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Comparison of two-dimensional echocardiographic and angiographic findings in arrhythmogenic right ventricular dysplasia
Comparison of Two-Dimensional Echocardiographic and Angiographic Findings in Arrhythmogenic Right Ventricular Dysplasia JEFFREYH. ROBERTSON,MD, GUST H. BARDY, MD, LAWRENCE D. GERMAN, MD, JOHN J. GALLAGHER,MD, and JOSEPH KISSLO, MD
Comparison of 2-dimensional (2-D) echocardlographic and right ventricular (RV) angiographk findings was performed in 10 patlents with arrhythmogenic RV dysplasia. Diagnosis was based on accepted electrocardiographic and angiographk criteria. Nine patients underwent invasive electrophysiologic study, which confirmed RV source of ventrkular tachycardia (VT) in 7. Biopsy findings of RV dysplasia were available in 3 patients. Twodimensional echocardkgraphy and angkgraphy corresponded closely when dfffuse RV enlargement and hypokinesiawere present. Buch dfffuse findings were not invarlably present. Localized abnormalities consisting of bulging or sacculation of the RV wall were noted by both techniques,even In the absence
of diffuse changes. Echocardiographk evidence of localized disease predicted the presence of similar kskns at angiography,but agreement as to specific kcatkn was poor. Bubjectivity in interpreting subtle RV abnormalities by either technique and the inherent differences in information provided by the 2 methods probably account for the inconsistencies. In the patient with suspected arrhythmogenk RV dysplasia, 2-D echocardiographic evidence of dlffuse RV enlargement, otherwise unexplained, strongly supports the diagnosis and angkgraphy may be avoided. Isolated local changes seen by echocardiography should increase suspicion of RV dysplasia, but complementary angiographic study ts warranted. (Am J Cardiol 1985;55:1508-1508)
Arrhythmogenic right ventricular (RV) dysplasia is a syndrome in which there is variable replacement of RV muscle with fatty and fibrous elements. Patients present with recurrent ventricular tachycardia (VT), typically of left bundle branch block morphologic pattern.l-7 Clinical diagnosis rests on documentation of an RV origin of the VT in association with verification of RV morphologic changes by ventriculography.4vs Widespread muscle replacement results in generalized RV dilatation and impaired function, whereas localized disease is manifest by focal wall thinning or aneurysmal dilatations and sacculations.4p5 Several limited reports suggest that echocardiography can identify RV morphologic abnormalities associated with this rare disorder.4J3-10 Marcus et al4 showed RV enlargement in 6 patients and Baran et al* reported
using 2-dimensional(2-D) echocardiography in 1 patient and found multiple outpouchings and sacculations of the RV confiied by angiography. The present study reports the results of a systematic comparison of the RV angiographic and 2-D echocardiographic findings in 10 patients with arrhythmogenic RV dysplasia.
From the Department of Medicine, Division of Cardiology, Duke UniVerSltY Medical Center, Durham, North Carolina. This work was supPOW in psrt by United States Public Health .%vlce Grants GM-29680, HL-12715 and HL-23783, National Institutes of Health, Bethesda, MatYiatId. Manuscript received June 19, 1984; revised manuscript received February 23, 1985, accepted February 26, 1985. Address for reprints: Joseph Klsslo, MD, Box 3818, Duke University Medical Center, Durham, North Carolina, 27710.
