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Multiform accelerated idioventricular rhythm in acute myocardial infarction
J. ELECTROCARDIOLOGY 11 (2), 1978, 197-200
Multiform Accelerated Idioventricular Rhythm in Acute Myocardial Infarction BY SAMUEL SCLAROVSKY, M.D., BORIS STRASBERG, M.D. AND JACOB AGMON, M.D.
60/min, blood pressure of 110/70, with no signs of heart failure. Serum cardiac enzymes (SGOT & LDH) demonstrated a curve typical for acute myocardial infarction. The admission electrocardiogram (ECG) was compatible with an acute postero-inferior myocardial infarction. Several hours l a t e r AIVR was observed. Figure 1 represents four non-continuous strips of the evolution of a paroxysm of AIVR recorded in lead V1. In the first strip the first two beats are from sinus origin and conducted with a prolonged P-R interval; the third beat is a fusion beat (FB) between the normal sinus impulse and the ectopic v e n t r i c u l a r r h y t h m (AIVR). This focus (F-l) has a regular rate of 81/min and shows a positive morphology s i m i l a r to r i g h t bundle b r a n c h block (RBBB). The 12th beat in the same strip is again a FB between the ectopic focus (F-l) and probably a second ectopic v e n t r i c u l a r focus (F-2) showing a left bundle branch block (LBBB) pattern. In strips 2 and 3 both ectopic foci take command of the heart rate intermittently with fusion beats between them (FB 1+ 2). The fourth strip shows the termination of the a r r h y t h m i a with a fusion beat of the second focus with LBBB pattern (F-2) and the normal sinus r h y t h m . The presence of QRS complexes with both a RBBB and LBBB morphology is of interest since t h e y represent ventricular ectopic foci of left and right ventricular origin respectively. 4'5 This phenomenon may be explained by infarction of both v e n t r i c l e s caused by the p o s t e r o - i n f e r i o r myocardial infarction. ~
SUMMARY The presence of accelerated idioventricular rhythm (AIVR) in its multiform variant in two patients with acute myocardial infarction is described. No difference was noted in the clinical evolution of this arrhythmia and the more commonly observed unifocal AIVR. Accelerated i d i o v e n t r i c u l a r r h y t h m is a well recognized a r r h y t h m i a of ectopic ventricu l a r origin a p p e a r i n g in different clinical states, 1 including acute myocardial infarction where it occurs fairly frequently during the first 24 hours. 2 Most of the reported cases of AIVR have shown a similar QRS configuration suggesting a unifocal origin. Multiform AIVR has also been described in three patients with severe congestive h e a r t failure and digitalis toxicity. 3 This report describes two cases of multiform A I V R o c c u r r i n g in p a t i e n t s w i t h a c u t e myocardial infarction.
CASE REPORTS Case I. A 60 year old m a n was admitted to our Intensive Coronary Care Unit (ICCU) following severe chest pain during the two hours prior to admission. Past history was unremarkable and he was not receiving drugs. Physical examination revealed a patient in good general condition with a normal pulse
Case II. A 53 year old man was admitted to our ICCU following a history of chest pain lasting four hours prior to admission. Past history was unremarkable. Pulse was 75/min and blood pressure 110/80. The ECG showed a pattern of acute anterior wall myocardial infarction. Cardiac enzymes (SGOT & LDH) curve was typical for acute myocardial infarction. Four hours after admission the presence of AIVR was recorded. Figure 2 shows four non-continuous strips of this a r r h y t h m i a (monitor lead). In the first strip, the first two beats are from sinus origin
From the Israel and Ione Massada Center for Heart Diseases, Intensive Coronary Care Unit and Institute for Cardiac Rehabilitation, BeilinsonMedicalCenter, Petah Tikva, Israel. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. 1734 solelyto indicate this fact. Reprint requests to: J. Agmon, M.D., The Massada Center for Heart Diseases, Beilinson Medical Center, Petah Tikva, Israel. 197
198
SCLAROVSKY ET AL
a-v v 780
780
740
r/40
L
740
740
L
740
-
L
J
a-v v -
720
-
720
-
720
~
700
700
700
700
70O
700
700
700
70O
Fig. 1. Four non-continuous strips of the evolution of AIVR in Case I (see text for explanation). NSR = normal sinus rhythm; FB -- fusion beat; F-1 = AIVR with RBBB pattern; F-2 = AIVR with LBBB pattern; FB 1+2 = fusion beats between F-1 and F-2. Numbers under schematic diagram = R-R intervals in msec.
