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Torsade de pointes induced by astemizole in a patient with prolongation of the QT interval
1436
Sakemi and VanNatta
American
presence of a fast and a slow atrioventricular conducting pathway.3,4v’ The fast pathway can be an accessory pathway, a fast atrioventricular nodal pathway, or a James tract, and the slow pathway can be the normal atrioventricular nodal His bundle pathway, a slow atrioventricular nodal pathway, or a slow accessory paraseptal accessory pathway. Thus when conduction delay occurs in the slow pathway during rapid pacing or extrastimulus testing, impulse conduction in both pathways may be out of phase so that the tissues at the other end are able to respond to the oncoming impulses from both the fast- and slow-conducting pathways. The retrograde fast pathway in our patient was likely to be the normal atrioventricular nodal pathway because the earliest atria1 activation during fast pathway conduction was registered from the His bundle recording catheter. The retrograde slow pathway was likely to be a slow paraseptal accessory pathway because the earliest atria1 activation during slow pathway conduction was registered from the ostium of the coronary sinus; the tachycardia could be terminated when a ventricular extrastimulus was delivered at the time the His bundle was refractory. That the tachycardia was terminated by a blocked ventricular extrastimulus excludes the possibility that the tachycardia was of atria1 reentry. REFERENCES
1. Grolleau R, Puech P, Cabasson J, Baissus C, Latour H. Particularites de la conduction auriculo-ventriculare dans un syndrome de Wolff-Parkinson-White. Arch Ma1 Coeur Vaiss i974;67:13-22. 2. Neuss H, Schlepper M, Spies HF. Double ventricular response to an atria1 extrasvstole in a natient with WPW syndrome type B. Eur J Cardio1”1974;2:175-9. 3. Wu D. Dual atrioventricular nodal pathways: a reappraisal. PACE 1982;5:72-89. 4. Lin FC, Yeh SJ, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. AM HEART J 1985;109:963-70. 5. Chang MS, Sung RJ, Tai TY, Lin SL, Liu Ph, Chang BN. Nodal and supraventricular tachycardia: an electrophysiologic study. J Am Co11 Cardiol 1983;2:894-903. 6. Brugada P, Vanagt EJ, Bar FWHM, Wellens HJJ. Incessant reciprocating atrioventricular tachycardia. Factors playing a role in the mechanism of the arrhythmia. PACE 1980;3:670-7. 7. Lin FC, Yeh SJ, Wu D. Double atria1 responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways. J Am Co11 Cardiol 1985;5:168-75.
Torsade de pointes induced by astemizole in a patient with prolongation of the QT interval Hideta Sakemi, MD, and Bruce VanNatta, Long Beach, Calif.
MD
From the Division of Cardiology, Long Beach Memorial Medical Center. Reprint requests: Bruce VanNatta, MD, 2699 Atlantic Ave., Long Beach, CA 90806. AM HEART J 1993;125:1436-1438. Copyright “’ 1993 by Mosby-Year Book, Inc. 000%8703/93/$1,00 + .I0 4/4/44909
Heart
my 1993 Journal
Administration 01 several antiarrhythmic agents. phe nothiazines. and tricyclic antidepressants has been associ. ated with t,he development of electrocardiographic QT interval prolongation and resultant torsade de pointes type tachyarrhythmias.’ Similar problems have been described with overdoses of nonsedating HI-receptor antagonists.‘, ’ We report a case of torsade de pointes occurring in a patient with possible congenital or mitral valve prolapse-associated prolongation of the QT interval who was receiving a therapeutic dose of astemizole. A 31-year-old woman was admitted in March 1991 to our hospital because of a second syncopal episode within 2 days. The patient was well until 1 day before admission, when she had a witnessed syncopal episode without warning. No seizure activity was noted. She regained consciousness within 1 minute without incontinence or a postictal syndrome. She was taken to another hospital where a complete blood cell count (CBC), serum glucose, and electrolyte levels were normal, but an electrocardiogram (ECG) was not taken. She was released from that institution but suffered another witnessed syncopal attack lasting about 30 seconds the following night. She was brought to our hospital, where the ECG was normal except for a prolonged QT, interval of 632 msec. The patient was an ex-hospital technician and had had an ECG taken in 