Methods The 10 patients (7 men, 3 women), aged 13 to 69 years (mean 29), were referred between 1978 and 1963 for evaluation of recurrent VT. All 10 patients had left bundle branch block morphologic pattern of the QRS complex during VT episodes, which were strongly suggestive of an RV source, and had local or diffuse RV changes by angiography. All had normal left ventricular function with no evidence of coronary artery disease by coronary angiography. Endocardial mapping studies were performed in 9 patients and unequivocally confirmed RV origin of the VT in 7. Biopsy proof of RV origin was available in 3 patients. Patients (Table I) were evaluated by 2-D echocardiography for the presence of morphologic abnormalities of the right ventricle using commercially available or research prototype 2-D scanners. In 8 of the 10 patients, echocardiograms were obtained using transducer frequencies of 2.5 MHz or lower. Standard and nonstandard intermediate planes were used for interrogation of the right ventricle.*
June 1. 1985
TABLE I
THE AMERICAN
OF CARDIOLOGY
Volume
55
1507
Results of Electrocardiography, Angiography and Echocardiography In 10 Patients wlth Arrhythmogenic Right Ventricular Dysplasia Angiographic Abnormalities
Patient
JOURNAL
Age (yr) 8 Sex
Diffuse
Localized
Echocardiographic Abnormalities Diffuse
Localized
+
Anterior Apex 0 0 Apex Anterior Apex 0
TH
31M
0
JS
19M 13F
0 0 Apex
+
Inferior Apex Outflow Inferior Outflow Apex
+ +
JMLL
20M
DG DD
19M 69M
EL
67F
ifs JH
22F 16M 18M
RV biplane angiograms and 2-D echocardiograms were reviewed retrospectively by 2 experienced observers, each blinded to the other’s findings. Ten additional normal echocardiographic and angiographic studies were mixed in the pool of studies to eliminate observer bias. Varying degrees of RV enlargement and or hypokinesia were classified as diffuse changes. Isolated bulges, sacculations or wall thinning were classified as localized abnormalities. For purposes of localization of isolated lesions, the RV free wall was divided into inferior, apical, anterior and outflow tract zones using a modified wall segment nomenclature system.il
EI::
++
+ 0” +
inferior Outflow Apex Inferior Apex
Discussion
Arrhythmogenic RV dysplasiais a rare disorderand the associatedVT may be life-threatening and fail to respondto medicalmeasures.RecognizingRV dysplasia as the causeof VT is important becausenew surgical techniquescan isolatethe arrhythmogenicsegmentsof the RV and make it possibleto reduceor eliminate this threat.lsJ3 In most patients, the diagnosisis made on
Results
Results of angiography and echocardiographyare listed in Table I. Examples of diffuse and localizedangiographic and echocardiographicchangesare shown in Figures 1 and 2. All normal angiogramsand echocardiogramswereinterpreted asnormal. Comparisonof angiographyand 2-D echocardiography for diffuse changesshoweda high degreeof concordance(in 9 of 10 patients). In the single exception, minor overall RV enlargementsuggestedby echocardiography was not confirmed by angiography.Both methods agreedasto the presenceor absenceof localized lesionsin 8 patients, but with little agreementas to their location.In all, 9 focal lesionsweredetectedby 2-D echocardiographyandin only 4 instances was there agreementas to specific location.
FIGURE 1. Anteroposterior angiograms from 2 patients with arrhythmogenic right ventricular (RV) dysplasia. A, systolic frame showing diffuse RV dilatation and hyponcontractility in a patient with diffuse involvement. Arrows denote fissuring of ths RV wall.’ B, diastolic frame showing a localized RV outpouching of the apex wlth dlsaete borders (arrows).
1508
RIGHT
VENTRICULAR
DYSPLASIA
the basis of the characteristic electrocardiogram findings combined with some evidence of RV structural abnormality by angiography. The role of 2-D echocardiography in this regard has not been adequately explored. Earlier studies using echocardiography relied on the measurement of the RVdeft ventricular (LV) diameter ratio by M-mode or 2-D echocardiography.4JcJ4 Because the presence of localized disease may be associated with a normal RV size7 and there are difficulties in measuring the absolute diameter of the right ventricle,15 the RV:LV ratio is not likely to be a very sensitive criterion. The results of this study indicate that the 2-D echocardiographic findings of diffuse RV enlargement and hypokinesia predict similar findings at angiography in patients with suspected RV dysplasia. A 2-D echocardiogram should be performed in the early assessment of patients with suspected arrhythmogenic RV dysplasia. Diffuse morphologic changes not otherwise explained would support the diagnosis of RV dysplasia and angiography might be obviated. The lack of correlation between the 2 techniques for detection of localized changes is discouraging, but not unexpected. Angiographic