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Successful catheter ablation of a noninducible ventricular tachycardia
Volume Number
114 6
Brief
II. Surgical model of mitral stenosis
Table
Dog no. 1 2 3 4 Mean
f SEM
Gradient pre valvotomy (mm Hd 9 29 7 15 15 k 5
Gradient
post valvotomy (mm f&J 0 2 3 0 1 2 1
(p = 0.03)
of approximately 11 cm, use of balloon circumferences proportionate to those in this study, i.e., double 30 mm balloons, would be expected to yield similar results. Nonetheless,thesefindings suggestthat caution should be exercisedin the clinical useof an oversized double balloon technique, in which the effective balloon circumference exceedsthe mitral annular circumference by >55%, for PMV. The circumference of the double balloonsin current clinical usedoesnot exceed that of a normal mitral anulus, and therefore this should not causethe damageobserved in the canine model. REFERENCES 1. Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical application of transvenous mitral commiasurotomy by a new balloon catheter. J Thorac Cardiovasc Surg 1984; 87:394. 2. Palacios IF, Block PC, Brandi SC, Blanc0 P, Casal H, Pulido JI, Munoz S, D’Empaire G, Ortega MA, Jacobs ML, Vlahakes G. Percutaneous balloon valvotomy for mitral stenosis [Abstract]. Circulation 1986;74(suppl II):II-208. 3. Lock JE, Khalilullah M, Shrivastava S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in rheumatic mitral stenosis. N Engl J Med 1985;313:1515. 4. McKay RG, Lock JE, Safian RD, Mandell VS, Bairn DS, Diver DJ, Royal HR, Come PC, Grossman W. Percutaneous balloon valvuloplasty in adult patients with critical mitral stenosis [Abstract]. Circulation 1986;74(suppl II):II-209. 5. Palacios I. Block PC. Brandi S. Blanc0 P. Casal H. Pulido JI. Munoz S,‘D’Empairk G, Ortega MA, Jacobs M, Vlahakes G: Percutaneous balloon valvotomy (PMV) for patients with severe mitral stenosis. Circulation 1987;75:778. 6. McKay CR, Ruiz C, Kawanishi D, Rahimtoola SH. Catheter balloon valvuloplasty treatment of mitral stenosis in adult patients: Initial experience with double balloon technique [Abstract]. Circulation 1986;74(suppl II):II-208.
Successful catheter ablation of a noninducible ventricular tachycardia Paul G. Colavita, M.D., W. Kenneth Haisty, Jr., M.D., and John S. Kelley, M.D. Winston-Salem, N.C. From the Department of Medicine, Bowman Gray School of Medicine. Reprint requests: Paul G. Colavita, M.D., Bowman Gray School Medicine, 300 S. Hawthorne Rd., Winston-Salem, NC 27103.
of
Communications
15 15
Ablation of ventricular tachycardia guided by electrophysiologic mapping’ or by visual inspection* has been accomplishedintraoperatively with much success.Catheter ablation of ventricular tachycardia has also been accomplished, but the experience is limited.3a4Prior to catheter ablation, endocardial activation mapping is required during ventricular tachycardia to isolate the area showing earliest endocardial activity relative to multiple reference leads. The purpose of this article is to report successfulcatheter ablation of a ventricular tachycardia focus guided by endocardial pace-mapping5without the aid of endocardial activation mapping. The patient suffered inferior and lateral myocardial infarctions in 1972 and 1980, respectively. Ventricular tachycardia with a right bundle branch morphology (RBBB) occurred in 1980 and was initially treated with quinidine and beta blockers. Quinidine was ineffective, and disopyramide was begun in 1981 with no recurrence until 1984. Ventricular tachycardia with a left bundle branch morphology (LBBB) wasalsonoted in September, 1984. An electrophysiologic study was performed in December, 1984, and the LBBB ventricular tachycardia was easily induced with premature atria1 stimulation. Amiodarone therapy was initiated, but combination therapy with tocainide, procainamide, or flecainide was required becauseof recurrent RBBB ventricular tachycardia. Flecainide and procainamide were discontinued due to exacerbation of congestive heart failure, and tocainide wasdiscontinued becauseof nauseaand