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Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction
as a Marker for MvocardialNecrosisand Reaerf;sion DuringThrombo&ticTherapyin Acute My&ardial Infarction ANTON P.M. GORGELS, MD, MARC A. VOS, MS, INGRID S. LETSCH, MD, ERIK A. VERSCHUUREN, MS, FRITS W.H.M. EIjiR, MD, JOHAN H.A. JANSSEN, MD, and HEIN J.J. WELLENS, MD
perfuskxt of the lefl anterior descendirrg branch showed meet configurations of AM? and with the least QRS wkfth. ReperfW~ of the circumflex branch never had a Ml bundle branch block-like configuration. AIVR from reperfusion of the r@ht coronary artery never had an inferior axfs. AIVR occurring durln9 per&tent ischemlc cheat pain is a marker for both myocardial necrosis and reperfMkm of the Infarct vessel. AM? starts wlth a I- coupling Interval and Is regular. The QRS configuration may be useful for the nonlnvaslve ktentlflcation of the infarct vessel.
The value of the accelerated kiloventr[cular rhythm (AIVR) as a marker for myocardlal necrosis and/or reperfuslon was prospectively studled In 87 patients admltted wlth pen&tent lschemk chest pain. All patients received streptoklnase. Necrosis was dlagnosed by new Q waves and an Increase In plasma enzymes. Reperfuslon was documented anglographically. Myocardial necmsls occurred in 72 patients and reperfualon In 70 patients, 58 of whom had myocardlal necroels. Of 27 patients with AlVR, 28 had both necmsls and reperfuslon (p
(Am J Cardiol 1988;61:231-235)
V
entricular tachycardia and fibrillation frequently occur during acute myocardial infarction and are a major cause of sudden cardiac death.* Ventricular rhythms with intermediate rates have also been described during acute myocardial infarction and in other disease states.2-20Until reentry, their pathophysiologic significance has been uncertain.3+6,7J1J4There has been much confusion about the terminology of these rhythms with rates from about 50 to 120 beats/ min. The term “accelerated idioventricular rhythm” (AIVR) as proposed by Marriott and Menendez2 is now generally accepted. For AIVR occurring in the
setting of acute myocardial infarction, a useful distinction has been madeI between AIVR in a restricted sense and slow ventricular tachycardia. AIVR is characterized by the following criteria: (1) the appearance of 23 successive ventricular beats with a rate between 50 and 120 beats/min and (21 an onset with a long coupling interval to the preceding sinus beat that frequently, but not always, terminates because the sinus rhythm is able to capture the ventricles. An example of such rhythm is shown in Figure 1. Slow ventricular tachycardias are defined by the following criteria: (1) a rate between 50 and 120 beats/ min, (2) a short coupling interval to the preceding sinus From the Department of Cardiology, Academic Hospital Maas- beat, (3) more irregularity and (4) frequent starts betricht, Maastricht, The Netherlands. Manuscript received June cause the rhythm stops abruptly. An example is shown 29, 1987;revised manuscript received September 18, 1987,ac- in Figure 2. We will use the term AIVR in the general cepted September 21,1987. sense to indicate all runs of ventricular ectopy beAddress for reprints: Anton P.M. Gorgels, MD, Academic tween 50 and 120 beats/min. Recently AIVR has been suggested to occur espeHospital Maastricht, Department of Cardiology, P.O. Box 1918, cially during the reperfusion phase of an acute myo6201BX Maastricht, The Netherlands. 231
232
ACCELERATED IDIOVENTFWJLAR RHYTHM
Coronary arteriography was performed 45 minutes after intravenous streptokinase and when chest pain and ST-segmentelevation persisted, the infarct artery was selectively perfused with 5,000 U/min during 50 minutes. Electrocardiograms were recorded on a simultaneous 6- or 12-channel electrocardiographic recorder (Siemens Elema). Samples of venous blood were obtained on admission and every 8 hours thereafter for determining plasma levels of creatinine phosMethods phokinase (upper value of normal 105 U/liter], serum Patients: Patients admitted to the coronary care unit glutamic oxaloacetic transferase (upper value of norbecause of ischemic chest pain were studied prospec- mal 40 U/liter) and lactic dehydrogenase (upper value tively when they fulfilled the following criteria: (11 of normal 400 U/liter] until the maximal plasma levels persistent chest pain was accompanied by ST-T seg were reached. Statistical analysis: Differences between means of ment changesindicating beginning of acute myocardial infarction; (2)streptokinase was administered intra- 2 groups were tested with the chi-square test and the venously or intracoronary within 3 hours after the unpaired t test. P values of
v2>
FIGURE 1. Simultaneous 124ead electrocardiogram of an acceierated idioventricuiar rhythm. Two runs of accelerated idioventricuiar rhythm are shown. Note the long coupling interval between the last sinus beat and the first QRS complex of accelerated idioventricuiar rhythm. The accelerated idioventricuiar rhythm is regular. The runs terminate because the sinus rhythm captures the ventricle. The infarct is located in the inferior wail. The accelerated ldioventricuiar rhythm also originates in that area.