and echocardiographic comparisons will never be exact because each method displays anatomic data differently% the angiogram provides an overall integrated image and the echocardiogram a cross-sectional image. There is also considerable subjectivity in interpretation of RV changes by both 2-D echocardiography and angiography. The absence of any established quantitative standards for either technique is an important limitation. Further work, as Guiraudon et a112have reported using angiography, must be done to correlate echocardiographic with anatomic findings. Newer 2-D echocardiographic systems using transducer frequencies of 5 MHz or more may improve echocardiographic visualization of involved segments of the right ventricle close to the chest wall. In the meantime, finding of localized RV abnormalities by echocardiography should increase the suspicion of RV dysplasia. Specificity and sensitivity of echocardiographic and angiographic findings are difficult to determine. We continue to see patients with morphologic changes compatible with RV dysplasia who do not have VT4 as
well as those with arrhythmogenic RV dysplasia in whom neither technique detects an RV abnormality. Other disorders may distort RV anatomy and may be associated with tachyarrhythmias. Among these are Ebstein’s anomaly, congenital absence of the right hemipericardium, atrial septal defect, partial anomalous pulmonary venous return, RV infarction and right-sided valvular insufficiency. Gross RV enlargement is also characteristic of Uhl’s anomaly, which may represent an extreme manifestation of RV dysplasia.5pg References I. Frank K, Fontaine 0, Vedel J, Mlalet G, Bol C. Gulraudon 0, Grosgogeat Y. Electrocardiologie de quatre cas de dy lasie ventrlculalre drotte arythmogene. Arch Mal Coeur 1978;71:963- T 72. 2. Fontaine G, Gulraudon G, Frank R, Cabrol C, Grosgogeat Y. Arrhythmu genic ri ht ventricular dysplasia: a previously unrecognized syndrome (abstr). 8 rrculation 1979;52 suppl ll:ll-65. 3. Fontalns G, Gulraudon 0, Frank R. Mechanism of ventricular tachycardia with and w&out associated chronic myocardial ischernla: surgical management based on epicardial mapping. In: Marula OS, ed. Cardiac Arrhythmias: Electrophysiology, Diagnosis and Management. Baltimore: Williams & Wilkins, 1979:523-530. 4. Marcus FI, Fontaine 0, Gulraudon 0, Frank R, Laurenceau JL, Malergue C, Grosgogeat Y. Right ventricular dysplasia: a report of 24 adult cases. Circulation 1982;05:384-398. 5. Fontaine 0, Gulraudon 0, Frank R, Tereau Y, Flllette F, Marcus FI, Chomette 0, Grosgogaat Y. Arrhythmogenic right ventricular dysplasia and Uhl’s disease. Arch Mal Coeur 1982;75:381 l-3671. 6. Rossl P, Massuml A, Gillette P, Hall R. Arrhythrnooenic rloht ventricular dysplasia: clinical featues, diagnostic techniques and-cwren. Am Heart J 1982:103:415-420. 7. Dungan Wl, Oar&n A Jr, Gllette PC. Arrhythogenic right ventricular dysplasia: a cause of ventricular tachyczudii in children with apparentty normal hearts. Am Heart J 1981;102:745-750. 8. Baran A, Nanda N, Falkott M, Barold BB, Gallaoher JJ. Twodirnenslonal echocardiographic detection of arrhythogenic r&t ventricular dysplasia. Am Heart J 1982;103:1066-1067. 9. Gaffney FA, Nicod P, Lln JC, Rude RE. Non-invasive ret nition of the parchment right ventricle (Uhl’s anomaly, arrh@mogenic rr3 t ventricular dysplasia) syndrome. Clin Cardiil 1983;6:235-242. 10. Laurenceau JL, Llenhart JF, Malergue MC, Gilbert M, Dumesnll JG. Donnees echocardiographlcs dans le syndrome du ventricule droit papyrace. Arch Mal Coeur 1979;72:258-262. 11. Henry WL, DeMarla A, Felgenbaum H, Kerber R, K&lo J, Weyman AE, Nanda N, Popp RL, Bahn D, Bchllter NB, lajlk AJ. Report of the American Society of Echccardiography Committee on Nomenctattre and Stat&n%: Identification of Myocardial Wall Segments. Irvine, CA: American Society of Echocardiooraohv. 1982. 12. Gulraudon 0, F&a& G, Frank R, Leandri R, Barra J, Cabrol C. Surgical treatment of ventricular tachycardla~guided by ventricular mapping in 23 paFs;owithout coronary artery drsease. Ann Thorac Surg 1981;32: 13. Guira& GM, Klein GJ, Gulamhuseln B, Palnvln GA DeICampo C Gonzalez X, Ko PT. Total disconnectlon of the right ver&cular free wall: surgical treatment of right ventricular tachycardtt associated with right ventricular dysplasia. Circulation 1983:67:463-470. 14. Laurenceau JL, Dumesmll JG. Right and left ventricular dimenstons as determinants of ventricular seotal motion. Chest 1978:69:388-393. 15. Bahn DJ, DaMarIa A, Klsslo’J, Weyman A. Measurement of M-mode echocardiograms: what lessons are there to be learned for the twodimensional approach? Clin Diagn Ultrasound 1980;4:7-19. 16. Klsslo JA. Robertson D, Gllbwt BW, van Ramm 0, Behar V. A comparison of real-time, two-dimensional echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 1977;55:134-141.
