormalities that were not apparent on static rightventricular MRI scans. This is probably due to the dynamic natureof the observed abnormalities . Wall thinning was more apparentduring systole than diastole . Similarly, hypokinetic or dyskineticsegments were apparent on the cine, but not the static, MRIscans. Although sagittal or obliquesagittal planes oriented alongthe long-axis of the right ventricular outflow tract were alsoimaged, the standard transaxial plane proved best for viewing the

JACC Vol. 24, No. 3September 1994 :720-7 RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TACHYCARDIA

abnormalities because most were in the anterior or lateral rightventricular outflow tract and the distal right ventricular free wall .

Comparisons of cine MRI with other imaging modalities .In our study, the structural abnormalities obFe!7 ,ed on the cineMRI scan in patients with right ventricular outflow tractventricular tachycardia were often not detected by echocardi-ography. When right ventricular abnormalities were detectedby echocardiography (two patients), more abnormalities wereapparent on the cine MRI scan . Thus, two patients manifestedonly right ventricular enlargement on echocardiogram. Thecine MRI scans of these patients demonstrated focal wallthickening and wall-motion abnormalities in the right ventric-ular outflow tract .

Comparisons of right ventricular angiography and the cineMRI scan for identifying right ventricular outflow tract struc-tural abnormalities in patients with right ventricular outflowtract ventricular tachycardia are difficult in this study becauseof the small number of patients (n := five) who underwent rightventricular angiography. However, observation of right ventric-ular outflow tract abnormalities on the cine MRI scan in twopatients with normal right ventricular angiograms suggests thatthe former technique defines more abnormalities .

The focal nature of the observed structural and functionalabnormalities may have decreased the utility of echocardiog-raphy and angiography. Several investigators (36-38) havenoted the limitations of conventional imaging modalities fordetecting focal myocardial disease . These limitations may alsoexplain the lack of an association in previous reports betweenright ventricular outflow tract ventricular tachycardia andstructural heart disease . Recent reports (19,20) suggest thatMRI scanning may be a more sensitive test for right ventricularstructural abnormalities .

Comparisons with other studies of right ventricular outflowtract ventricular tachycardia . Some investigators (39,40) havedemonstrated focal wall motion abnormalities in patients withidiopathic ventricular tachycardia . Although most studies haveconcluded that right ventricular outflow tract ventricular tachy-cardia occurs in patients with structurally normal hearts, a fewinvestigators have noted abnormalities in a minority of pa-tients . Using echocardiography or cine angiography, Proclemeret al. (41) detected right ventricular structural abnormalities in20% to 27% of patients with right ventricular outflow tractventricular tachycardia. Abnormalities included right ventric-ular dilatation and wall motion abnormalities suggestive ofarrhythmogenic right ventricular dysplasia . Kunze et al . (35)detected right ventricular outflow tract aneurysms by cineangiography in 4 of 11 patients with right ventricular outflowtract ventricular tachycardia . We do not know whether theseaneurysms correspond to the abnormalities observed in ourstudy. However, the prevalence (5 of 22) of anatomic rightventricular abnormalities demonstrated by echocardiographyand cine angiography in our study was similar to that describedin previous reports. By contrast, the prevalence of functionalabnormalities of right ventricular free wall contraction de-tected by cine MRI in our study was much higher than thatpreviously reported .