FIGURE 2. Simultaneous B-lead electrocardiogram of a “slow ventricular tachycardia.” Note the short coupling interval, the irreguiarity and the abrupt cessation of ventricular rhythm.
February 1, 1988
TABLE I Divlslon of Patients According to the Presence of Myocardial Necrosis, Reperfuslon and Accelerated ldioventrlcular Rhythm (AIVR)
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 61
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TABLE II Characteristics of Patients With Necrosis and Reperfusion With and Without Accelerated ldioventricular Rhythm (AIVR)
Pts
With AIVR
Without AIVR
57f 10 23:3 12:14
58f 10 24~8 14:17
Necrosis Reperfusion AIVR + = with; - = without.
AIVR occurred in 27 patients, 26 of whom had both myocardial necrosis and reperfusion of the infarct artery. Therefore, in patients with both necrosis and reperfusion, AIVR was seen in 26 of 58 (46%], in contrast to 1 of 29 patients in whom neither necrosis nor reperfusion was present (p
Electrocardiographic characteristics of accelerated idioventricular rhythm: Rhythm: An example of AIVR is shown in Figure 1. It characteristically starts after a long pause resulting in a long interval between the last sinus beat and the first QRS complex of AIVR. AIVR is regular and terminates because the sinus rhythm captures the ventricle. The infarct is located in the inferior wall. The AIVR also originates in this area. The relation between the last QRS interval during sinus rhythm and the interval to the first QRS complex could be measured in 24 patients. Data of different AIVRs that started during regular sinus rhythm were analyzed (n = 43). The remaining AIVRs started after a premature beat or the one configuration changed into another one without interrupting sinus beats. A linear relation was found between the last sinus beat interval and the coupling interval between the sinus beat to AIVR (y = 0.91x + 84) [r = 0.91). The mean and standard deviation of the cycle lengths of AIVRs studied were measured from a maximum of 10 consecutive intervals during a single run of AIVR. The majority (50 episodes) had a cycle length between 600 and 800 ms. Of the remaining runs of AIVR, 20 were between 800 and 1,000 ms, 5 between 1,000 and 1,100 and 9 between 500 and 600. The stan-
Age b-4 Male/female Anterior/inferior infarct location Killip class 1 CPK maximum (U/liter) SGOT maximum (U/liter) Potassium (mmol/liter) Creatinine (~mollliter) Lidocaine AP rep time (hrs) Sinus rate (beatslmin)
4 f 1,363 i 160 f 0.51 f 23 16 3.45 f 1.30 79% 14
2,466 273 3.92 101
3 i 1,307 f 117 4~ 0.81 f 36 11 4.08 f 2.30 85i 13
2,142 201 3.72 105
AP = onset of chest pain: AP rep time = time from the start of chest pain to moment of reperfusion; CPK = creatinine phosphokinase; SGDT = serum glutanic oxaloacetic transferase.