Comparison of 2-dimensional (2-D) echocardlographic and right ventricular (RV) angiographk findings was performed in 10 patlents with arrhythmogenic RV dysplasia. Diagnosis was based on accepted electrocardiographic and angiographk criteria. Nine patients underwent invasive electrophysiologic study, which confirmed RV source of ventrkular tachycardia (VT) in 7. Biopsy findings of RV dysplasia were available in 3 patients. Twodimensional echocardkgraphy and angkgraphy corresponded closely when dfffuse RV enlargement and hypokinesiawere present. Buch dfffuse findings were not invarlably present. Localized abnormalities consisting of bulging or sacculation of the RV wall were noted by both techniques,even In the absence
of diffuse changes. Echocardiographk evidence of localized disease predicted the presence of similar kskns at angiography,but agreement as to specific kcatkn was poor. Bubjectivity in interpreting subtle RV abnormalities by either technique and the inherent differences in information provided by the 2 methods probably account for the inconsistencies. In the patient with suspected arrhythmogenk RV dysplasia, 2-D echocardiographic evidence of dlffuse RV enlargement, otherwise unexplained, strongly supports the diagnosis and angkgraphy may be avoided. Isolated local changes seen by echocardiography should increase suspicion of RV dysplasia, but complementary angiographic study ts warranted. (Am J Cardiol 1985;55:1508-1508)
Arrhythmogenic right ventricular (RV) dysplasia is a syndrome in which there is variable replacement of RV muscle with fatty and fibrous elements. Patients present with recurrent ventricular tachycardia (VT), typically of left bundle branch block morphologic pattern.l-7 Clinical diagnosis rests on documentation of an RV origin of the VT in association with verification of RV morphologic changes by ventriculography.4vs Widespread muscle replacement results in generalized RV dilatation and impaired function, whereas localized disease is manifest by focal wall thinning or aneurysmal dilatations and sacculations.4p5 Several limited reports suggest that echocardiography can identify RV morphologic abnormalities associated with this rare disorder.4J3-10 Marcus et al4 showed RV enlargement in 6 patients and Baran et al* reported
using 2-dimensional(2-D) echocardiography in 1 patient and found multiple outpouchings and sacculations of the RV confiied by angiography. The present study reports the results of a systematic comparison of the RV angiographic and 2-D echocardiographic findings in 10 patients with arrhythmogenic RV dysplasia.
From the Department of Medicine, Division of Cardiology, Duke UniVerSltY Medical Center, Durham, North Carolina. This work was supPOW in psrt by United States Public Health .%vlce Grants GM-29680, HL-12715 and HL-23783, National Institutes of Health, Bethesda, MatYiatId. Manuscript received June 19, 1984; revised manuscript received February 23, 1985, accepted February 26, 1985. Address for reprints: Joseph Klsslo, MD, Box 3818, Duke University Medical Center, Durham, North Carolina, 27710.
