1382
Brief communications
American
unusual and bizarre atria1 electrogram at electrophysiologic study.3 (4) The disease may not be confined to atria or sinus node and may involve lower conduction systems and subsidiary pacemakers,4*g as in case No. 1. (5) The natural history of the disease is not known. Ventricular pacing seems to be an effective mode of treatment to prevent bradyarrhythmic symptoms9 and possibly sudden death. Anticoagulant therapy seems to be advisable, although its efficacy remains to be proved. REFERENCES
1.
2. 3. 4. 5. 6.
Ruff P, Leier CV, Sahaal SF. Temporary atrial standstill. AM HEART J 1979;98:413-20. Disertori M, Guarnerio M, Vergara G, et al. Familial endemic persistent atria1 standstill in a small mountain community. Eur Heart J 1983;4:354-61. Ward DE, Ho SY, Shinebourne EA. Familial atrial standstill and inexcitability in childhood. Am J Cardiol 19&1;53:965-7. Rosen KM, Rahimtoola SH, Gunnar RM, Lev M. Transient and persistent atrial standstill with His bundle lesions. Circulation 1971;44:220-36. Levy S, Pauget B, Lacaze JC, Clementy J, Bricand H. Partial atria1 standstill: report of 3 cases and review of clinical and electrophysiologic features. Eur Heart J 1980;1:107-16. Bensaid J. Le paralvsie auriculaire. Ann Cardiol Aneeiol 1975;24:509-17.
-
-
I. Baldwin AJ, Talley RC, Johnson C, Nutler 0. Permanent paralysis
of the atrium
in a patient
with
facioscapulohumeral
muscular dystrophy. Am J Cardiol 1973;31:649-53. 8. Allensworth DC, Rice GJ, Lowe GW. Persistent atria1 standstillinafamily withmyocardialdisease. Am J Med 1969;47:77584. 9. Pierard LA, Henrard L, Demoulin JC. Persistent atria1 standstill in familial Ebstein’s anomaly. Br Heart J 1985;53:594-7. 10. Sumimoto T, Hamada M. Naaae A. Kazatani Y. Hiwada K. Low levels of atria1 natriuretic factor in patients with atria1 standstill. AM HEART J 1990;120:210-11. 11. Effendy
partial
FN, Blongnesi
R, Bianchy
G, Visioli
and total atria1 standstill.
0. Alternation
J Electrocardiol
of
1979;
12:121-7.
Cosecretion of atrial and brain natriuretic peptides during supraventricular tachyarrhythmias Masakazu Kohno, MD, Takeshi Horio, MD, Iku Toda, MD, Kaname Akioka, MD, Akira Tahara, MD, Masakazu Teragaki, MD, Kazuhide Takeuchi, MD, Naotsugu Kurihara, MD, and Tadanao Takeda, MD. Osaka, Japan
From the First Department of Internal Medicine, Osaka City University Medical School. Reprint requests: Masakazu Kohno, MD, First Department of Internal Medicine, Osaka City University Medical School, l-5-7 Asahi-machi, Abeno-ku, Osaka 545, Japan. 4/4/35982
May 1992 Heart Journal
Atria1 natriuretic peptide (ANP) is a diuretic, natriuretic, and vasodilatory peptide hormone originally isolated from the mammalian heart. Brain natriuretic peptide (BNP) was first identified in the porcine brain,’ and later isolated from the porcine heart.2 Porcine BNP consists of 26 amino acid residues with a remarkable homology to but definitely distinct from the sequence of ANP.i BNP elicits a spectrum of diuretic, natriuretic, and hypotensive effects very similar to those of ANP.’ Recently, a low molecular weight form of human BNP, human BNP-32, which corresponds to the C-terminal sequence (77-108) of the human BNP precursor deduced from the complementary deoxyribonucleic acid (cDNA) sequence, was found in the human atriimmunoreactive BNP was found in um. 3 Subsequently, human plasma; its concentration is high in plasma from patients with congestive heart failure.4 The purpose of this study was to measure changes in plasma concentrations of ANP and BNP in patients with paroxysmal supraventricular tachycardia and rapid atria1 fibrillation. We also examined the circulating forms of immunoreactive ANP and BNP in these patients by reverse-phase high-pressure liquid chromatography (HPLC).5 Four patients with paroxysmal supraventricular tachycardia