vomiting. During a repeat electrophysiology study in April, 1986, RBBB ventricular tachycardia waseasily induced with pacing at 400 msecfrom the right ventricular apex, despite therapy with amiodarone and mexiletine. The patient was not considered a suitable candidate for ablative surgery and catheter ablation of the RBBB ventricular tachycardia focus was performed after we obtained informed consent. The patient wasbrought to the cardiac catheterization laboratory in the fasting, nonsedated state, after all antiarrhythmic drugs had been discontinued for at least 5 half-lives (except amiodarone). With the extrastimulus technique, RBBB ventricular tachycardia was initially induced from the right ventricular outflow tract after a prolonged effort. Following introduction of a No. 7F tripolar catheter (USCI, Billerica Mass.) into the left ventricle, ventricular tachycardia could not be reinitiated despite burst pacing, single,double, and triple extrastimuli at two cycle lengths from the right ventricular apex, outflow tract, and from multiple sites in the left ventricle. With the use of a No. 6F steerable tripolar catheter (Electra-Catheter Corp., Rahway, N. J.), pace-mapping was performed from multiple sites in the left ventricle.5 Pace-mappingfrom a localized area on the posteromedial left ventricular wall resulted in a QRS morphology almost identical to the clinical RBBB ventricular tachycardia (Fig. 1). Slight shifts in catheter position would produce dramatic changesin QRS morphology, particularly in lead V,. Slow ventricular conduction wasconfirmed in this area by latency from stimulus to onset of ventricular activation
1516
Brief
Communications
Fig.
Fig.
1A. Electrocardiogram obtained during the ablation procedure, showing normal sinus rhythm.
1B. Electrocardiogram obtained during the ablation procedure, showingventricular tachycardia.
and by fragmented electrograms (Fig. 2). After adequate anesthesiawas achieved, a single 200 J shock was delivered between the distal electrode and a back plate, as previously described.6 Following the countershock, the fragmented electrograms were markedly decreased in amplitude (Fig. 3). The patient tolerated the procedure well without any acute adverse effects. A follow-up Holter monitor revealed 4,290 ventricular ectopic beats with occasional couplets, but no sustained tachyarrhythmias. The patient has remained asymptomatic in spite of recurrent slow LBBB ventricular tacbycardia while receiving no antiarrhythmic therapy for 8 months. There has been no recurrence of the RBBB ventricular tachycardia since the ablation.
The present caseis interesting for several reasons:(1) the enormouslatency from stimulus to onset of ventricular activation; (2) the marked reduction in the amplitude of the fragmented electrograms following the shock and; (3) the successfulablation of a ventricular tachycardia focus guided only by pace-mapping. Latency can be defined asthe time that elapsesbetween the stimulus and the response,which is madeup of the stimulus-excitation latency in the vicinity of the stimulating electrode and the conduction time from the stimulus site to the recording site. Local electrograms were not recorded during left ventricular pacing to separate the two components of latency, but during normal sinus rhythm and right ventricular pacing local electrogramswere fragmented consis-
Volume Number
114 6
Brief
Communications
1517
1C. Electrocardiogram obtained during the ablation procedure, showing endocardial ventricular pacing from posteromedial left ventricle. Note the latency from stimulus to onset of ventricular activation. Fig.
DLV ~200ms
1
2. Electrograms initially recorded during normal sinus rhythm demonstrating slow fragmented potentials from the site of ablation in the left ventricle (Lb’). All intracardiac electrogramswere recorded with an Electronics for Medicine paper recorder at a speedof 100mm/set. Tracings from top to bottom are ECG leadsI, II, and V1, bipolar RV electrogram, and unipolar LV electrograms(proximal [P], middle [MI, and distal [o], respectively).