Methods The 10 patients (7 men, 3 women), aged 13 to 69 years (mean 29), were referred between 1978 and 1963 for evaluation of recurrent VT. All 10 patients had left bundle branch block morphologic pattern of the QRS complex during VT episodes, which were strongly suggestive of an RV source, and had local or diffuse RV changes by angiography. All had normal left ventricular function with no evidence of coronary artery disease by coronary angiography. Endocardial mapping studies were performed in 9 patients and unequivocally confirmed RV origin of the VT in 7. Biopsy proof of RV origin was available in 3 patients. Patients (Table I) were evaluated by 2-D echocardiography for the presence of morphologic abnormalities of the right ventricle using commercially available or research prototype 2-D scanners. In 8 of the 10 patients, echocardiograms were obtained using transducer frequencies of 2.5 MHz or lower. Standard and nonstandard intermediate planes were used for interrogation of the right ventricle.*
June 1. 1985
TABLE I
THE AMERICAN
OF CARDIOLOGY
Volume
55
1507
Results of Electrocardiography, Angiography and Echocardiography In 10 Patients wlth Arrhythmogenic Right Ventricular Dysplasia Angiographic Abnormalities
Patient
JOURNAL
Age (yr) 8 Sex
Diffuse
Localized
Echocardiographic Abnormalities Diffuse
Localized
+
Anterior Apex 0 0 Apex Anterior Apex 0
TH
31M
0
JS
19M 13F
0 0 Apex
+
Inferior Apex Outflow Inferior Outflow Apex
+ +
JMLL
20M
DG DD
19M 69M
EL
67F
ifs JH
22F 16M 18M
RV biplane angiograms and 2-D echocardiograms were reviewed retrospectively by 2 experienced observers, each blinded to the other’s findings. Ten additional normal echocardiographic and angiographic studies were mixed in the pool of studies to eliminate observer bias. Varying degrees of RV enlargement and or hypokinesia were classified as diffuse changes. Isolated bulges, sacculations or wall thinning were classified as localized abnormalities. For purposes of localization of isolated lesions, the RV free wall was divided into inferior, apical, anterior and outflow tract zones using a modified wall segment nomenclature system.il
EI::
++
+ 0” +
inferior Outflow Apex Inferior Apex
Discussion
Arrhythmogenic RV dysplasiais a rare disorderand the associatedVT may be life-threatening and fail to respondto medicalmeasures.RecognizingRV dysplasia as the causeof VT is important becausenew surgical techniquescan isolatethe arrhythmogenicsegmentsof the RV and make it possibleto reduceor eliminate this threat.lsJ3 In most patients, the diagnosisis made on
Results
Results of angiography and echocardiographyare listed in Table I. Examples of diffuse and localizedangiographic and echocardiographicchangesare shown in Figures 1 and 2. All normal angiogramsand echocardiogramswereinterpreted asnormal. Comparisonof angiographyand 2-D echocardiography for diffuse changesshoweda high degreeof concordance(in 9 of 10 patients). In the single exception, minor overall RV enlargementsuggestedby echocardiography was not confirmed by angiography.Both methods agreedasto the presenceor absenceof localized lesionsin 8 patients, but with little agreementas to their location.In all, 9 focal lesionsweredetectedby 2-D echocardiographyandin only 4 instances was there agreementas to specific location.
FIGURE 1. Anteroposterior angiograms from 2 patients with arrhythmogenic right ventricular (RV) dysplasia. A, systolic frame showing diffuse RV dilatation and hyponcontractility in a patient with diffuse involvement. Arrows denote fissuring of ths RV wall.’ B, diastolic frame showing a localized RV outpouching of the apex wlth dlsaete borders (arrows).
1508
RIGHT
VENTRICULAR
DYSPLASIA
the basis of the characteristic electrocardiogram findings combined with some evidence of RV structural abnormality by angiography. The role of 2-D echocardiography in this regard has not been adequately explored. Earlier studies using echocardiography relied on the measurement of the RVdeft ventricular (LV) diameter ratio by M-mode or 2-D echocardiography.4JcJ4 Because the presence of localized disease may be associated with a normal RV size7 and there are difficulties in measuring the absolute diameter of the right ventricle,15 the RV:LV ratio is not likely to be a very sensitive criterion. The results of this study indicate that the 2-D echocardiographic findings of diffuse RV enlargement and hypokinesia predict similar findings at angiography in patients with suspected RV dysplasia. A 2-D echocardiogram should be performed in the early assessment of patients with suspected arrhythmogenic RV dysplasia. Diffuse morphologic changes not otherwise explained would support the diagnosis of RV dysplasia and angiography might be obviated. The lack of correlation between the 2 techniques for detection of localized changes is discouraging, but not unexpected. Angiographic