and three patients with rapid atria1 fibrillation were studied (Table I). Of the seven patients, none had congestive heart failure or renal failure. Heart rate was determined during tachyarrhythmias and 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. Heart rate and rhythm were recorded by electrocardiogram. The tachycardia samples were drawn 0.5 to 6 hours after supratachyarrhythmias occurred. The post-tachycardia samples were drawn 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. Blood samples for ANP and BNP were taken from a forearm vein with the subject in the supine resting position and were drawn directly into ice-chilled siliconized disposable tubes containing aprotinin (500 KIU/ml) and ethylenediamine tetraacetic acid (EDTA) (1 mg/ml). Plasma was separated by centrifugation for 10 minutes at 4’ C, and was then immediately frozen and stored at -80” C for several days. Immunoreactive ANP or BNP was extracted from plasma using a Sep-Pak Cl 8 cartridge (Waters Associates, Milford, Mass.), as described previously.6 The recovery rate of human ANP(l-28) and human BNP-32 was 667’ and 62 ‘;, respectively. The concentration of plasma immunoreactive ANP was measured as previously reported.6 The concentration of plasma immunoreactive BNP was measured with antibody against synthetic human BNP-32 and 1251-labelled human BNP-32 (Peninsula Laboratories Inc., Belmont, Calif.), as reported for ANP radioimmunoassay. This antibody reacts 100% with human BNP-32 and cross-reacts 0.05?; with rat BNP-32. This antibody did not cross-react with porcine BNP-26, rat BNP-45, a-human ANP(l-28), cu-rat ANP(l-28), angiotensin II, vasopressin, or endothelin-1. The interassay variations of ANP and BNP were 12.6?; and 11.7 % , and the intraassay variations of ANP and BNP were 6.2 % and 7.0%) respectively. Reverse-phase HPLC was performed with an octadecyl-
Volume Number
123 5
1383
Brief communications
s E
3
E .
o-
0-
TACHY
POST
TACHY
TACHY
POST
TACHY
Fig. 1. Plasma concentrations of ANP (left panel) and BNP (right panel) during and after supraventricular tachyarrhythmias (Z’ACHY). The hatched area is the normal range in control subjects.
Table I. Characteristics
of the seven patients
with supraventricular
tachyarrhythmias Heart
Age Patient
PSVT,
No.
& Sex
1
72 F
2 3
47 F
60 F
4
73 M
5 6 7
67 M 64 M 56 F
Paroxysmal
supraventricular
rate
(beatslmin)
fyr)
Arrhythmia
Underlying
AF, atrial
TACHY
Systemic hypertension None Systemic hypertension Lung cancer (adenocarcinoma) CAD Lung cancer (adenocarcinoma) Systemic hypertension
PSVT PSVT PSVT PSVT Rapid AF Rapid AF Rapid AF tachycardia;
disease
fibrillation;
CAD,
silica column (4.6 X 250 mm, Tosoh, Tokyo, Japan),5 which was eluted with a linear gradient of acetonitrile from 15 % to 60% in 0.09% trifluoroacetic acid with a flow rate of 1 ml/min; 1 ml fractions were collected and assayed by radioimmunoassay. Fig. 1 shows plasma concentrations of ANP and BNP during and after supraventricular tachyarrhythmias. Mean plasma concentrations of ANP and BNP in clinically normal subjects were 31 + 10 pg/ml (n = 32) and 2.1 + 0.4 pg/ml (n = 25), respectively. These normal subjects were checked by routine laboratory studies including assays of serum electrolytes, serum creatinine, blood urea nitrogen, and the fasting blood glucose level, liver function test, urinalysis, a chest roentgenogram, and an electrocardiogram. Significantly high levels of ANP and BNP during supraventricular tachycardia and rapid atria1 fibrillation were observed compared with normal levels, respectively (p < 0.05, p < 0.05). Ten to 20 minutes after restoration of normal sinus rhythm or normal heart rate, both peptide
coronary
artery
disease;
186 166 180 164 132 150 160 TACHY,
tachyarrhythmias;
Post TACHY 92 (SR) 90 (SR)
96 (SR) 86 (SR) 80 (AF) 90 (AF) 72 (SR) SR, sinus
rhythm.