1986, showing a QT, interval of 546 msec (Fig. 1). She denied any previous history of cardiac diseases, syncopal episodes, palpitations, shortness of breat,h, or exercise intolerance. There was no past history of liver disease. ‘The patient drank alcohol socially but denied smoking or use of illicit drugs. She had been taking astemizole (Hismanal, Janssen Pharmacentica, Piscataway, NJ.), 10 mg daily, for 6 weeks before admission. The medication had been prescribed for prophylaxis of her food-induced urticaria. The last dose was taken in the morning on the day of admission. She denied taking more than 10 mg a day or taking any other medication while she was taking astemizole. The patient’s father had mitral valve prolapse but no electrocardiographic abnormalities. Her mother had no electrocardiographic abnormalities. The patient had one healthy sister who never had an ECG taken. Her uncle had died of an acute myocardial infarction at the age of 51. Her cousin, a heavy drug and alcohol abuser, had a sudden death at the age of 29. There was no consanguinity bet.ween the patient’s parents. On admission, the temperature was 37.3’ C (99.2’ F), the respiratory rate was 18, the pulse rate was 60 beats/min, and blood pressure was 96/76 mm Hg without an orthostatic drop. Cardiac examination revealed a II/VI systolic murmur at the apex with a midsystolic click. No other cardiovascular or respiratory abnormalities were appreciated. Her hearing was normal. Laboratory tests on admission showed a normal CBC and normal serum electrolytes, with a potassium level of 3.7 mg/dl (normal 3.3 to 5.0 mg/dl), a calcium level of 9.0 mg/dl (normal 9.0 to 10.5 mg/dl) and a magnesium level of 2.1 mg/dl (normal 1.6 to 3.0 mg/dl). The serum concentration of astemizole or its hydroxylated metabolites was not determined. Echocardiography revealed normal left ventricular size and systolic function and probable mitral valve prolapse, with trace mitral regurgitation. The left atria1 dimension was 40 mm. About 12 hours after admission, the patient developed another syncopal attack.
Volume 125, Number 5, Part 1 American Heart Journal
Sakemi and VanNatta
1437
. i i
*
i.
1.
Fig. 1. ECG rhythm strip made in 1986,5 years before admission.The QT, interval is 546 msec.
Torsade de pointes-type ventricular tachyarrhythmia was documented on the heart monitor (Fig. 2). The QT, interval immediately before the ventricular tachycardia was680 msec.The patient wastreated with a lidocainedrip and oral metoprolol for 2 days in the intensive care unit. The signal-averagedECG while the patient was receiving metoprolol was negative for delayed potentials. The patient had no recurrence of ventricular tachycardia and was dischargedhomeon the sixth hospital day taking oral magnesiumsupplementation. She wasadvisednot to take astemizole in the future. The patient’s follow-up ECG taken 4 days after dischargeshowed a QT, interval of 577 msec. The patient experienced no recurrence of syncopeor palpitations. A follow-up ECG taken 5 months after discharge revealed a QT, interval of 509 msec(Fig. 3). Astemizole (Hismanal) is one of the nonsedatingHi-receptor antagonists,having virtually no anticholinergic side effects and no central nervous systempenetration. It is almost exclusively metabolized in the liver and excreted in the feces.The plasmahalf-life of astemizoleand its active metabolite following long-term administration is biphasic with an initial Ti/s of 7 to 9 days and a terminal Ti/s of 17 days. It has beenin clinical usein the United Kingdom for about a decade,and hasbeenavailable in the United States sincelate 1988.Astemizole hasbeenreported to causeprolongation of the QT interval and torsade de pointes when usedin excess23 3 The first suchcasewasreported in 1986. Terfenadine, the other nonsedating Hi-receptor antagonist, has alsobeen reported to causethe sameabnormality when an overdoseis taken4 or when taken with ketoconazole, a well-known inhibitor of the P-450 metabolic pathwayin the liver. The exact physiologicmechanismby which these nonsedating Hi-blockers cause prolongation of the QT interval is still unknown, although stimulation of the histamine receptors is known to increaseintracellular cy-
Fig. 2. ECG rhythm strip made 12 hours after admission. A torsadesde pointes-type ventricular tachyarrhythmia is documented.
