Volume
Number
122
Brief Communications
5
0
-1 MAXIMUM
-2 ST
-3 SEGMENT
-4
-5
DEPRESSION
-6
-7 (mm)
Fig. 1. The maximum amount of ST segmentdepression present in the 12-leadelectrocardiogram during PSVT in 100 patients.
this study. Electrocardiograms were recorded at a paper speedof 25 mm/set and at a gain setting of 10 mm/mV. The magnitude of ST segmentdepressionwasmeasuredmanually in every lead to the nearestmillimeter, 80 msecafter the J point, using the TP segmentas a baseline.Intraobserver reproducibility was 98% and interobserver reproducibility between two observerswas97%. The data were analyzed using Student’s t test, chi square,and linear regressionanalysisand by analysisof covariance.ST segment depressionof 1 mm or more waspresent during PSVT in at least one lead in 89 of 100PSVTs. The meannumber of leads per electrocardiogram that demonstrated 1 mm or moreof ST segmentdepressionwas6.5 + 2. The maximum amount of ST segment depressionin the 100 PSVTs is shown in Fig. 1. ST segmentdepressionof 1 mm or more was present more often in leadsII, III, aVF, and V4 to Vs (68% to 84% ) than in the other leads(p < 0.01). The mean magnitude of ST segmentdepressionamongthe leadsthat demonstratedST segmentdepressionwas2.2 i 1 mm, and the mean maximum magnitude of ST segmentdepression for each PSVT was3.0 * 1.4 mm. There wasa significant direct correlation between the rate of PSVT and the number of leadsthat demonstrated rl mm of ST segmentdepression (r = 0.3, p < 0.01) and also with the maximum magnitude of ST segmentdepression(r = 0.44,p < 0.001). The meanrate of the 46 orthodromic tachycardias, 190 f 24 beats/min, wassignificantly greater than the mean rate of the 52 AV nodal reentrant tachycardias, 173 + 32 beats/ min (p < 0.01). The maximum amount of ST segmentdepressionin the orthodromic tachycardias, 3.2 & 1 mm, was significantly greater than in the AV nodal reentrant tachycardias, 2.6 f 1 mm (p < 0.05). However, after correcting for heart rate, there wasnot a significant difference in the amount of ST segmentdepressionbetween the two types
1487
of PSVT. Neither the number of leadsdemonstrating ~1 mm of ST segmentdepressionnor the meanor maximum magnitude of ST segmentdepressionwasrelated to the age of the patients, the presenceof structural heart disease,or the presenceof overt preexcitation during sinusrhythm. The results of this study demonstrate that ST segment depressionis quite commonduring PSVT, with 21 mm of ST segment depressionbeing present in approximately 90% of the 100 PSVTs in this series.Marked ST segment depressionof 4 mm or morewaspresentin 26% of patients. ST segmentdepressionwasfound to be a rate-related phenomenonthat wasindependent of patient ageand underlying heart disease.This is consistentwith the results of a prior study’ that demonstrated that ST segmentdepression during PSVT is a physiologic responsethat is unrelated to myocardial ischemia. Although ST segment depressionoccursto a greater degreein orthodromic tachycardia than in AV nodal reentrant tachycardia, this is accounted for by the higher mean rate of orthodromic tachycardia. In conclusion, ST segment depressionoccurs commonly during PSVT and is a rate-related phenomenon that provides no independent diagnostic information either regardingthe mechanismof the PSVT or the presence of underlying coronary artery disease. REFERENCES
1.
2.
Nelson SD, Kou WH, Anneeley T, de Buitleir M, Morady F. Significance of ST segment depression during paroxysmal supraventricular tachycardia. J Am Co11Cardiol 1988;12:383-7. Leitch J, Klein GJ, Yee R, Murdock C. Invasive electrophysiologic evaluation of patients with supraventricular tachycardia. In: Scheinman MM. ed. Cardioloev-.. clinics: Sunraventricular tachycardia. Vol 8. No. 3. Philadelphia: W. B. Saunders co, 1990:465-77.