values fell toward normal levels. The concentrations of both peptides were correlated with each other (n = 14, r = 0.85, p < 0.01). Fig. 2 shows elution profiles of extracts of pooled plasma obtained from patients with supraventricular tachyarrhythmias. The major peak with immunoreactive BNP emerged at 13 minutes, which was the same retention time as that of synthetic human BNP-32. Immunoreactive ANP eluted at the same elution position as human ANP(l-28). These results suggest that human ANP( l-28) and human BNP-32 are cosecreted from the heart during supraventricular tachyarrhythmias. The precise cause of the increase in the plasma BNP concentration during supraventricular tachyarrhythmias remains to be established, but an increase in atrial pressure during these arrhythmias is one likely possibility. Atria1 stretch may induce the secretion of BNP in the same way it does for ANP. The post-tachycardia ANP and BNP levels were above the normal range. The circulating half-lives of these peptides are 3 to
1384
Brief communications
American
0
5
10
15
Retention
20
time
25
II
Hearl
May 1992 Journal
45
(mio)
Fig. 2. Profiles by reverse-phase HPLC of immunoreactive ANP (upper panel) and BNP (lower panel) in extracts of pooled plasma obtained from patients with supraventricular tachyarrhythmias. The plasma samples were concentrated with the use of a Sep-Pak Cl 8 cartridge (see text). The elution positions of standard human BNP-32 and human ANP(l-28) are shown by arrows.
5 minutes. Therefore one possible explanation is that a considerable amount of ANP and BNP secreted during tachyarrhythmias may influence the plasma levels of these peptides even at 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. ANP is proposed to be a contributing factor to the polyuria sometimes associated with paroxysmal supraventricular tachyarrhythmias.7 The raised BNP concentration during supraventricular tachyarrhythmias may also play a role in this polyuria. However, the BNP concentration required to induce natriuresis in man needs to be carefully determined before we can conclude that both BNP and ANP are truly responsible for this polyuria. REFERENCES
1. Sudoh T, Kangawa K, Minamino N, Matsuo H. A new natriuretic peptide in porcine brain. Nature 1988;332:78-81. 2. Minamino N, Aburaya M, Ueda S, Kangawwa K, Matsuo H. The presence of brain natriuretic peptide of 12,000 daltons in porcine heart. Biochem Biophys Res Commun 1988;155:740-6. 3. Kambayashi Y, Nakao K, Mukoyama M, Saito Y, Ogawa Y, Shiono S, et al. Isolation and sequence determination of human brain natriuretic peptide in human atrium. FEBS Lett 1990;259:341-5. 4. Mukoyama M, Nakao K, Saito Y, Ogawa Y, Hosoda K, Suga S, et al. Human brain natriuretic peptide, a novel cardiac hormone. Lancet 1990;335:801-2. 5. Kohno M, Yasunari K, Murakawa K, Yokokawa K, Horio T, Fukui T, Takeda T. Plasma immunoreactive endothelin in essential hypertension. Am J Med 1990;88:614-8. 6. Kohno M, Murakawa K, Yasunari K, Nishizawa Y, Morii H, Takeda T. Circulating atria1 natriuretic peptides in hyperthyroidism and hypothyroidism. Am J Med 1987;83:648-52. 7. Yamaji T, Ishibashi M, Nakaoka H, Imataka H, Amano M, Fujii J. Possible role for atrial natriuretic peptide in polyuria associated with paroxysmal atria1 arrhythmias [Letter]. Lancet 1985;1:1211.
Successful radiofrequency catheter ablation of an atrial ectopic tachycardia in an adolescent Yung R. Lau, MD, Paul C. Gillette, MD, Matthew M. Wienecke, MD, and Christopher L. Case, MD. Charleston, S.C.
Atria1 ectopic tachycardia (AET) is frequently incessant and is extremely difficult to control with medications. While the effectiveness of radiofrequency (RF) catheter ablation for accessory pathways has been established in adults,l* 2 only two successful RF catheter ablations of AET have been reported in adults.3 The full scope of RF ablation has not yet been established in the pediatric population. While previous reports have shown successful directcurrent (DC) ablation of AET in the pediatric population4, 5 successful RF ablation of AET has been reported in abstract form only.6 We herein describe a case of a 15year-old with incessant AET and cardiomyopathy who was successfully treated with RF catheter ablation and whose cardiomyopathy has subsequently resolved. CV, a previously healthy, asymptomatic 15-year-old white male. was found to have an elevated heart rate dur-
From Heart Reprint Children’s 4/4/35976
the Medical Center. requests: Heart
University
of South
Yung R. Lau, MD, Center, 171 Ashley
Carolina,
South
Medical University Ave., Charleston,
Carolina
Children’s
of South Carolina, SC 29425.