followed by an AIVR (F1) with a frequency of 75/min. This r h y t h m is interrupted by an extrasystole (E) and followed by two ventricular complexes with different QRS morphology (F2). The following beat is a FB between these two QRS morphologies (F1 + F2). The second strip shows the termination and genesis of a paroxysm of AIVR with positive QRS morphology (F2) with a frequency of 65/min. The t h i r d s t r i p s h o w s t h e t e r m i n a t i o n of a paroxysm of AIVR with positive QRS morphology (F2) with a FB between the negative ectopic focus (F1) and either the sinus r h y t h m or the positive ectopic focus (F2); the following two beats are from sinus origin and the 6th beat is a FB between the sinus r h y t h m and the AIVR with negative QRS morphology (F0. In the 4th strip the first four beats are an AIVR with positive QRS morphology (F2) followed by two sinus beats, the next beat (7th) shows the same morphology as the first four and is followed by a FB between the previous positive QRS morphology (F2) and the negative QRS morphology (F0.
DISCUSSION The literature referring to AIVR is still confusing since different terminology was used to describe it. Common terms used are idiovent r i c u l a r t a c h y c a r d i a , ~ slow v e n t r i c u l a r
tachycardia, s accelerated isorhythmic vent r i c u l a r r h y t h m , z and accelerated idiovent r i c u l a r r h y t h m (AIVR) 9, adopted in this report. The ventricular origin of this r h y t h m has been proved by His bundle technique recording, z~ Abnormal automaticity in the Purkinje fibers in acute myocardial infarction is considered the responsible mechanism. Until recent years this r h y t h m has been accepted as a benign a r r h y t h m i a 9 with generally no need for treatment. Later reports have cont r a d i c t e d the previous observations since a high percentage of cases have shown an association between AIVR and fast ventricular tachycardia, zz,,2 The presence of multiform ventricular ectopic r h y t h m with the characteristics of vent r i c u l a r parasystole h a s been reported by R o e l a n d t 13 a n d E 1 - S h e r i f . ~4 M u l t i f o r m r h y t h m with AIVR characteristics has been described by Rothfeld,3 who reported this arr h y t h m i a in three cases with severe heart failure and digitalis toxicity. Our cases resemble Rothfeld's report, showing two different ventricular QRS morphologies with the presence of fusion beats between the sinus r h y t h m and both QRS morphologies. In addition, fusion beats between these two different QRS morphologies were recorded favoring the existence of two different ventricular ectopic foci appearing in the infarcted area during J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978
MULTIFORM AIVR
FI
t
760
920
860
,
F2
9
800
199
l
~0
800
800 480 E 880
840
880 FB 800
800
800 4
F2
9~
920
9~
920
1
740 r2
' I
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f Jl
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T Jl I
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i,F~ 9
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Fi
.
A J
880
880
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760
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980
880 feel 880
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Fig. 2. Four non-continuous strips of the evolution of AIVR in Case II (see text for explanation). E = extrasystole; FB = fusion beat; F~ = AIVR with negative QRS morphology; F2 = AIVR with positive QRS morphology; Numbers under the electrocardiogram recording = R-R intervals in msec.
a c u t e m y o c a r d i a l infarction. As s t r e s s e d by Rothfeld, 3 this a r r h y t h m i a did not fulfill the c r i t e r i a for a p a r a s y s t o l i c origin. 1~ In c o n t r a s t to Rothfeld's observations, however, we did not find a n y o m i n o u s prognosis for this arr h y t h m i a since it lasted for short periods, was self-limited and t h e clinical evolution of both cases was benign, as described for unifocal AIVR2
4. LIeMAN, B S AND MASSIE, E: In Clinical Scalar
5. 6.
7. Acknowledgement: We gratefully acknowledge the secretarial assistance of Mrs. Cecile Strasberg.
8.
9.
REFERENCES 1. MASSUMI, R A AND ALI, N: A c c e l e r a t e d isorhythmic ventricular rhythms. Am J Cardiol 26:170, 1970 2. BIGGER,J T, JR, DRESDALE,R J, HEISSENBUTTEL, R H, WELD, F M AND WIT, A L: Ventricular arrhythmias in ischemic heart disease: mechanism, prevalence, significance, and management. Prog Cardiovasc Dis 19:255, 1977 3. ROTHFELD, E L AND ZUCKER, I R: Multiform accelerated idioventricular rhythm. Angiology 25:457, 1974 J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978
10.