dard deviations of the measured intervals were small: in 55 runs between 0 and 40 ms and in the remaining runs between 40 and 80. From these findings it can be concluded that the AIVR occurring during the reperfusion phase of acute myocardial infarction is generally a regular rhythm. Configuration of accelerated idioventricular rhythm: During the reperfusion phase of myocardial infarction, an AIVR with different configurations could be observed. These QRS configurations always suggested an origin in the infarcted and reperfused area. This is illustrated by the example in Figure 3. In that case reperfusion of a large obtuse marginal branch was obtained. A continuous AIVR was recorded during 18 minutes showing 8 different configurations, which changed gradually from a right’ bundle branch block-like pattern with intermediate axis, to a right bundle branch block-like pattern with right axis. The polarity of the QRS complex became completely inverted in leads I, aVL and V, through Vg. These electrocardiographic changes indicate that during reperfusion of the obtuse marginal branch, impulse formation initially started in the posterobasal part of the left ventricle and gradually changed to a more inferolateral location. Table III shows different aspects of the QRS configuration of AIVR in relation to the infarct artery. It was found that the greatest number of AIVR configurations per patient occurred in patiknts with reperfusion of the left anterior descending branch with a maximum of 8. Left and right bundle branch block-like patterns occurred during reperfusion of both the left anterior descending branch and the right coronary artery. In contrast restoration of flow through the circumflex branch only caused AIVR with a right bundle branch block morphology. The frontal axis could point in all directions in either circumflex or left anterior descending branch reperfusion. Right coronary artery reperfusion, however, caused only a superior axis. Concerning QRS width, lactic dehydrogenase reperfusion of the
234
ACCELERATED
IDIOVENTRICULAR
TABLE III Artery
RHYTHM
ORB Configuration
of Accelerated
AlVRlFl
ldioventrlcular
Configuration
Rhythm (AIVR) in Relation to Infarct
Electrical
QRS Width
artery
Rts
(no)
1 2 3 4 5 6 7 8 LBBB RBBB 0 to 90° 90 to 190° 0 to -90’
LAD LC Right
12 7 7
49 10 17
5 24 15
2 2 2 1 1 1
19 0 7
30 18 10
17 3
14 4
LAD = left anterior descending branch: LBBB = left bundle branch block-like branch; RBBB = right bundle branch block-like configuration.
left anterior descending branch induced AIVR with a less wide QRS compared with reperfusion of the circumflex and the right coronary artery (130vs 150ms, p
Discussion In the setting of acute ischemic heart disease the occurrence of ventricular arrhythmias, varying from premature beats and accelerated rhythms to ventricular tachycardia and fibrillation, is well known. Ac-
A
Axis
AIVR
Coronary
B I
3
-9Oto-180’
10 7 15 configuration:
8 4 2
W-4 131 f 25 148 f 23 150 f 20
LC = left circumflex
cording to studies before thrombolytic therapy for acute myocardial infarction was available, the incidence of AIVR varies between 8 and 46%. This figure is affected by the differences in accepted upper rate for AIVR. This arrhythmia has intrigued cardiologists for a long time in respect to its pathophysiology and, prognostic significance. For instance, AIVR has been considered to be a ventricular tachycardia with 2 or 3:1 exit block5J1J3g24 and also a marker for the risk of more severe ventricular arrhythmias.3*6*7JlJ4
4
5
6
7
8
avr
FtGURE 3. A, simultaneous 12-lead electrocardiograms from a patient with an Inferolateral infarction caused by an obtuse marglnal branch occlusion recorded during sfnus rhythm. 6, shows 8 different accelerated ldloventrlculai rhythms recorded during reperfuslon. The GRB configuration shows a right bundle branch block pattern with a gradual shift toward right axis devlatlon In the frontal plane and development of left lateral negativity In the horlrontal plane. This suggests that impulse formatlon started In the posterobasal part and gradually changed to an inferolateral location. This Is compatible with gradual reperfuslon of the myocardlum along the obtuse marginal branch. V, we8 not recorded in E, 4 through 8, to allow visualization of the maln stem of the left coronary artery during angiography.