Fig.
tent with slow, inhomogeneousconduction in this area.lq8 Although the excitatory response evoked by cathodal stimulation during phase 3 may travel slowly, the action potential duration would not have been expected to be equal to the pacing cycle length, even with amiodarone, and would not explain the latency noted. The stimulus strength, which was one and one-half times diastolic threshold, would also not explain the latency noted. The best explanation for the latency is slow inhomogeneous conduction through this area. During reentry, an impulse must conduct over a path-
way that is functionally isolated from the rest of the heart? This region of slowconduction must have excitable entry and exit points, but be laterally protected by inexcitable boundaries. Only if the stimulating electrode was located in an area of slow orthodromic conduction leading to the exit site could the similarity of the paced and tachycardia QRS morphology be explained. This area wasalsoprotected laterally with no intervening myocardiurn activated despite 240 msec of latency. The marked reduction in the amplitude of the late fragmental electrograms by the countershock and the lack of arrhythmia
1518
Brief
Communications
American
December 1997 Heart Journal
PLV ML”
DLV I200ms
1
3. Electrograms recorded following ablation during normal sinusrhythm from the samearea shown in Fig. 2. Note the marked reduction in amplitude of the fragmental electrograms.Abbreviations are asin Fig. 2. Fig.
recurrence over the past 8 months is final proof that this area was indeed an integral part of the reentrant circuit. Ventricular tachycardia is occasionally rendered noninducible in the operating room following induction of general anesthesiaor after a ventriculotomy is performed. Our failure to induce the RBBB tachycardia is difficult to explain, considering its easeof induction 6 days prior to ablation. Possibleexplanations include a change in autonomic tone, improvement in congestive heart failure, or catheter trauma to the tachycardia circuit. Unipolar endocardial pace-mapping at the cycle length of the tachycardia wasperformed only after a prolonged effort to induce ventricular tachycardia wasunsuccessful.Josephsonet aL5 found endocardial pace-mapping “neither easier, more accurate, nor quicker” than endocardial activation mapping, and felt it to be of limited clinical use and that it should not replace activation mapping. We agree that pace-mapping should only be used as a corroborative method of localizing the ventricular tachycardia focus, but feel that careful pace-mappingmay allow one to successfully ablate an endocardial focus when activation mapping is not possible.The findings of exaggerated latency and fragmented electrogramsmay enhance the successof the ablation. REFERENCES
1. Josephson ME, Harken AH, Horowitz LN. Endocardial excision: a new surgical technique for the treatment of malignant ventricular tachycardia. Circulation 1979;60:143039. 2. Moran JM, Kehoe RF, Loeb JM, Lichtenthal PR, Sanders JH, Michaelis LL. Extended endocardial resection for the treatment of ventricular tachycardia and ventricular fibrillation. Ann Thorac Surg 1982;34:538-50. 3. Hartzler GO, Electrode catheter ablation of refractory focal ventriculartachycsrdia.J Am Coil Cardiol 1983;2:1107-13. 4. Fontaine G, Tonet JL, Frank R, Gallas Y, Fareng G, Grosgogeat Y. La fulguration endocavitaire. Une nouvelle methode
5.
6.
7.
8.
9.
de traitment des troubles du rhythme? Ann Cardiol Angeol 1984;33:543-61. Josephson ME, Waxman HL, Cain ME, Gardner MJ, Buxton AE. Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia. Am J Cardiol 1982;50:11-22. Gallagher JJ, Svenson RH, Kasell JH, German LD, Bardy GH, Broughton A, Critelli G. Catheter technique for closedchest ablation of the atrioventricular conduction system. N Engl J Med 1982;306:194-200. El-Sherif N, Scherlag BJ, Lazzara R, Hope RR. Re-entrant ventricular arrhythmias in the late myocardial infarction period. 1. Conduction characteristics in the infarction zone. Circulation 1977;55:686-702. Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia. Circulation 1978;57:659-65. Wit AL, Rosen MR, Hoffman BF. Electrophysiology and pharmacology of cardiac arrhythmias. II. Relationship of normal and abnormal electrical activity of cardiac fibers to the genesis of arrhythmias. B. Re-entry. AM HEART J 1974;88:664-70.
Echocardiographic diagnosis of anastomotic stricture following surgical correction of supra4~dkc t43tM anomskus putmonary venous connection Maurice P. Leung, M.B.,B.S.,* C.K. Mok, M.B.,B.S., David L.C. Cheung, M.B.,Ch.B, and K.C. Lau, M.B.,B.S.* Hong Kong From the Departments of *Paediatrics and Surgery, University of Hong Kong, Grantham Hospital. Reprint requests: Maurice P. Leung, Department of Paediatrics, The Grantham Hospital, 125 Wong Chuk Hang Road, Hong Kong.