11.
12.
E l e c t r o c a r d i o g r a p h y , 5th ed. Year Book, Chicago, 1965, Chap 13, p 395 STOCK, J P P AND WILLIAMS, D O: The Diagnosis and Treatment of Cardiac Arrhythmias. Butterworths, London, 1974, Chap 6, p 72 SCHAMROTH,L: The Electrocardiology of Coronary Artery Disease, Blackwell Scientific Publications, Oxford and Edinburgh, 1975, Chap 17, p 176 SCHAMROTH,L: Idioventricular tachycardia. J Electrocardiol 1:205, 1968 CASTELLANOS, A, JR, LEMBERG, L AND ARCEBAL, A G: Mechanism of slow ventricular tachycardias in acute myocardial infarction. Dis Chest 51:520, 1967 MARRIOTT, H J L: Practical Electrocardiography. Williams & Wilkins, Baltimore, 1972, Chap 10, p 116 GALLAGHER,J J, DAMATO,A N AND LAU, S H: Electrophysiological studies during accelerated i d i o v e n t r i c u l a r r h y t h m . Circulation 44:671, 1971 DE SOYZA, N, BISSETT, J K, KANE, J J, MURPHY, M L AND DOHERTY, J E: Association of a c c e l e r a t e d i d i o v e n t r i c u l a r r h y t h m and paroxysmal ventricular tachycardia in acute myocardial infarction. Am J Cardiol 34:667, 1974 LICHSTEIN,E, RIBAS-MENECLIER,C, GUPTA, P K AND CHADDA,K D: Incidence and description
200
SCLAROVSKY ET AL
of accelerated ventricular rhythm complicating acute myocardial infarction. Am J Med 58:192, 1975 13. ROELANDT, J, POOL, J AND SCHAMROTH, L: Ventricular parasystole. J Electrocardiol 5:86, 1972
14. EL-SHERIF, N AND SAMET P: Multiform ventricular ectopic rhythm; evidence for multiple parasystolic activity. Circulation 51:492, 1975 15. SCHAMROTH, L: The Disorders of Cardiac Rhythm. Blackwell Scientific Publications, Oxford and Edinburgh, 1971, Chap 22, p 95
J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978
Multiform Accelerated Idioventricular Rhythm in Acute Myocardial Infarction BY SAMUEL SCLAROVSKY, M.D., BORIS STRASBERG, M.D. AND JACOB AGMON, M.D.
60/min, blood pressure of 110/70, with no signs of heart failure. Serum cardiac enzymes (SGOT & LDH) demonstrated a curve typical for acute myocardial infarction. The admission electrocardiogram (ECG) was compatible with an acute postero-inferior myocardial infarction. Several hours l a t e r AIVR was observed. Figure 1 represents four non-continuous strips of the evolution of a paroxysm of AIVR recorded in lead V1. In the first strip the first two beats are from sinus origin and conducted with a prolonged P-R interval; the third beat is a fusion beat (FB) between the normal sinus impulse and the ectopic v e n t r i c u l a r r h y t h m (AIVR). This focus (F-l) has a regular rate of 81/min and shows a positive morphology s i m i l a r to r i g h t bundle b r a n c h block (RBBB). The 12th beat in the same strip is again a FB between the ectopic focus (F-l) and probably a second ectopic v e n t r i c u l a r focus (F-2) showing a left bundle branch block (LBBB) pattern. In strips 2 and 3 both ectopic foci take command of the heart rate intermittently with fusion beats between them (FB 1+ 2). The fourth strip shows the termination of the a r r h y t h m i a with a fusion beat of the second focus with LBBB pattern (F-2) and the normal sinus r h y t h m . The presence of QRS complexes with both a RBBB and LBBB morphology is of interest since t h e y represent ventricular ectopic foci of left and right ventricular origin respectively. 4'5 This phenomenon may be explained by infarction of both v e n t r i c l e s caused by the p o s t e r o - i n f e r i o r myocardial infarction. ~
SUMMARY The presence of accelerated idioventricular rhythm (AIVR) in its multiform variant in two patients with acute myocardial infarction is described. No difference was noted in the clinical evolution of this arrhythmia and the more commonly observed unifocal AIVR. Accelerated i d i o v e n t r i c u l a r r h y t h m is a well recognized a r r h y t h m i a of ectopic ventricu l a r origin a p p e a r i n g in different clinical states, 1 including acute myocardial infarction where it occurs fairly frequently during the first 24 hours. 2 Most of the reported cases of AIVR have shown a similar QRS configuration suggesting a unifocal origin. Multiform AIVR has also been described in three patients with severe congestive h e a r t failure and digitalis toxicity. 3 This report describes two cases of multiform A I V R o c c u r r i n g in p a t i e n t s w i t h a c u t e myocardial infarction.