An incessant form of junctional ectopic tachycardia in an adult responsive to a class 1C agent JamesR. Cook, MD, and Jonathan S. Steinberg, MD. New York, N.Y.
An incessantform of junctional ectopic tachycardia (JET) has been well described during early chi1dhood.l Also a distinct catecholamine-sensitiveparoxysmal JET hasbeen observed in adults. The adult form sharesmany features with the infant variety but in contrast is almost always paroxysmal, is associatedwith a distinctly more benign From the Division of Cardiology, Department of Medicine, Columbia-Presbyterian Medical Center. Supported in part by an Investigatorship from the American Heart Association, New York City Affiliate (Dr. Steinberg). Reprint requests: James R. Cook, MD, Division of Cardiology, Baystate Medical Center, 759 Chestnut St., Springfield, MA 01199. 4/4/31763
1488
Brief Communications
Fig.
American
November 1991 Heart Journal
1. Twelve-lead ECG representing narrow complex tachycardia with AV dissociation.
Fig. 2. Surface (I, aVF, VI) and intracardiac (high right atrium [HRA] and His bundle recording [HBE]) electrical recordingsobtained during tachycardia. Atria1 depolarization (A), His bundle potential (H), and ventricular depolarization (V) are labeled. Note that each ventricular depolarization is preceded by His potential.
course, and has an excellent responseto beta blocker therapyB2Herein we describea caseof incessantrapid JET in an adult, which was unresponsiveto beta blockers but respondedto a classIC agent, flecainide. The patient, a 19-year-old man, had had palpitations since age 16. The episodeswere exacerbated by exertion and tobacco use and were associatedwith fatigue and lightheadedness.Two years before the current presenta-
tion, he had beentreated with metoprolol but discontinued therapy because of fatigue. On March 8, 1990 he was admitted to a hospital with profound hypotension and near-syncope.A 12-leadECG revealed an irregular narrow complex tachycardia with a ventricular rate varying between 170 and 220 beats/min and atrioventricular (AV) dissociation (Fig. 1). The blood pressurewasbarely palpable and the patient was in obvious distress. Results of
Volume Number
122 5
physical examination showed Cannon “A” waves and an intermittent third heart sound. He received multiple doses of verapamil, propranolol, esmolol, and digoxin over the next several hours without demonstrable effect. Repeated trials of electrical cardioversion (50 to 400 joules direct current) were unsuccessful in terminating the tachycardia. The patient was transferred to the electrophysiology laboratory at Columbia-Presbyterian Medical Center. Intracardiac recordings were obtained from the high right atrium and the bundle of His (Fig. 2). The sinus rate was 64 beats/min, and a junctional tachycardia was also present with a rate of approximately 220 beats/min. Nearly complete AV dissociation was present, and each ventricular complex was preceded by a His bundle potential (Fig. 2). There was no retrograde atria1 activation. The HV interval remained constant (45 msec) whether the QRS complex was generated from the sinus node or from the junctional focus. The tachycardia was highly irregular. This irregularity was not entirely due to intermittent sinus capture but rather appeared to represent an intrinsic quality of the tachycardia. The rate of the tachycardia was unaffected by ‘7 mg, (0.1 mg/kg) of intravenous propranolol. Burst atria1 pacing at a variety of rates had inconsistent effects-at times accelerating and occasionally slowing the tachycardia. However, because of the irregular nature of the tachycardia neither effect was reproducible. Ventricular pacing had no effect on the tachycardia. We concluded that this was an incessant form of JET, likely of an automatic mechanism. The patient was started on a regimen of oral flecainide at a dose of 200 mg/day (100 mg twice a day), which was subsequently increased to 300 mglday (150 mg twice a day). After two dosesof flecainide the pulse stabilized between 90 and 100beatslmin with the ectopic focus remaining as the dominant rhythm. Frequent periods of sinusrhythm with ventricular capture werealsoevident on monitored strips. A flecainide level wasobtained and measured0.7 