114 6
Brief
II. Surgical model of mitral stenosis
Table
Dog no. 1 2 3 4 Mean
f SEM
Gradient pre valvotomy (mm Hd 9 29 7 15 15 k 5
Gradient
post valvotomy (mm f&J 0 2 3 0 1 2 1
(p = 0.03)
of approximately 11 cm, use of balloon circumferences proportionate to those in this study, i.e., double 30 mm balloons, would be expected to yield similar results. Nonetheless,thesefindings suggestthat caution should be exercisedin the clinical useof an oversized double balloon technique, in which the effective balloon circumference exceedsthe mitral annular circumference by >55%, for PMV. The circumference of the double balloonsin current clinical usedoesnot exceed that of a normal mitral anulus, and therefore this should not causethe damageobserved in the canine model. REFERENCES 1. Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical application of transvenous mitral commiasurotomy by a new balloon catheter. J Thorac Cardiovasc Surg 1984; 87:394. 2. Palacios IF, Block PC, Brandi SC, Blanc0 P, Casal H, Pulido JI, Munoz S, D’Empaire G, Ortega MA, Jacobs ML, Vlahakes G. Percutaneous balloon valvotomy for mitral stenosis [Abstract]. Circulation 1986;74(suppl II):II-208. 3. Lock JE, Khalilullah M, Shrivastava S, Bahl V, Keane JF. Percutaneous catheter commissurotomy in rheumatic mitral stenosis. N Engl J Med 1985;313:1515. 4. McKay RG, Lock JE, Safian RD, Mandell VS, Bairn DS, Diver DJ, Royal HR, Come PC, Grossman W. Percutaneous balloon valvuloplasty in adult patients with critical mitral stenosis [Abstract]. Circulation 1986;74(suppl II):II-209. 5. Palacios I. Block PC. Brandi S. Blanc0 P. Casal H. Pulido JI. Munoz S,‘D’Empairk G, Ortega MA, Jacobs M, Vlahakes G: Percutaneous balloon valvotomy (PMV) for patients with severe mitral stenosis. Circulation 1987;75:778. 6. McKay CR, Ruiz C, Kawanishi D, Rahimtoola SH. Catheter balloon valvuloplasty treatment of mitral stenosis in adult patients: Initial experience with double balloon technique [Abstract]. Circulation 1986;74(suppl II):II-208.
Successful catheter ablation of a noninducible ventricular tachycardia Paul G. Colavita, M.D., W. Kenneth Haisty, Jr., M.D., and John S. Kelley, M.D. Winston-Salem, N.C. From the Department of Medicine, Bowman Gray School of Medicine. Reprint requests: Paul G. Colavita, M.D., Bowman Gray School Medicine, 300 S. Hawthorne Rd., Winston-Salem, NC 27103.
of
Communications
15 15
Ablation of ventricular tachycardia guided by electrophysiologic mapping’ or by visual inspection* has been accomplishedintraoperatively with much success.Catheter ablation of ventricular tachycardia has also been accomplished, but the experience is limited.3a4Prior to catheter ablation, endocardial activation mapping is required during ventricular tachycardia to isolate the area showing earliest endocardial activity relative to multiple reference leads. The purpose of this article is to report successfulcatheter ablation of a ventricular tachycardia focus guided by endocardial pace-mapping5without the aid of endocardial activation mapping. The patient suffered inferior and lateral myocardial infarctions in 1972 and 1980, respectively. Ventricular tachycardia with a right bundle branch morphology (RBBB) occurred in 1980 and was initially treated with quinidine and beta blockers. Quinidine was ineffective, and disopyramide was begun in 1981 with no recurrence until 1984. Ventricular tachycardia with a left bundle branch morphology (LBBB) wasalsonoted in September, 1984. An electrophysiologic study was performed in December, 1984, and the LBBB ventricular tachycardia was easily induced with premature atria1 stimulation. Amiodarone therapy was initiated, but combination therapy with tocainide, procainamide, or flecainide was required becauseof recurrent RBBB ventricular tachycardia. Flecainide and procainamide were discontinued due to exacerbation of congestive heart failure, and tocainide wasdiscontinued becauseof nauseaand vomiting. During a repeat electrophysiology study in April, 1986, RBBB