clic adenosinemonophosphate(AMP) of cardiac muscles and to exert inotropic and chronotropic effects. On the other hand, prolongation of the QT intervals in generalcan be either congenital, asin the Romano-.Wardsyndromeand Jervell-Lange-Nielsen syndrome, or acquired. Conditions associatedwith acquired QT prolongation are ischemic
1438
Greenberg,
Robinson,
and Birrer
American
May 1993 Heart Journal
Fig. 3. Folio, f-up ECG rhythm strip made 5 months after discharge.The QT, interval is 509 msec.
heart disease, cardiomyopathy, postresuscitation state, electrolyte disorders,hypothyroidism, complete atrioventricular (AV) block, mitral valve prolapse, hypothermia. subarachnoid hemorrhage, postneurosurgical state, and the administration of various drugssuchasantiarrhythmic agents,phenothiazines, and tricyclic antidepressants.’ Our casehad documented QT prolongation in 1986and continued to have the sameabnormality asof August 1991. Her family history and normal hearing however did not suggestan inherited disorder, although incomplete penetrance could not be excluded. The patient’s father had mitral valve prolapse, and the patient wasfound to have mitral valve prolapse by echocardiography during this admission.Since conflicting studiesexist asto the association between mitral valve prolapseand prolongation of the QT interval,5a6it is difficult to determine at this time whether QT prolongation in our caseis congenital, with weak penetration among family members, or acquired, associated with mitral valve prolapse.Regardlessof the cause,it does appearthat our patient’s baselineQT interval prolongation may have made her more susceptibleto the development of torsade de pointes in the presenceof therapeutic doses of astemizole.In light of our caseand a review of the literature, we would recommendcaution in the useof astemizole in patients with known prolongation of the QT interval. REFERENCES
SurawiczB, Knoebel SB. Long QT: good, bad or indifferent. J Am Co11 Cardiol 1984;4:398-413. 2. Craft TM. Torsade de pointes after astemizole overdose. Br Med J 1986;292:660. 3. Bishop RO, Gaudry PL. Prolonged Q-T interval following astemizole overdose. Arch Emerg Med 1989;6:63-5. 4. Monahan BP, Ferguson CL, Kilieavy ES, Kellerman 53. Torsade de pointes occurring in association with terfenadine use. JAMA 1990;264:2788-90. ,5. Cowan MD, Fye WB. Prevalence of QT, prolongation in women with mitral valve prolapse. Am J Cardiol1989;63:133-4. 6. Drory Y, Fisman EZ, Pines A, Lloyd BK, Troy J, Cantilena LR. Exercise response in young woman with mitral valve pro1.
lapse.
Chest
1989;96:1076-80.
Atrial fibrillation after intravenous administration of gasoline Michael David Greenberg, MD, Timothy Robinson,DO, and Richard Birrer, MD Jamaica, N.Y.
Toxicity from commercialgasolineingestion is well recognized, both as a result of intentional and accidental ingesti0n.l
The vast majority
of reported
cases involve oral in-
gestion or inhalation. We report the caseof a young intravenous drug user, who self-injected between 5 and 15 cm3 of commercial gasoline. A 3%year-old man presented to the emergencydepartment with complaints of nausea, weakness, and palpitations. The symptoms appeared suddenly approximately 30 minutes before his arrival in the emergency department.
The patient admitted to having intentionally self-injected himself with between 5 and 15 cm3 of “93 octane” gasoline, which he obtained at a commercial gas station 1 hour before arrival at the hospital. His medical history was unre-
markable and the patient denied any history of cardiovascular disease. He also denied any previous “palpitations“ or history or “irregular heart beat.” There was no surgical history, and he was taking no prescription medications. The patient admitted to heavy tobacco use, although he denied alcohol use or use of cocaine within the previous week. Physical examination revealed a young man in no
acute distress.Vital signswere blood pressure,138/92mm Hg; pulse, 120 to 140 beats/min and irregular; respirations, From Emergency Medical Services Institute, Catholic Medical Brooklyn & Queens, Department of Emergency Medicine.
Center
Reprint Institute, Jamaica,
Services 153rd St..
requests: Michael Catholic Medical NY 11432.
AM HEART
D. Greenberg, MD, Center of Brooklyn
.J 1993;125:1438-1439.
Copyright 199:i 0002-8703/93/$1.00
by Mosby-.Year Houk, + .10 414144912
Inc.