rg/ml. An exercisetolerance test wasperformed, and the patient exercisedfor 13minutes and 25 secondsof a Bruce protocol, attaining a maximum heart rate of 170 beats/min. Sinus rhythm was the sole rhythm noted throughout the exercise period. Echocardiography was done and results were interpreted asnormal. The patient wasdischargedon a regimenof flecainideand hasremained symptom free for 9 months with a pulse rate of approximately 90 to 100 beats/min. Rapid narrow complex tachycardias in adults most commonly result from reentrant circuits involving a bypass tract or within the AV node,However, analysisof the ECG from the patient previously describedreveals a distinctly irregular arrhythmia and obvious AV dissociation. These two characteristics exclude the incorporation of a bypass tract in a reentrant circuit and makeAV nodal reentry very unlikely. 4*5 Furthermore, the diagnosisof JET was confirmed by electrophysiologic criteria.2 Ruder et a1.2described five adult patients with automatic junctional tachycardias that were accelerated with infusion of isoproterenol and responsive to beta blocker therapy. The investigators surmisedthat the mechanismfor the arrhythmia wascatecholamine-enhancedautomaticity. Automatic
Brief Communications
1489
tachycardias are resistant to overdrive pacing, cardioversion,and frequently to drug therapy. This wasthe casewith our patient. Kuck et al3 studied three adult patients with JET (two with spontaneousJET and onewith an incessant variety) and treated them with classIC agents.They found that encainide or flecainide could effectively suppressthe arrhythmia in thosepatients with spontaneousJET. These investigators postulated that drug efficacy was based on depressionof automaticity in ectopic pacemakers,which has been shown experimentally.4 Interestingly the one adult patient with incessantJET did not tolerate an intravenousdoseof flecainide becauseof profound hypotension, and consequently a classIC agent was not prescribed for this patient. The few casesof JET describedin adults have been paroxysmal and mainly responsive to beta blocker therapy. This report is the first description of incessant JET in an adult successfullytreated with a classIC agent. Flecainide wassuccessfulbecauseit markedly reducedthe rate of dischargeof a presumed automatic focus. Persistence of rapid automatic rates with exit block wasunlikely given the normal AV conduction seenwith sinusbeatsbut could not be excluded. The slowerrates, more frequent sinus capture, and AV synchrony resulted in marked hemodynamic improvement. REFERENCES
1.
2.
3.
4.
5.
Garson A, Gillette PC. Junctional ectopic tachycardia in children: electrocardiography, electrophysiology and pharmacologic response. Am J Cardiol 1979;44:298. Ruder RA, Davis JC, Eldar M, Abbott JA, Griffin JC, Seger JJ, Scheinman MM. Clinical and electrophysiologic characterization of automatic junctional tachycardia in adults. Circulation 1986;78:930. Kuck HK, Kunze KP, Sluter M, Duckeck W. Encainide versus flecainide for chronic atria1 and junctional ectopic tachycardia. Am J Cardiol 1988;62:37L. Ko PT, Naccarelli GV, Gulamhusein S, Prystowsky EN, Zipes DP, Klein GJ. Atrioventricular dissociation during paroxysmal junctional tachycardia. PACE 1981;4:670. Bauernfeind RA, Wu D, Denes P, Rosen KM. Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia. Am J Cardiol 1978;42:499.
Pentamidine-induced
torsade
de pointes
Abraham Gonzalez, MD, Philip T. Sager, MD, Bisher Akil, MD, Shahbudin H. Rahimtoola, MB, FRCP, and Anil K. Bhandari, MD. Los Angeles, Calif. From the Division of Cardiology, Department of Medicine, LAC + USC Medical Center, University of Southern California School of Medicine, Los Angeles. Supported in part by a Grant (MO1 RR-43 GCRC, DRR, NIH) from the General Clinical Research Centera Program of the Division of Research Resources, National Institutes of Health. Reprint requests: Shahbudin H. Rahimtoola, MD, Division of Cardiology, USC School of Medicine, 2025 &ma1 Ave., Los Angeles, CA 90033. 414132463
Number
122
Brief Communications
5
0
-1 MAXIMUM
-2 ST
-3 SEGMENT
-4
-5
DEPRESSION
-6
-7 (mm)
Fig. 1. The maximum amount of ST segmentdepression present in the 12-leadelectrocardiogram during PSVT in 100 patients.