ventricular tachycardia waseasily induced with pacing at 400 msecfrom the right ventricular apex, despite therapy with amiodarone and mexiletine. The patient was not considered a suitable candidate for ablative surgery and catheter ablation of the RBBB ventricular tachycardia focus was performed after we obtained informed consent. The patient wasbrought to the cardiac catheterization laboratory in the fasting, nonsedated state, after all antiarrhythmic drugs had been discontinued for at least 5 half-lives (except amiodarone). With the extrastimulus technique, RBBB ventricular tachycardia was initially induced from the right ventricular outflow tract after a prolonged effort. Following introduction of a No. 7F tripolar catheter (USCI, Billerica Mass.) into the left ventricle, ventricular tachycardia could not be reinitiated despite burst pacing, single,double, and triple extrastimuli at two cycle lengths from the right ventricular apex, outflow tract, and from multiple sites in the left ventricle. With the use of a No. 6F steerable tripolar catheter (Electra-Catheter Corp., Rahway, N. J.), pace-mapping was performed from multiple sites in the left ventricle.5 Pace-mappingfrom a localized area on the posteromedial left ventricular wall resulted in a QRS morphology almost identical to the clinical RBBB ventricular tachycardia (Fig. 1). Slight shifts in catheter position would produce dramatic changesin QRS morphology, particularly in lead V,. Slow ventricular conduction wasconfirmed in this area by latency from stimulus to onset of ventricular activation
1516
Brief
Communications
Fig.
Fig.
1A. Electrocardiogram obtained during the ablation procedure, showing normal sinus rhythm.
1B. Electrocardiogram obtained during the ablation procedure, showingventricular tachycardia.
and by fragmented electrograms (Fig. 2). After adequate anesthesiawas achieved, a single 200 J shock was delivered between the distal electrode and a back plate, as previously described.6 Following the countershock, the fragmented electrograms were markedly decreased in amplitude (Fig. 3). The patient tolerated the procedure well without any acute adverse effects. A follow-up Holter monitor revealed 4,290 ventricular ectopic beats with occasional couplets, but no sustained tachyarrhythmias. The patient has remained asymptomatic in spite of recurrent slow LBBB ventricular tacbycardia while receiving no antiarrhythmic therapy for 8 months. There has been no recurrence of the RBBB ventricular tachycardia since the ablation.
The present caseis interesting for several reasons:(1) the enormouslatency from stimulus to onset of ventricular activation; (2) the marked reduction in the amplitude of the fragmented electrograms following the shock and; (3) the successfulablation of a ventricular tachycardia focus guided only by pace-mapping. Latency can be defined asthe time that elapsesbetween the stimulus and the response,which is madeup of the stimulus-excitation latency in the vicinity of the stimulating electrode and the conduction time from the stimulus site to the recording site. Local electrograms were not recorded during left ventricular pacing to separate the two components of latency, but during normal sinus rhythm and right ventricular pacing local electrogramswere fragmented consis-
Volume Number
114 6
Brief
Communications
1517
1C. Electrocardiogram obtained during the ablation procedure, showing endocardial ventricular pacing from posteromedial left ventricle. Note the latency from stimulus to onset of ventricular activation. Fig.
DLV ~200ms
1
2. Electrograms initially recorded during normal sinus rhythm demonstrating slow fragmented potentials from the site of ablation in the left ventricle (Lb’). All intracardiac electrogramswere recorded with an Electronics for Medicine paper recorder at a speedof 100mm/set. Tracings from top to bottom are ECG leadsI, II, and V1, bipolar RV electrogram, and unipolar LV electrograms(proximal [P], middle [MI, and distal [o], respectively).