CARLSON ET AL . 725

Mechanisms of right ventricular outflow tract ventriculartachycardia. The findings of this study have significant impli-cations with regard to the mechanisms of right ventricularoutflow tract ventricular tachycardia. In the absence of appar-ent structural heart disease, many investigators have suggestedthat right ventricular outflow tract ventricular tachycardia isassociated with primary electrical disease, possibly at thecellular level . Lerman et al . (15) described idiopathic ventric-ular tachycardia that was cyclic adenosine monophosphatedependent, but the mechanism of this dependency remainsunknown. The association between right ventricular outflowtract ventricular tachycardia and exercise or the administrationof exogenous catecholamines and the response of the arrhyth-mia to calcium-channel blocking drugs has led some investiga . .torn to suggest that the arrhythmia is due to triggered activity .However, the myocardial structural abnormalities observed inour study suggest that right ventricular outflow tract ventricu-lar tachycardia may result from structural abnormalities ratherthan from either a primary electrical or a biochemical distur-bance. Although wall motion abnormalities might result fromabnormal electrical activation, the wall thinning and focalexcavations cannot be explained by such an abnormality . Theproximity of the right ventricular outflow tract structuralabnormalities to the earliest electrical activation during ven-tricular tachycardia in 10 patients supports the hypothesis thatthese abnormalities were related to the ventricular tachycardia .The presence of abnormalities at sites remote from the ven-tricular tachycardia onset site suggests that these abnormalitiesmay not always be associated with ventricular tachycardia .

Some investigators believe that idiopathic ventricular tachy-cardia is a manifestation of subclinical or occult cardiomyop-athy that will become clinically overt after a latency period .However, data from long-term studies indicate that mostpatients with right ventricular outflow tract ventricular tachy-cardia do not develop structural cardiac disease duringfollow-up (30,32,33,39,40,42-49) . Whether some of the pa-tients in our study will develop overt cardiomyopathy remainsto be seen .

Study limitations. In our study comparison of cine MRIscanning and right ventricular angiography is difficult becauseonly five patients underwent angiography. The detection ratefor right ventricular angiography (three of five) suggests thatthis test may be reasonably effective in determining the pres-ence of right ventricular outflow tract abnormalities. However,one of the patients with a normal right ventricular angiogramhad one of the most abnormal cine MRI scans . Thus, cine MRIdetected some abnormalities that were not appreciated byangiography. In these patients cine MRI revealed informationabout wall thickness that could not be appreciated on theangiogram . Furthermore, in contrast to angiography, cine MRIoffers a noninvasive means of evaluating the right ventricle andright ventricular outflow tract .

Our study does not address the cause of the observedstructural abnormalities . We did not perform endomyocardialbiopsies of the right ventricular outflow tract in any of thepatients because of concerns that the myocardial thinning and

726 CARLSON ET AL . .RIGHT VENTRICULAR OUTFLOW TRACT VENTRICULAR TAC'HYC'ARDIA September 1994:720-7

the location of the lesions in the right ventricular outflow tractmight increase the risk of cardiac perforation associated withthe procedure . Furthermore, the patchy nature of the abnor-malities may decrease the diagnostic yield of conventional rightventricular endomyocardial biopsy .

Although the clinical characteristics of the patients weremost consistent with idiopathic right ventricular outflow tractventricular tachycardia, we cannot exclude the possibility thatsome may have had arrhythmogenic right ventricular dysplasia.Auffermann et al . (50) and Blake et al. (51) described MRIfindings in patients with arrhythmogenic right ventriculardysplasia . Some of the cine MRI findings in our study weresimilar to those observed in patients with arrhythmogenic rightventricular dysplasia (18,50-54) . However, typical MRI char-acteristics associated with arrhythmogenic right ventriculardysplasia (fatty infiltrates of the right ventricle myocardiumand multiple ventricular tachycardia ORS complex configura-lions) were not present in our patients .

Conclusions. Right ventricular outflow tract ventriculartachycardia, previously considered to be "idiopathic," is asso-ciated with focal anatomic and functional wall motion abnor-malities of the right ventricular outflow tract . In this study,New abnormalities were best seen on cine MRI and werefrequently missed by other imaging modalities. Thus, cine MRIprovides a simple, reliable, noninvasive technique in the diag-nosis of right ventricular outflow tract ventricular tachycardia .Furthermore, the frequency of the right ventricular outflowtract abnormalities associated with right ventricular outflowtract ventricular tachycardia provides a stimulus for furtherstudy to characterize the abnormality more fully .

We thank Sandra Kruner for help in preparing the manuscript.

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