this study. Electrocardiograms were recorded at a paper speedof 25 mm/set and at a gain setting of 10 mm/mV. The magnitude of ST segmentdepressionwasmeasuredmanually in every lead to the nearestmillimeter, 80 msecafter the J point, using the TP segmentas a baseline.Intraobserver reproducibility was 98% and interobserver reproducibility between two observerswas97%. The data were analyzed using Student’s t test, chi square,and linear regressionanalysisand by analysisof covariance.ST segment depressionof 1 mm or more waspresent during PSVT in at least one lead in 89 of 100PSVTs. The meannumber of leads per electrocardiogram that demonstrated 1 mm or moreof ST segmentdepressionwas6.5 + 2. The maximum amount of ST segment depressionin the 100 PSVTs is shown in Fig. 1. ST segmentdepressionof 1 mm or more was present more often in leadsII, III, aVF, and V4 to Vs (68% to 84% ) than in the other leads(p < 0.01). The mean magnitude of ST segmentdepressionamongthe leadsthat demonstratedST segmentdepressionwas2.2 i 1 mm, and the mean maximum magnitude of ST segmentdepression for each PSVT was3.0 * 1.4 mm. There wasa significant direct correlation between the rate of PSVT and the number of leadsthat demonstrated rl mm of ST segmentdepression (r = 0.3, p < 0.01) and also with the maximum magnitude of ST segmentdepression(r = 0.44,p < 0.001). The meanrate of the 46 orthodromic tachycardias, 190 f 24 beats/min, wassignificantly greater than the mean rate of the 52 AV nodal reentrant tachycardias, 173 + 32 beats/ min (p < 0.01). The maximum amount of ST segmentdepressionin the orthodromic tachycardias, 3.2 & 1 mm, was significantly greater than in the AV nodal reentrant tachycardias, 2.6 f 1 mm (p < 0.05). However, after correcting for heart rate, there wasnot a significant difference in the amount of ST segmentdepressionbetween the two types
1487
of PSVT. Neither the number of leadsdemonstrating ~1 mm of ST segmentdepressionnor the meanor maximum magnitude of ST segmentdepressionwasrelated to the age of the patients, the presenceof structural heart disease,or the presenceof overt preexcitation during sinusrhythm. The results of this study demonstrate that ST segment depressionis quite commonduring PSVT, with 21 mm of ST segment depressionbeing present in approximately 90% of the 100 PSVTs in this series.Marked ST segment depressionof 4 mm or morewaspresentin 26% of patients. ST segmentdepressionwasfound to be a rate-related phenomenonthat wasindependent of patient ageand underlying heart disease.This is consistentwith the results of a prior study’ that demonstrated that ST segmentdepression during PSVT is a physiologic responsethat is unrelated to myocardial ischemia. Although ST segment depressionoccursto a greater degreein orthodromic tachycardia than in AV nodal reentrant tachycardia, this is accounted for by the higher mean rate of orthodromic tachycardia. In conclusion, ST segment depressionoccurs commonly during PSVT and is a rate-related phenomenon that provides no independent diagnostic information either regardingthe mechanismof the PSVT or the presence of underlying coronary artery disease. REFERENCES
1.
2.
Nelson SD, Kou WH, Anneeley T, de Buitleir M, Morady F. Significance of ST segment depression during paroxysmal supraventricular tachycardia. J Am Co11Cardiol 1988;12:383-7. Leitch J, Klein GJ, Yee R, Murdock C. Invasive electrophysiologic evaluation of patients with supraventricular tachycardia. In: Scheinman MM. ed. Cardioloev-.. clinics: Sunraventricular tachycardia. Vol 8. No. 3. Philadelphia: W. B. Saunders co, 1990:465-77.