February 1, 1988
Since the introduction of thrombolytic therapy, more insight has been gained in the pathophysiologic mechanism of AIVR. It was recognized that AIVR especially occurred during restoration of blood flow during acute myocardial infarction.16 This finding is supported by our study although the group of patients without reperfusion was small. Further, we found that the occurrence of an AIVR was always accompanied by an enzyme increase indicative of myocardial necrosis. Apparently, both reperfusion and necrosis are necessary to induce AIVR. This finding is of practical clinical importance. It may help to recognize reperfusion after administration of thrombolytic agents when coronary angiography is not performed. It might also be useful to diagnose spontaneous reperfusion when no thrombolytic agents are administered. The configuration of AIVR, although not highly specific, may be of help in the noninvasive identification of the infarct vessel. For instance multiple configurations and narrow QRS width point to the left anterior descending branch. A left bundle branch blocklike configuration virtually excludes the circumflex branch as the occluded artery: AIVR with an electrical axis between 0 and 180’ in the frontal plane makes the right coronary artery unlikely to be the infarct vessel, a finding in agreement with other studies.17 AIVR always started with a long coupling interval. This finding is of interest because it is in agreement with one of the criteria advanced for triggered activity based on delayed after-depolarizations as the underlying arrhythmogenic mechanism.25 In the isolated tissue preparation delayed after-depolarizations and triggered rhythms have been demonstrated during conditions mimicking reperfusion after an ischemic episode.26The possibility that AIVR is caused by triggered activity is not supported by our observation that AIVR was seen equally often in patients with and without the administration of lidocaine. Lidocaine is well known to suppress triggered activity induced by delayed after-depolarization.27 As previously noted, ventricular arrhythmias with intermediate rates have been divided into “accelerated idiov&tricular rhythms” in the restricted sense and “slow ventricular tachycardias.” Our study demonstrates that during the reperfusion phase of acute myocardial infarction especially, the accelerated idioventricular rhythm in the restricted sense is observed. In our (preliminary] experience “slow ventricular tachycardia” also occurs frequently during the first 24 hours of infarction but after the direct phase of reperfusion. The pathophysiologic significance of slow ventricular tachycardia is still a matter of investigation. No variables could be found to predict the all or none occurrence of AIVR in patients with reperfusion and myocardial necrosis (Table II). Although there was a trend for a higher enzyme increase to occur more often in the presence of AIVR, this relation did not achieve statistical significance. Indeed, we have observed that
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even very small infarcts could be accompanied by long-lasting sustained AIVR. Acknowledgment: J. Haenen is acknowledged for his assistance in collecting patient data and Arno Muytjens for his statistical advice.
References
1. Myerburg RS. Conde CA, Sung RJ, Mallon SM. Sheps DS, Appel R, Castellanes A. Prehospital cardiac arrest: early and long term clinical and electrophysiologic characteristics. In: Kulbertus HE, Wellens HJJ, eds. Sudden Death. Developments in Cardiovascular Medicine 4. The Hague: Martinus Nijhoff, 1980:219-231. 2. Marriott JCJL,Menendez MM. A-V dissociation revisited. Prog Cardiovasc Dis 1966;8:522-538. 3. Rothfeld EL, Zucker JR, Parsonnet V. Alinsonorin CA. Idioventricular rhythm in acute myocardial infarction. Circulation 1968;27:203-209. 4. Schamroth L. Idioventricular tachycardia. J Electrocardiol1968;1:205-212. 5. Castellanos A Jr, Lemberg L, Arcebal AG. Mechanisms of slow ventriculbr tachycardias in acute myocardial infarction. Dis Chest 1969:56:470-476. 6. Massumi RA, Ali N. Accelerated isorhythmic ventricular rhythms. Am J Cardiol 1970;26:170-185. 7. Norris RM. Mercer CI. Yeates SE. Idioventricular rhvthm comnficating . . acute myocarhial infarctyon. Br Heart J 1970;32:617-621.’ 8. Gallagher JJ, Damato AN, Lau SH. Electrophysiological studies during occeleroied i&oventricular rhythms. Circulation 1971:44:671-677. 9. Zipes DP, Fisch C. Accelerated ventricular rhythm. Arch Intern Med 1972;129:651-652.