Emergency & Queens,
Medical 88-25
of
Sakemi and VanNatta
American
presence of a fast and a slow atrioventricular conducting pathway.3,4v’ The fast pathway can be an accessory pathway, a fast atrioventricular nodal pathway, or a James tract, and the slow pathway can be the normal atrioventricular nodal His bundle pathway, a slow atrioventricular nodal pathway, or a slow accessory paraseptal accessory pathway. Thus when conduction delay occurs in the slow pathway during rapid pacing or extrastimulus testing, impulse conduction in both pathways may be out of phase so that the tissues at the other end are able to respond to the oncoming impulses from both the fast- and slow-conducting pathways. The retrograde fast pathway in our patient was likely to be the normal atrioventricular nodal pathway because the earliest atria1 activation during fast pathway conduction was registered from the His bundle recording catheter. The retrograde slow pathway was likely to be a slow paraseptal accessory pathway because the earliest atria1 activation during slow pathway conduction was registered from the ostium of the coronary sinus; the tachycardia could be terminated when a ventricular extrastimulus was delivered at the time the His bundle was refractory. That the tachycardia was terminated by a blocked ventricular extrastimulus excludes the possibility that the tachycardia was of atria1 reentry. REFERENCES
1. Grolleau R, Puech P, Cabasson J, Baissus C, Latour H. Particularites de la conduction auriculo-ventriculare dans un syndrome de Wolff-Parkinson-White. Arch Ma1 Coeur Vaiss i974;67:13-22. 2. Neuss H, Schlepper M, Spies HF. Double ventricular response to an atria1 extrasvstole in a natient with WPW syndrome type B. Eur J Cardio1”1974;2:175-9. 3. Wu D. Dual atrioventricular nodal pathways: a reappraisal. PACE 1982;5:72-89. 4. Lin FC, Yeh SJ, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. AM HEART J 1985;109:963-70. 5. Chang MS, Sung RJ, Tai TY, Lin SL, Liu Ph, Chang BN. Nodal and supraventricular tachycardia: an electrophysiologic study. J Am Co11 Cardiol 1983;2:894-903. 6. Brugada P, Vanagt EJ, Bar FWHM, Wellens HJJ. Incessant reciprocating atrioventricular tachycardia. Factors playing a role in the mechanism of the arrhythmia. PACE 1980;3:670-7. 7. Lin FC, Yeh SJ, Wu D. Double atria1 responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways. J Am Co11 Cardiol 1985;5:168-75.
Torsade de pointes induced by astemizole in a patient with prolongation of the QT interval Hideta Sakemi, MD, and Bruce VanNatta, Long Beach, Calif.
MD
From the Division of Cardiology, Long Beach Memorial Medical Center. Reprint requests: Bruce VanNatta, MD, 2699 Atlantic Ave., Long Beach, CA 90806. AM HEART J 1993;125:1436-1438. Copyright “’ 1993 by Mosby-Year Book, Inc. 000%8703/93/$1,00 + .I0 4/4/44909
Heart
my 1993 Journal
Administration 01 several antiarrhythmic agents. phe nothiazines. and tricyclic antidepressants has been associ. ated with t,he development of electrocardiographic QT interval prolongation and resultant torsade de pointes type tachyarrhythmias.’ Similar problems have been described with overdoses of nonsedating HI-receptor antagonists.‘, ’ We report a case of torsade de pointes occurring in a patient with possible congenital or mitral valve prolapse-associated prolongation of the QT interval who was receiving a therapeutic dose of astemizole. A 31-year-old woman was admitted in March 1991 to our hospital because of a second syncopal episode within 2 days. The patient was well until 1 day before admission, when she had a witnessed syncopal episode without warning. No seizure activity was noted. She regained consciousness within 1 minute without incontinence or a postictal syndrome. She was taken to another hospital where a complete blood cell count (CBC), serum glucose, and electrolyte levels were normal, but an electrocardiogram (ECG) was not taken. She was released from that institution but suffered another witnessed syncopal attack lasting about 30 seconds the following night. She was brought to our hospital, where the ECG was normal except for a prolonged QT, interval of 632 msec. The patient was an ex-hospital technician and had had an ECG taken in 1986, showing a QT, interval of 546 msec (Fig. 1). She denied