Brief communications
American
unusual and bizarre atria1 electrogram at electrophysiologic study.3 (4) The disease may not be confined to atria or sinus node and may involve lower conduction systems and subsidiary pacemakers,4*g as in case No. 1. (5) The natural history of the disease is not known. Ventricular pacing seems to be an effective mode of treatment to prevent bradyarrhythmic symptoms9 and possibly sudden death. Anticoagulant therapy seems to be advisable, although its efficacy remains to be proved. REFERENCES
1.
2. 3. 4. 5. 6.
Ruff P, Leier CV, Sahaal SF. Temporary atrial standstill. AM HEART J 1979;98:413-20. Disertori M, Guarnerio M, Vergara G, et al. Familial endemic persistent atria1 standstill in a small mountain community. Eur Heart J 1983;4:354-61. Ward DE, Ho SY, Shinebourne EA. Familial atrial standstill and inexcitability in childhood. Am J Cardiol 19&1;53:965-7. Rosen KM, Rahimtoola SH, Gunnar RM, Lev M. Transient and persistent atrial standstill with His bundle lesions. Circulation 1971;44:220-36. Levy S, Pauget B, Lacaze JC, Clementy J, Bricand H. Partial atria1 standstill: report of 3 cases and review of clinical and electrophysiologic features. Eur Heart J 1980;1:107-16. Bensaid J. Le paralvsie auriculaire. Ann Cardiol Aneeiol 1975;24:509-17.
-
-
I. Baldwin AJ, Talley RC, Johnson C, Nutler 0. Permanent paralysis
of the atrium
in a patient
with
facioscapulohumeral
muscular dystrophy. Am J Cardiol 1973;31:649-53. 8. Allensworth DC, Rice GJ, Lowe GW. Persistent atria1 standstillinafamily withmyocardialdisease. Am J Med 1969;47:77584. 9. Pierard LA, Henrard L, Demoulin JC. Persistent atria1 standstill in familial Ebstein’s anomaly. Br Heart J 1985;53:594-7. 10. Sumimoto T, Hamada M. Naaae A. Kazatani Y. Hiwada K. Low levels of atria1 natriuretic factor in patients with atria1 standstill. AM HEART J 1990;120:210-11. 11. Effendy
partial
FN, Blongnesi
R, Bianchy
G, Visioli
and total atria1 standstill.
0. Alternation
J Electrocardiol
of
1979;
12:121-7.
Cosecretion of atrial and brain natriuretic peptides during supraventricular tachyarrhythmias Masakazu Kohno, MD, Takeshi Horio, MD, Iku Toda, MD, Kaname Akioka, MD, Akira Tahara, MD, Masakazu Teragaki, MD, Kazuhide Takeuchi, MD, Naotsugu Kurihara, MD, and Tadanao Takeda, MD. Osaka, Japan
From the First Department of Internal Medicine, Osaka City University Medical School. Reprint requests: Masakazu Kohno, MD, First Department of Internal Medicine, Osaka City University Medical School, l-5-7 Asahi-machi, Abeno-ku, Osaka 545, Japan. 4/4/35982
May 1992 Heart Journal
Atria1 natriuretic peptide (ANP) is a diuretic, natriuretic, and vasodilatory peptide hormone originally isolated from the mammalian heart. Brain natriuretic peptide (BNP) was first identified in the porcine brain,’ and later isolated from the porcine heart.2 Porcine BNP consists of 26 amino acid residues with a remarkable homology to but definitely distinct from the sequence of ANP.i BNP elicits a spectrum of diuretic, natriuretic, and hypotensive effects very similar to those of ANP.’ Recently, a low molecular weight form of human BNP, human BNP-32, which corresponds to the C-terminal sequence (77-108) of the human BNP precursor deduced from the complementary deoxyribonucleic acid (cDNA) sequence, was found in the human atriimmunoreactive BNP was found in um. 3 Subsequently, human plasma; its concentration is high in plasma from patients with congestive heart failure.4 The purpose of this study was to measure changes in plasma concentrations of ANP and BNP in patients with paroxysmal supraventricular tachycardia and rapid atria1 fibrillation. We also examined the circulating forms of immunoreactive ANP and BNP in these patients by reverse-phase high-pressure liquid chromatography (HPLC).5 Four patients with paroxysmal supraventricular tachycardia