10. Norris RM, Mercer CJ. Significance of idioventricular rhythms in acute myocardial infarction. Prog Cardiovasc Dis 1974;16:455-467. 11. de Soyza N, Bisset JK, Kane JJ, Murphy ML, Doherty JE. Association of accelerated idioventricular rhythm and paroxysmal ventricular tachycardia in acute myocardiaf infarction. Am J Cardiol 1974;34:667-670. 12. Basu D, Scheinman M. Sustained accelerated idioventricular rhythm. Am Heart J 1975;89:227-231. 13. Licbstein E, Ribas-Meneclier C. Gupta PK, Chadda KD. Incidence and descriotion of accelerated ventricular rh&hm comdicatinn . - acute mvocardiol infarciion. A’m r Med 1975;58:193-198. . 14. Talbot S. Greaves M. Association of ventricular extrasystoles and ventricular tachycordia with idioventricular rhythm. Br Heort J 1975;38:457-464, 15. Bigger JT Jr, Dresdale R], Heissenbuttel RH, Weld FM, Wit AL. Ventricufar arrhythmias in ischemic heart disease: mechanism, prevalence, significance and management. Prog Cardiovasc Dis 1977;19:255-300. 16. Goldberg S, Greenspan AJ. Urban PL, Muza B, Berger B, Walinsky P, Maroko PR. Reperfusion arrhythmia: a marker of restoration of anterograde flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart I 1983:105:26-32. 17. Sclarovsky S, Strasberg B, Fuchs J, Lewin RF, Arditi A, Klainman E, Kracoff OH, Agmon J. Multiform accelerated idioventriculor rhythm in acute myocardial infarction: electrocardiographic characteristics and response to verapamil. Am J Cardiol 1983x72:43-47. 18. Buckineham TA. Devine IE. Redd RM. Kennedv HL. Reperfusion orrhythmios &ring coronary &perfusion in man. Chest 1986;90:348-351. 19. Sclarovsky S, Strasberg B, Martonovich G, Agmon J. Ventricular rhythms with intermediate rates in acute myocordial infarction. Chest 1976;74:180182. 20. Wellens HJJ. The electrocardiogram in digitalis intoxication. In: Yu PN, Goodwin IF. eds. Progress in Cardiology-. 5. Philadelphia: Leo and Febiger, 1976:271-290.
-
21. Rentrop KP, Blanke H, Karsch KR. Effects of nonsurgical coronary reperfusion in the left ventricle in human subjects compared with conventional treatment. Am J Cardiol 1982;49:1-7. 22. Simoons ML, Serruys PW, vd Brand M, de Zwaan C, Blr FW, Res J, Verheugt FWA, Krause-XH. Remme WJ, Vermeer F, Lubsen J. Improved survival after early thrombolysis in acute myocardial infarction. Loncet 1985:2:578-582. 23. &moons ML, Serruys PW. vd Brand M, Res J, Verheugt FW, Krauss XH. Remme WJ. BBr FW, de Zwaan C, van der Laarse A, Vermeer F, Lubsen J. Thrombolvsis in acute myocardiol infarction: limitation of infarct size and improved.survivaf. JACK 1987;7:717-728. 24. Schamroth L. Genesis and evolution of ectopic ventricular rhythm. Br Heort J 1966;28:244-248. 25. Rosen MR. Fisch C, Hoffmann BF, Danilo P, Lovelace DF, Knoebel SB. Can adcelerated otrioventricular junctional escape rhythms be explained by delayed after-depolarizations? Am J Cardiol 1980;45:1272-1284. 26. Ferrier GR. Moffat MP, Lukas A. Possible mechanisms of ventricular arrhythmias elicited by ischemio followed by reperfusion. Circ Res 1985;56: 184-194. 27. Eisner DA, Lederer WJ. A cellular basis for lidocaine’s antiorrhythmic action. 1 Physiol 1979;295:25-26.