any previous history of cardiac diseases, syncopal episodes, palpitations, shortness of breat,h, or exercise intolerance. There was no past history of liver disease. ‘The patient drank alcohol socially but denied smoking or use of illicit drugs. She had been taking astemizole (Hismanal, Janssen Pharmacentica, Piscataway, NJ.), 10 mg daily, for 6 weeks before admission. The medication had been prescribed for prophylaxis of her food-induced urticaria. The last dose was taken in the morning on the day of admission. She denied taking more than 10 mg a day or taking any other medication while she was taking astemizole. The patient’s father had mitral valve prolapse but no electrocardiographic abnormalities. Her mother had no electrocardiographic abnormalities. The patient had one healthy sister who never had an ECG taken. Her uncle had died of an acute myocardial infarction at the age of 51. Her cousin, a heavy drug and alcohol abuser, had a sudden death at the age of 29. There was no consanguinity bet.ween the patient’s parents. On admission, the temperature was 37.3’ C (99.2’ F), the respiratory rate was 18, the pulse rate was 60 beats/min, and blood pressure was 96/76 mm Hg without an orthostatic drop. Cardiac examination revealed a II/VI systolic murmur at the apex with a midsystolic click. No other cardiovascular or respiratory abnormalities were appreciated. Her hearing was normal. Laboratory tests on admission showed a normal CBC and normal serum electrolytes, with a potassium level of 3.7 mg/dl (normal 3.3 to 5.0 mg/dl), a calcium level of 9.0 mg/dl (normal 9.0 to 10.5 mg/dl) and a magnesium level of 2.1 mg/dl (normal 1.6 to 3.0 mg/dl). The serum concentration of astemizole or its hydroxylated metabolites was not determined. Echocardiography revealed normal left ventricular size and systolic function and probable mitral valve prolapse, with trace mitral regurgitation. The left atria1 dimension was 40 mm. About 12 hours after admission, the patient developed another syncopal attack.
Volume 125, Number 5, Part 1 American Heart Journal
Sakemi and VanNatta
1437
. i i
*
i.
1.
Fig. 1. ECG rhythm strip made in 1986,5 years before admission.The QT, interval is 546 msec.
Torsade de pointes-type ventricular tachyarrhythmia was documented on the heart monitor (Fig. 2). The QT, interval immediately before the ventricular tachycardia was680 msec.The patient wastreated with a lidocainedrip and oral metoprolol for 2 days in the intensive care unit. The signal-averagedECG while the patient was receiving metoprolol was negative for delayed potentials. The patient had no recurrence of ventricular tachycardia and was dischargedhomeon the sixth hospital day taking oral magnesiumsupplementation. She wasadvisednot to take astemizole in the future. The patient’s follow-up ECG taken 4 days after dischargeshowed a QT, interval of 577 msec. The patient experienced no recurrence of syncopeor palpitations. A follow-up ECG taken 5 months after discharge revealed a QT, interval of 509 msec(Fig. 3). Astemizole (Hismanal) is one of the nonsedatingHi-receptor antagonists,having virtually no anticholinergic side effects and no central nervous systempenetration. It is almost exclusively metabolized in the liver and excreted in the feces.The plasmahalf-life of astemizoleand its active metabolite following long-term administration is biphasic with an initial Ti/s of 7 to 9 days and a terminal Ti/s of 17 days. It has beenin clinical usein the United Kingdom for about a decade,and hasbeenavailable in the United States sincelate 1988.Astemizole hasbeenreported to causeprolongation of the QT interval and torsade de pointes when usedin excess23 3 The first suchcasewasreported in 1986. Terfenadine, the other nonsedating Hi-receptor antagonist, has alsobeen reported to causethe sameabnormality when an overdoseis taken4 or when taken with ketoconazole, a well-known inhibitor of the P-450 metabolic pathwayin the liver. The exact physiologicmechanismby which these nonsedating Hi-blockers cause prolongation of the QT interval is still unknown, although stimulation of the histamine receptors is known to increaseintracellular cy-
Fig. 2. ECG rhythm strip made 12 hours after admission. A torsadesde pointes-type ventricular tachyarrhythmia is documented.