Fig.
tent with slow, inhomogeneousconduction in this area.lq8 Although the excitatory response evoked by cathodal stimulation during phase 3 may travel slowly, the action potential duration would not have been expected to be equal to the pacing cycle length, even with amiodarone, and would not explain the latency noted. The stimulus strength, which was one and one-half times diastolic threshold, would also not explain the latency noted. The best explanation for the latency is slow inhomogeneous conduction through this area. During reentry, an impulse must conduct over a path-
way that is functionally isolated from the rest of the heart? This region of slowconduction must have excitable entry and exit points, but be laterally protected by inexcitable boundaries. Only if the stimulating electrode was located in an area of slow orthodromic conduction leading to the exit site could the similarity of the paced and tachycardia QRS morphology be explained. This area wasalsoprotected laterally with no intervening myocardiurn activated despite 240 msec of latency. The marked reduction in the amplitude of the late fragmental electrograms by the countershock and the lack of arrhythmia
1518
Brief
Communications
American
December 1997 Heart Journal
PLV ML”
DLV I200ms
1
3. Electrograms recorded following ablation during normal sinusrhythm from the samearea shown in Fig. 2. Note the marked reduction in amplitude of the fragmental electrograms.Abbreviations are asin Fig. 2. Fig.
recurrence over the past 8 months is final proof that this area was indeed an integral part of the reentrant circuit. Ventricular tachycardia is occasionally rendered noninducible in the operating room following induction of general anesthesiaor after a ventriculotomy is performed. Our failure to induce the RBBB tachycardia is difficult to explain, considering its easeof induction 6 days prior to ablation. Possibleexplanations include a change in autonomic tone, improvement in congestive heart failure, or catheter trauma to the tachycardia circuit. Unipolar endocardial pace-mapping at the cycle length of the tachycardia wasperformed only after a prolonged effort to induce ventricular tachycardia wasunsuccessful.Josephsonet aL5 found endocardial pace-mapping “neither easier, more accurate, nor quicker” than endocardial activation mapping, and felt it to be of limited clinical use and that it should not replace activation mapping. We agree that pace-mapping should only be used as a corroborative method of localizing the ventricular tachycardia focus, but feel that careful pace-mappingmay allow one to successfully ablate an endocardial focus when activation mapping is not possible.The findings of exaggerated latency and fragmented electrogramsmay enhance the successof the ablation. REFERENCES
1. Josephson ME, Harken AH, Horowitz LN. Endocardial excision: a new surgical technique for the treatment of malignant ventricular tachycardia. Circulation 1979;60:143039. 2. Moran JM, Kehoe RF, Loeb JM, Lichtenthal PR, Sanders JH, Michaelis LL. Extended endocardial resection for the treatment of ventricular tachycardia and ventricular fibrillation. Ann Thorac Surg 1982;34:538-50. 3. Hartzler GO, Electrode catheter ablation of refractory focal ventriculartachycsrdia.J Am Coil Cardiol 1983;2:1107-13. 4. Fontaine G, Tonet JL, Frank R, Gallas Y, Fareng G, Grosgogeat Y. La fulguration endocavitaire. Une nouvelle methode
5.
6.
7.
8.
9.
de traitment des troubles du rhythme? Ann Cardiol Angeol 1984;33:543-61. Josephson ME, Waxman HL, Cain ME, Gardner MJ, Buxton AE. Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia. Am J Cardiol 1982;50:11-22. Gallagher JJ, Svenson RH, Kasell JH, German LD, Bardy GH, Broughton A, Critelli G. Catheter technique for closedchest ablation of the atrioventricular conduction system. N Engl J Med 1982;306:194-200. El-Sherif N, Scherlag BJ, Lazzara R, Hope RR. Re-entrant ventricular arrhythmias in the late myocardial infarction period. 1. Conduction characteristics in the infarction zone. Circulation 1977;55:686-702. Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia. Circulation 1978;57:659-65. Wit AL, Rosen MR, Hoffman BF. Electrophysiology and pharmacology of cardiac arrhythmias. II. Relationship of normal and abnormal electrical activity of cardiac fibers to the genesis of arrhythmias. B. Re-entry. AM HEART J 1974;88:664-70.
Echocardiographic diagnosis of anastomotic stricture following surgical correction of supra4~dkc t43tM anomskus putmonary venous connection Maurice P. Leung, M.B.,B.S.,* C.K. Mok, M.B.,B.S., David L.C. Cheung, M.B.,Ch.B, and K.C. Lau, M.B.,B.S.* Hong Kong From the Departments of *Paediatrics and Surgery, University of Hong Kong, Grantham Hospital. Reprint requests: Maurice P. Leung, Department of Paediatrics, The Grantham Hospital, 125 Wong Chuk Hang Road, Hong Kong.