CASE REPORTS Case I. A 60 year old m a n was admitted to our Intensive Coronary Care Unit (ICCU) following severe chest pain during the two hours prior to admission. Past history was unremarkable and he was not receiving drugs. Physical examination revealed a patient in good general condition with a normal pulse
Case II. A 53 year old man was admitted to our ICCU following a history of chest pain lasting four hours prior to admission. Past history was unremarkable. Pulse was 75/min and blood pressure 110/80. The ECG showed a pattern of acute anterior wall myocardial infarction. Cardiac enzymes (SGOT & LDH) curve was typical for acute myocardial infarction. Four hours after admission the presence of AIVR was recorded. Figure 2 shows four non-continuous strips of this a r r h y t h m i a (monitor lead). In the first strip, the first two beats are from sinus origin
From the Israel and Ione Massada Center for Heart Diseases, Intensive Coronary Care Unit and Institute for Cardiac Rehabilitation, BeilinsonMedicalCenter, Petah Tikva, Israel. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. 1734 solelyto indicate this fact. Reprint requests to: J. Agmon, M.D., The Massada Center for Heart Diseases, Beilinson Medical Center, Petah Tikva, Israel. 197
198
SCLAROVSKY ET AL
a-v v 780
780
740
r/40
L
740
740
L
740
-
L
J
a-v v -
720
-
720
-
720
~
700
700
700
700
70O
700
700
700
70O
Fig. 1. Four non-continuous strips of the evolution of AIVR in Case I (see text for explanation). NSR = normal sinus rhythm; FB -- fusion beat; F-1 = AIVR with RBBB pattern; F-2 = AIVR with LBBB pattern; FB 1+2 = fusion beats between F-1 and F-2. Numbers under schematic diagram = R-R intervals in msec.
followed by an AIVR (F1) with a frequency of 75/min. This r h y t h m is interrupted by an extrasystole (E) and followed by two ventricular complexes with different QRS morphology (F2). The following beat is a FB between these two QRS morphologies (F1 + F2). The second strip shows the termination and genesis of a paroxysm of AIVR with positive QRS morphology (F2) with a frequency of 65/min. The t h i r d s t r i p s h o w s t h e t e r m i n a t i o n of a paroxysm of AIVR with positive QRS morphology (F2) with a FB between the negative ectopic focus (F1) and either the sinus r h y t h m or the positive ectopic focus (F2); the following two beats are from sinus origin and the 6th beat is a FB between the sinus r h y t h m and the AIVR with negative QRS morphology (F0. In the 4th strip the first four beats are an AIVR with positive QRS morphology (F2) followed by two sinus beats, the next beat (7th) shows the same morphology as the first four and is followed by a FB between the previous positive QRS morphology (F2) and the negative QRS morphology (F0.
DISCUSSION The literature referring to AIVR is still confusing since different terminology was used to describe it. Common terms used are idiovent r i c u l a r t a c h y c a r d i a , ~ slow v e n t r i c u l a r
tachycardia, s accelerated isorhythmic vent r i c u l a r r h y t h m , z and accelerated idiovent r i c u l a r r h y t h m (AIVR) 9, adopted in this report. The ventricular origin of this r h y t h m has been proved by His bundle technique recording, z~ Abnormal automaticity in the Purkinje fibers in acute myocardial infarction is considered the responsible mechanism. Until recent years this r h y t h m has been accepted as a benign a r r h y t h m i a 9 with generally no need for treatment. Later reports have cont r a d i c t e d the previous observations since a high percentage of cases have shown an association between AIVR and fast ventricular tachycardia, zz,,2 The presence of multiform ventricular ectopic r h y t h m with the characteristics of vent r i c u l a r parasystole h a s been reported by R o e l a n d t 13 a n d E 1 - S h e r i f . ~4 M u l t i f o r m r h y t h m with AIVR characteristics has been described by Rothfeld,3 who reported this arr h y t h m i a in three cases with severe heart failure and digitalis toxicity. Our cases resemble Rothfeld's report, showing two different ventricular QRS morphologies with the presence of fusion beats between the sinus r h y t h m and both QRS morphologies. In addition, fusion beats between these two different QRS morphologies were recorded favoring the existence of two different ventricular ectopic foci appearing in the infarcted area during J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978
MULTIFORM AIVR
FI
t
760
920
860
,
F2
9
800
199
l
~0
800
800 480 E 880
840
880 FB 800
800
800 4
F2
9~
920
9~
920
1
740 r2
' I
" r~
f Jl
_i
T
T Jl I
J
i,F~ 9
740
Fi
.