and three patients with rapid atria1 fibrillation were studied (Table I). Of the seven patients, none had congestive heart failure or renal failure. Heart rate was determined during tachyarrhythmias and 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. Heart rate and rhythm were recorded by electrocardiogram. The tachycardia samples were drawn 0.5 to 6 hours after supratachyarrhythmias occurred. The post-tachycardia samples were drawn 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. Blood samples for ANP and BNP were taken from a forearm vein with the subject in the supine resting position and were drawn directly into ice-chilled siliconized disposable tubes containing aprotinin (500 KIU/ml) and ethylenediamine tetraacetic acid (EDTA) (1 mg/ml). Plasma was separated by centrifugation for 10 minutes at 4’ C, and was then immediately frozen and stored at -80” C for several days. Immunoreactive ANP or BNP was extracted from plasma using a Sep-Pak Cl 8 cartridge (Waters Associates, Milford, Mass.), as described previously.6 The recovery rate of human ANP(l-28) and human BNP-32 was 667’ and 62 ‘;, respectively. The concentration of plasma immunoreactive ANP was measured as previously reported.6 The concentration of plasma immunoreactive BNP was measured with antibody against synthetic human BNP-32 and 1251-labelled human BNP-32 (Peninsula Laboratories Inc., Belmont, Calif.), as reported for ANP radioimmunoassay. This antibody reacts 100% with human BNP-32 and cross-reacts 0.05?; with rat BNP-32. This antibody did not cross-react with porcine BNP-26, rat BNP-45, a-human ANP(l-28), cu-rat ANP(l-28), angiotensin II, vasopressin, or endothelin-1. The interassay variations of ANP and BNP were 12.6?; and 11.7 % , and the intraassay variations of ANP and BNP were 6.2 % and 7.0%) respectively. Reverse-phase HPLC was performed with an octadecyl-
Volume Number
123 5
1383
Brief communications
s E
3
E .
o-
0-
TACHY
POST
TACHY
TACHY
POST
TACHY
Fig. 1. Plasma concentrations of ANP (left panel) and BNP (right panel) during and after supraventricular tachyarrhythmias (Z’ACHY). The hatched area is the normal range in control subjects.
Table I. Characteristics
of the seven patients
with supraventricular
tachyarrhythmias Heart
Age Patient
PSVT,
No.
& Sex
1
72 F
2 3
47 F
60 F
4
73 M
5 6 7
67 M 64 M 56 F
Paroxysmal
supraventricular
rate
(beatslmin)
fyr)
Arrhythmia
Underlying
AF, atrial
TACHY
Systemic hypertension None Systemic hypertension Lung cancer (adenocarcinoma) CAD Lung cancer (adenocarcinoma) Systemic hypertension
PSVT PSVT PSVT PSVT Rapid AF Rapid AF Rapid AF tachycardia;
disease
fibrillation;
CAD,
silica column (4.6 X 250 mm, Tosoh, Tokyo, Japan),5 which was eluted with a linear gradient of acetonitrile from 15 % to 60% in 0.09% trifluoroacetic acid with a flow rate of 1 ml/min; 1 ml fractions were collected and assayed by radioimmunoassay. Fig. 1 shows plasma concentrations of ANP and BNP during and after supraventricular tachyarrhythmias. Mean plasma concentrations of ANP and BNP in clinically normal subjects were 31 + 10 pg/ml (n = 32) and 2.1 + 0.4 pg/ml (n = 25), respectively. These normal subjects were checked by routine laboratory studies including assays of serum electrolytes, serum creatinine, blood urea nitrogen, and the fasting blood glucose level, liver function test, urinalysis, a chest roentgenogram, and an electrocardiogram. Significantly high levels of ANP and BNP during supraventricular tachycardia and rapid atria1 fibrillation were observed compared with normal levels, respectively (p < 0.05, p < 0.05). Ten to 20 minutes after restoration of normal sinus rhythm or normal heart rate, both peptide
coronary
artery
disease;
186 166 180 164 132 150 160 TACHY,
tachyarrhythmias;
Post TACHY 92 (SR) 90 (SR)
96 (SR) 86 (SR) 80 (AF) 90 (AF) 72 (SR) SR, sinus
rhythm.