An incessant form of junctional ectopic tachycardia in an adult responsive to a class 1C agent JamesR. Cook, MD, and Jonathan S. Steinberg, MD. New York, N.Y.
An incessantform of junctional ectopic tachycardia (JET) has been well described during early chi1dhood.l Also a distinct catecholamine-sensitiveparoxysmal JET hasbeen observed in adults. The adult form sharesmany features with the infant variety but in contrast is almost always paroxysmal, is associatedwith a distinctly more benign From the Division of Cardiology, Department of Medicine, Columbia-Presbyterian Medical Center. Supported in part by an Investigatorship from the American Heart Association, New York City Affiliate (Dr. Steinberg). Reprint requests: James R. Cook, MD, Division of Cardiology, Baystate Medical Center, 759 Chestnut St., Springfield, MA 01199. 4/4/31763
1488
Brief Communications
Fig.
American
November 1991 Heart Journal
1. Twelve-lead ECG representing narrow complex tachycardia with AV dissociation.
Fig. 2. Surface (I, aVF, VI) and intracardiac (high right atrium [HRA] and His bundle recording [HBE]) electrical recordingsobtained during tachycardia. Atria1 depolarization (A), His bundle potential (H), and ventricular depolarization (V) are labeled. Note that each ventricular depolarization is preceded by His potential.
course, and has an excellent responseto beta blocker therapyB2Herein we describea caseof incessantrapid JET in an adult, which was unresponsiveto beta blockers but respondedto a classIC agent, flecainide. The patient, a 19-year-old man, had had palpitations since age 16. The episodeswere exacerbated by exertion and tobacco use and were associatedwith fatigue and lightheadedness.Two years before the current presenta-
tion, he had beentreated with metoprolol but discontinued therapy because of fatigue. On March 8, 1990 he was admitted to a hospital with profound hypotension and near-syncope.A 12-leadECG revealed an irregular narrow complex tachycardia with a ventricular rate varying between 170 and 220 beats/min and atrioventricular (AV) dissociation (Fig. 1). The blood pressurewasbarely palpable and the patient was in obvious distress. Results of
Volume Number
122 5
physical examination showed Cannon “A” waves and an intermittent third heart sound. He received multiple doses of verapamil, propranolol, esmolol, and digoxin over the next several hours without demonstrable effect. Repeated trials of electrical cardioversion (50 to 400 joules direct current) were unsuccessful in terminating the tachycardia. The patient was transferred to the electrophysiology laboratory at Columbia-Presbyterian Medical Center. Intracardiac recordings were obtained from the high right atrium and the bundle of His (Fig. 2). The sinus rate was 64 beats/min, and a junctional tachycardia was also present with a rate of approximately 220 beats/min. Nearly complete AV dissociation was present, and each ventricular complex was preceded by a His bundle potential (Fig. 2). There was no retrograde atria1 activation. The HV interval remained constant (45 msec) whether the QRS complex was generated from the sinus node or from the junctional focus. The tachycardia was highly irregular. This irregularity was not entirely due to intermittent sinus capture but rather appeared to represent an intrinsic quality of the tachycardia. The rate of the tachycardia was unaffected by ‘7 mg, (0.1 mg/kg) of intravenous propranolol. Burst atria1 pacing at a variety of rates had inconsistent effects-at times accelerating and occasionally slowing the tachycardia. However, because of the irregular nature of the tachycardia neither effect was reproducible. Ventricular pacing had no effect on the tachycardia. We concluded that this was an incessant form of JET, likely of an automatic mechanism. The patient was started on a regimen of oral flecainide at a dose of 200 mg/day (100 mg twice a day), which was subsequently increased to 300 mglday (150 mg twice a day). After two dosesof flecainide the pulse stabilized between 90 and 100beatslmin with the ectopic focus remaining as the dominant rhythm. Frequent periods of sinusrhythm