A J
880
880
880
760
820
980
880 feel 880
J
880
/
880
880
l
Fig. 2. Four non-continuous strips of the evolution of AIVR in Case II (see text for explanation). E = extrasystole; FB = fusion beat; F~ = AIVR with negative QRS morphology; F2 = AIVR with positive QRS morphology; Numbers under the electrocardiogram recording = R-R intervals in msec.
a c u t e m y o c a r d i a l infarction. As s t r e s s e d by Rothfeld, 3 this a r r h y t h m i a did not fulfill the c r i t e r i a for a p a r a s y s t o l i c origin. 1~ In c o n t r a s t to Rothfeld's observations, however, we did not find a n y o m i n o u s prognosis for this arr h y t h m i a since it lasted for short periods, was self-limited and t h e clinical evolution of both cases was benign, as described for unifocal AIVR2
4. LIeMAN, B S AND MASSIE, E: In Clinical Scalar
5. 6.
7. Acknowledgement: We gratefully acknowledge the secretarial assistance of Mrs. Cecile Strasberg.
8.
9.
REFERENCES 1. MASSUMI, R A AND ALI, N: A c c e l e r a t e d isorhythmic ventricular rhythms. Am J Cardiol 26:170, 1970 2. BIGGER,J T, JR, DRESDALE,R J, HEISSENBUTTEL, R H, WELD, F M AND WIT, A L: Ventricular arrhythmias in ischemic heart disease: mechanism, prevalence, significance, and management. Prog Cardiovasc Dis 19:255, 1977 3. ROTHFELD, E L AND ZUCKER, I R: Multiform accelerated idioventricular rhythm. Angiology 25:457, 1974 J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978
10.
11.
12.
E l e c t r o c a r d i o g r a p h y , 5th ed. Year Book, Chicago, 1965, Chap 13, p 395 STOCK, J P P AND WILLIAMS, D O: The Diagnosis and Treatment of Cardiac Arrhythmias. Butterworths, London, 1974, Chap 6, p 72 SCHAMROTH,L: The Electrocardiology of Coronary Artery Disease, Blackwell Scientific Publications, Oxford and Edinburgh, 1975, Chap 17, p 176 SCHAMROTH,L: Idioventricular tachycardia. J Electrocardiol 1:205, 1968 CASTELLANOS, A, JR, LEMBERG, L AND ARCEBAL, A G: Mechanism of slow ventricular tachycardias in acute myocardial infarction. Dis Chest 51:520, 1967 MARRIOTT, H J L: Practical Electrocardiography. Williams & Wilkins, Baltimore, 1972, Chap 10, p 116 GALLAGHER,J J, DAMATO,A N AND LAU, S H: Electrophysiological studies during accelerated i d i o v e n t r i c u l a r r h y t h m . Circulation 44:671, 1971 DE SOYZA, N, BISSETT, J K, KANE, J J, MURPHY, M L AND DOHERTY, J E: Association of a c c e l e r a t e d i d i o v e n t r i c u l a r r h y t h m and paroxysmal ventricular tachycardia in acute myocardial infarction. Am J Cardiol 34:667, 1974 LICHSTEIN,E, RIBAS-MENECLIER,C, GUPTA, P K AND CHADDA,K D: Incidence and description
200
SCLAROVSKY ET AL
of accelerated ventricular rhythm complicating acute myocardial infarction. Am J Med 58:192, 1975 13. ROELANDT, J, POOL, J AND SCHAMROTH, L: Ventricular parasystole. J Electrocardiol 5:86, 1972
14. EL-SHERIF, N AND SAMET P: Multiform ventricular ectopic rhythm; evidence for multiple parasystolic activity. Circulation 51:492, 1975 15. SCHAMROTH, L: The Disorders of Cardiac Rhythm. Blackwell Scientific Publications, Oxford and Edinburgh, 1971, Chap 22, p 95
J. ELECTROCARDIOLOGY, VOL. 11, NO. 2, 1978