and echocardiographic comparisons will never be exact because each method displays anatomic data differently% the angiogram provides an overall integrated image and the echocardiogram a cross-sectional image. There is also considerable subjectivity in interpretation of RV changes by both 2-D echocardiography and angiography. The absence of any established quantitative standards for either technique is an important limitation. Further work, as Guiraudon et a112have reported using angiography, must be done to correlate echocardiographic with anatomic findings. Newer 2-D echocardiographic systems using transducer frequencies of 5 MHz or more may improve echocardiographic visualization of involved segments of the right ventricle close to the chest wall. In the meantime, finding of localized RV abnormalities by echocardiography should increase the suspicion of RV dysplasia. Specificity and sensitivity of echocardiographic and angiographic findings are difficult to determine. We continue to see patients with morphologic changes compatible with RV dysplasia who do not have VT4 as
well as those with arrhythmogenic RV dysplasia in whom neither technique detects an RV abnormality. Other disorders may distort RV anatomy and may be associated with tachyarrhythmias. Among these are Ebstein’s anomaly, congenital absence of the right hemipericardium, atrial septal defect, partial anomalous pulmonary venous return, RV infarction and right-sided valvular insufficiency. Gross RV enlargement is also characteristic of Uhl’s anomaly, which may represent an extreme manifestation of RV dysplasia.5pg References I. Frank K, Fontaine 0, Vedel J, Mlalet G, Bol C. Gulraudon 0, Grosgogeat Y. Electrocardiologie de quatre cas de dy lasie ventrlculalre drotte arythmogene. Arch Mal Coeur 1978;71:963- T 72. 2. Fontaine G, Gulraudon G, Frank R, Cabrol C, Grosgogeat Y. Arrhythmu genic ri ht ventricular dysplasia: a previously unrecognized syndrome (abstr). 8 rrculation 1979;52 suppl ll:ll-65. 3. Fontalns G, Gulraudon 0, Frank R. Mechanism of ventricular tachycardia with and w&out associated chronic myocardial ischernla: surgical management based on epicardial mapping. In: Marula OS, ed. Cardiac Arrhythmias: Electrophysiology, Diagnosis and Management. Baltimore: Williams & Wilkins, 1979:523-530. 4. Marcus FI, Fontaine 0, Gulraudon 0, Frank R, Laurenceau JL, Malergue C, Grosgogeat Y. Right ventricular dysplasia: a report of 24 adult cases. Circulation 1982;05:384-398. 5. Fontaine 0, Gulraudon 0, Frank R, Tereau Y, Flllette F, Marcus FI, Chomette 0, Grosgogaat Y. Arrhythmogenic right ventricular dysplasia and Uhl’s disease. Arch Mal Coeur 1982;75:381 l-3671. 6. Rossl P, Massuml A, Gillette P, Hall R. Arrhythrnooenic rloht ventricular dysplasia: clinical featues, diagnostic techniques and-cwren. Am Heart J 1982:103:415-420. 7. Dungan Wl, Oar&n A Jr, Gllette PC. Arrhythogenic right ventricular dysplasia: a cause of ventricular tachyczudii in children with apparentty normal hearts. Am Heart J 1981;102:745-750. 8. Baran A, Nanda N, Falkott M, Barold BB, Gallaoher JJ. Twodirnenslonal echocardiographic detection of arrhythogenic r&t ventricular dysplasia. Am Heart J 1982;103:1066-1067. 9. Gaffney FA, Nicod P, Lln JC, Rude RE. Non-invasive ret nition of the parchment right ventricle (Uhl’s anomaly, arrh@mogenic rr3 t ventricular dysplasia) syndrome. Clin Cardiil 1983;6:235-242. 10. Laurenceau JL, Llenhart JF, Malergue MC, Gilbert M, Dumesnll JG. Donnees echocardiographlcs dans le syndrome du ventricule droit papyrace. Arch Mal Coeur 1979;72:258-262. 11. Henry WL, DeMarla A, Felgenbaum H, Kerber R, K&lo J, Weyman AE, Nanda N, Popp RL, Bahn D, Bchllter NB, lajlk AJ. Report of the American Society of Echccardiography Committee on Nomenctattre and Stat&n%: Identification of Myocardial Wall Segments. Irvine, CA: American Society of Echocardiooraohv. 1982. 12. Gulraudon 0, F&a& G, Frank R, Leandri R, Barra J, Cabrol C. Surgical treatment of ventricular tachycardla~guided by ventricular mapping in 23 paFs;owithout coronary artery drsease. Ann Thorac Surg 1981;32: 13. Guira& GM, Klein GJ, Gulamhuseln B, Palnvln GA DeICampo C Gonzalez X, Ko PT. Total disconnectlon of the right ver&cular free wall: surgical treatment of right ventricular tachycardtt associated with right ventricular dysplasia. Circulation 1983:67:463-470. 14. Laurenceau JL, Dumesmll JG. Right and left ventricular dimenstons as determinants of ventricular seotal motion. Chest 1978:69:388-393. 15. Bahn DJ, DaMarIa A, Klsslo’J, Weyman A. Measurement of M-mode echocardiograms: what lessons are there to be learned for the twodimensional approach? Clin Diagn Ultrasound 1980;4:7-19. 16. Klsslo JA. Robertson D, Gllbwt BW, van Ramm 0, Behar V. A comparison of real-time, two-dimensional echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 1977;55:134-141.