values fell toward normal levels. The concentrations of both peptides were correlated with each other (n = 14, r = 0.85, p < 0.01). Fig. 2 shows elution profiles of extracts of pooled plasma obtained from patients with supraventricular tachyarrhythmias. The major peak with immunoreactive BNP emerged at 13 minutes, which was the same retention time as that of synthetic human BNP-32. Immunoreactive ANP eluted at the same elution position as human ANP(l-28). These results suggest that human ANP( l-28) and human BNP-32 are cosecreted from the heart during supraventricular tachyarrhythmias. The precise cause of the increase in the plasma BNP concentration during supraventricular tachyarrhythmias remains to be established, but an increase in atrial pressure during these arrhythmias is one likely possibility. Atria1 stretch may induce the secretion of BNP in the same way it does for ANP. The post-tachycardia ANP and BNP levels were above the normal range. The circulating half-lives of these peptides are 3 to
1384
Brief communications
American
0
5
10
15
Retention
20
time
25
II
Hearl
May 1992 Journal
45
(mio)
Fig. 2. Profiles by reverse-phase HPLC of immunoreactive ANP (upper panel) and BNP (lower panel) in extracts of pooled plasma obtained from patients with supraventricular tachyarrhythmias. The plasma samples were concentrated with the use of a Sep-Pak Cl 8 cartridge (see text). The elution positions of standard human BNP-32 and human ANP(l-28) are shown by arrows.
5 minutes. Therefore one possible explanation is that a considerable amount of ANP and BNP secreted during tachyarrhythmias may influence the plasma levels of these peptides even at 10 to 20 minutes after restoration of normal sinus rhythm or normal heart rate. ANP is proposed to be a contributing factor to the polyuria sometimes associated with paroxysmal supraventricular tachyarrhythmias.7 The raised BNP concentration during supraventricular tachyarrhythmias may also play a role in this polyuria. However, the BNP concentration required to induce natriuresis in man needs to be carefully determined before we can conclude that both BNP and ANP are truly responsible for this polyuria. REFERENCES
1. Sudoh T, Kangawa K, Minamino N, Matsuo H. A new natriuretic peptide in porcine brain. Nature 1988;332:78-81. 2. Minamino N, Aburaya M, Ueda S, Kangawwa K, Matsuo H. The presence of brain natriuretic peptide of 12,000 daltons in porcine heart. Biochem Biophys Res Commun 1988;155:740-6. 3. Kambayashi Y, Nakao K, Mukoyama M, Saito Y, Ogawa Y, Shiono S, et al. Isolation and sequence determination of human brain natriuretic peptide in human atrium. FEBS Lett 1990;259:341-5. 4. Mukoyama M, Nakao K, Saito Y, Ogawa Y, Hosoda K, Suga S, et al. Human brain natriuretic peptide, a novel cardiac hormone. Lancet 1990;335:801-2. 5. Kohno M, Yasunari K, Murakawa K, Yokokawa K, Horio T, Fukui T, Takeda T. Plasma immunoreactive endothelin in essential hypertension. Am J Med 1990;88:614-8. 6. Kohno M, Murakawa K, Yasunari K, Nishizawa Y, Morii H, Takeda T. Circulating atria1 natriuretic peptides in hyperthyroidism and hypothyroidism. Am J Med 1987;83:648-52. 7. Yamaji T, Ishibashi M, Nakaoka H, Imataka H, Amano M, Fujii J. Possible role for atrial natriuretic peptide in polyuria associated with paroxysmal atria1 arrhythmias [Letter]. Lancet 1985;1:1211.
Successful radiofrequency catheter ablation of an atrial ectopic tachycardia in an adolescent Yung R. Lau, MD, Paul C. Gillette, MD, Matthew M. Wienecke, MD, and Christopher L. Case, MD. Charleston, S.C.
Atria1 ectopic tachycardia (AET) is frequently incessant and is extremely difficult to control with medications. While the effectiveness of radiofrequency (RF) catheter ablation for accessory pathways has been established in adults,l* 2 only two successful RF catheter ablations of AET have been reported in adults.3 The full scope of RF ablation has not yet been established in the pediatric population. While previous reports have shown successful directcurrent (DC) ablation of AET in the pediatric population4, 5 successful RF ablation of AET has been reported in abstract form only.6 We herein describe a case of a 15year-old with incessant AET and cardiomyopathy who was successfully treated with RF catheter ablation and whose cardiomyopathy has subsequently resolved. CV, a previously healthy, asymptomatic 15-year-old white male. was found to have an elevated heart rate dur-
From Heart Reprint Children’s 4/4/35976
the Medical Center. requests: Heart
University
of South
Yung R. Lau, MD, Center, 171 Ashley
Carolina,
South
Medical University Ave., Charleston,
Carolina
Children’s
of South Carolina, SC 29425.