with ventricular capture werealsoevident on monitored strips. A flecainide level wasobtained and measured0.7 rg/ml. An exercisetolerance test wasperformed, and the patient exercisedfor 13minutes and 25 secondsof a Bruce protocol, attaining a maximum heart rate of 170 beats/min. Sinus rhythm was the sole rhythm noted throughout the exercise period. Echocardiography was done and results were interpreted asnormal. The patient wasdischargedon a regimenof flecainideand hasremained symptom free for 9 months with a pulse rate of approximately 90 to 100 beats/min. Rapid narrow complex tachycardias in adults most commonly result from reentrant circuits involving a bypass tract or within the AV node,However, analysisof the ECG from the patient previously describedreveals a distinctly irregular arrhythmia and obvious AV dissociation. These two characteristics exclude the incorporation of a bypass tract in a reentrant circuit and makeAV nodal reentry very unlikely. 4*5 Furthermore, the diagnosisof JET was confirmed by electrophysiologic criteria.2 Ruder et a1.2described five adult patients with automatic junctional tachycardias that were accelerated with infusion of isoproterenol and responsive to beta blocker therapy. The investigators surmisedthat the mechanismfor the arrhythmia wascatecholamine-enhancedautomaticity. Automatic
Brief Communications
1489
tachycardias are resistant to overdrive pacing, cardioversion,and frequently to drug therapy. This wasthe casewith our patient. Kuck et al3 studied three adult patients with JET (two with spontaneousJET and onewith an incessant variety) and treated them with classIC agents.They found that encainide or flecainide could effectively suppressthe arrhythmia in thosepatients with spontaneousJET. These investigators postulated that drug efficacy was based on depressionof automaticity in ectopic pacemakers,which has been shown experimentally.4 Interestingly the one adult patient with incessantJET did not tolerate an intravenousdoseof flecainide becauseof profound hypotension, and consequently a classIC agent was not prescribed for this patient. The few casesof JET describedin adults have been paroxysmal and mainly responsive to beta blocker therapy. This report is the first description of incessant JET in an adult successfullytreated with a classIC agent. Flecainide wassuccessfulbecauseit markedly reducedthe rate of dischargeof a presumed automatic focus. Persistence of rapid automatic rates with exit block wasunlikely given the normal AV conduction seenwith sinusbeatsbut could not be excluded. The slowerrates, more frequent sinus capture, and AV synchrony resulted in marked hemodynamic improvement. REFERENCES
1.
2.
3.
4.
5.
Garson A, Gillette PC. Junctional ectopic tachycardia in children: electrocardiography, electrophysiology and pharmacologic response. Am J Cardiol 1979;44:298. Ruder RA, Davis JC, Eldar M, Abbott JA, Griffin JC, Seger JJ, Scheinman MM. Clinical and electrophysiologic characterization of automatic junctional tachycardia in adults. Circulation 1986;78:930. Kuck HK, Kunze KP, Sluter M, Duckeck W. Encainide versus flecainide for chronic atria1 and junctional ectopic tachycardia. Am J Cardiol 1988;62:37L. Ko PT, Naccarelli GV, Gulamhusein S, Prystowsky EN, Zipes DP, Klein GJ. Atrioventricular dissociation during paroxysmal junctional tachycardia. PACE 1981;4:670. Bauernfeind RA, Wu D, Denes P, Rosen KM. Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia. Am J Cardiol 1978;42:499.
Pentamidine-induced
torsade
de pointes
Abraham Gonzalez, MD, Philip T. Sager, MD, Bisher Akil, MD, Shahbudin H. Rahimtoola, MB, FRCP, and Anil K. Bhandari, MD. Los Angeles, Calif. From the Division of Cardiology, Department of Medicine, LAC + USC Medical Center, University of Southern California School of Medicine, Los Angeles. Supported in part by a Grant (MO1 RR-43 GCRC, DRR, NIH) from the General Clinical Research Centera Program of the Division of Research Resources, National Institutes of Health. Reprint requests: Shahbudin H. Rahimtoola, MD, Division of Cardiology, USC School of Medicine, 2025 &ma1 Ave., Los Angeles, CA 90033. 414132463