clic adenosinemonophosphate(AMP) of cardiac muscles and to exert inotropic and chronotropic effects. On the other hand, prolongation of the QT intervals in generalcan be either congenital, asin the Romano-.Wardsyndromeand Jervell-Lange-Nielsen syndrome, or acquired. Conditions associatedwith acquired QT prolongation are ischemic
1438
Greenberg,
Robinson,
and Birrer
American
May 1993 Heart Journal
Fig. 3. Folio, f-up ECG rhythm strip made 5 months after discharge.The QT, interval is 509 msec.
heart disease, cardiomyopathy, postresuscitation state, electrolyte disorders,hypothyroidism, complete atrioventricular (AV) block, mitral valve prolapse, hypothermia. subarachnoid hemorrhage, postneurosurgical state, and the administration of various drugssuchasantiarrhythmic agents,phenothiazines, and tricyclic antidepressants.’ Our casehad documented QT prolongation in 1986and continued to have the sameabnormality asof August 1991. Her family history and normal hearing however did not suggestan inherited disorder, although incomplete penetrance could not be excluded. The patient’s father had mitral valve prolapse, and the patient wasfound to have mitral valve prolapse by echocardiography during this admission.Since conflicting studiesexist asto the association between mitral valve prolapseand prolongation of the QT interval,5a6it is difficult to determine at this time whether QT prolongation in our caseis congenital, with weak penetration among family members, or acquired, associated with mitral valve prolapse.Regardlessof the cause,it does appearthat our patient’s baselineQT interval prolongation may have made her more susceptibleto the development of torsade de pointes in the presenceof therapeutic doses of astemizole.In light of our caseand a review of the literature, we would recommendcaution in the useof astemizole in patients with known prolongation of the QT interval. REFERENCES
SurawiczB, Knoebel SB. Long QT: good, bad or indifferent. J Am Co11 Cardiol 1984;4:398-413. 2. Craft TM. Torsade de pointes after astemizole overdose. Br Med J 1986;292:660. 3. Bishop RO, Gaudry PL. Prolonged Q-T interval following astemizole overdose. Arch Emerg Med 1989;6:63-5. 4. Monahan BP, Ferguson CL, Kilieavy ES, Kellerman 53. Torsade de pointes occurring in association with terfenadine use. JAMA 1990;264:2788-90. ,5. Cowan MD, Fye WB. Prevalence of QT, prolongation in women with mitral valve prolapse. Am J Cardiol1989;63:133-4. 6. Drory Y, Fisman EZ, Pines A, Lloyd BK, Troy J, Cantilena LR. Exercise response in young woman with mitral valve pro1.
lapse.
Chest
1989;96:1076-80.
Atrial fibrillation after intravenous administration of gasoline Michael David Greenberg, MD, Timothy Robinson,DO, and Richard Birrer, MD Jamaica, N.Y.
Toxicity from commercialgasolineingestion is well recognized, both as a result of intentional and accidental ingesti0n.l
The vast majority
of reported
cases involve oral in-
gestion or inhalation. We report the caseof a young intravenous drug user, who self-injected between 5 and 15 cm3 of commercial gasoline. A 3%year-old man presented to the emergencydepartment with complaints of nausea, weakness, and palpitations. The symptoms appeared suddenly approximately 30 minutes before his arrival in the emergency department.
The patient admitted to having intentionally self-injected himself with between 5 and 15 cm3 of “93 octane” gasoline, which he obtained at a commercial gas station 1 hour before arrival at the hospital. His medical history was unre-
markable and the patient denied any history of cardiovascular disease. He also denied any previous “palpitations“ or history or “irregular heart beat.” There was no surgical history, and he was taking no prescription medications. The patient admitted to heavy tobacco use, although he denied alcohol use or use of cocaine within the previous week. Physical examination revealed a young man in no
acute distress.Vital signswere blood pressure,138/92mm Hg; pulse, 120 to 140 beats/min and irregular; respirations, From Emergency Medical Services Institute, Catholic Medical Brooklyn & Queens, Department of Emergency Medicine.
Center
Reprint Institute, Jamaica,
Services 153rd St..
requests: Michael Catholic Medical NY 11432.
AM HEART
D. Greenberg, MD, Center of Brooklyn
.J 1993;125:1438-1439.
Copyright 199:i 0002-8703/93/$1.00
by Mosby-.Year Houk, + .10 414144912
Inc.
Emergency & Queens,
Medical 88-25
of