perfuskxt of the lefl anterior descendirrg branch showed meet configurations of AM? and with the least QRS wkfth. ReperfW~ of the circumflex branch never had a Ml bundle branch block-like configuration. AIVR from reperfusion of the r@ht coronary artery never had an inferior axfs. AIVR occurring durln9 per&tent ischemlc cheat pain is a marker for both myocardial necrosis and reperfMkm of the Infarct vessel. AM? starts wlth a I- coupling Interval and Is regular. The QRS configuration may be useful for the nonlnvaslve ktentlflcation of the infarct vessel.
The value of the accelerated kiloventr[cular rhythm (AIVR) as a marker for myocardlal necrosis and/or reperfuslon was prospectively studled In 87 patients admltted wlth pen&tent lschemk chest pain. All patients received streptoklnase. Necrosis was dlagnosed by new Q waves and an Increase In plasma enzymes. Reperfuslon was documented anglographically. Myocardial necmsls occurred in 72 patients and reperfualon In 70 patients, 58 of whom had myocardlal necroels. Of 27 patients with AlVR, 28 had both necmsls and reperfuslon (p
(Am J Cardiol 1988;61:231-235)
V
entricular tachycardia and fibrillation frequently occur during acute myocardial infarction and are a major cause of sudden cardiac death.* Ventricular rhythms with intermediate rates have also been described during acute myocardial infarction and in other disease states.2-20Until reentry, their pathophysiologic significance has been uncertain.3+6,7J1J4There has been much confusion about the terminology of these rhythms with rates from about 50 to 120 beats/ min. The term “accelerated idioventricular rhythm” (AIVR) as proposed by Marriott and Menendez2 is now generally accepted. For AIVR occurring in the
setting of acute myocardial infarction, a useful distinction has been madeI between AIVR in a restricted sense and slow ventricular tachycardia. AIVR is characterized by the following criteria: (1) the appearance of 23 successive ventricular beats with a rate between 50 and 120 beats/min and (21 an onset with a long coupling interval to the preceding sinus beat that frequently, but not always, terminates because the sinus rhythm is able to capture the ventricles. An example of such rhythm is shown in Figure 1. Slow ventricular tachycardias are defined by the following criteria: (1) a rate between 50 and 120 beats/ min, (2) a short coupling interval to the preceding sinus From the Department of Cardiology, Academic Hospital Maas- beat, (3) more irregularity and (4) frequent starts betricht, Maastricht, The Netherlands. Manuscript received June cause the rhythm stops abruptly. An example is shown 29, 1987;revised manuscript received September 18, 1987,ac- in Figure 2. We will use the term AIVR in the general cepted September 21,1987. sense to indicate all runs of ventricular ectopy beAddress for reprints: Anton P.M. Gorgels, MD, Academic tween 50 and 120 beats/min. Recently AIVR has been suggested to occur espeHospital Maastricht, Department of Cardiology, P.O. Box 1918, cially during the reperfusion phase of an acute myo6201BX Maastricht, The Netherlands. 231
232
ACCELERATED IDIOVENTFWJLAR RHYTHM
Coronary arteriography was performed 45 minutes after intravenous streptokinase and when chest pain and ST-segmentelevation persisted, the infarct artery was selectively perfused with 5,000 U/min during 50 minutes. Electrocardiograms were recorded on a simultaneous 6- or 12-channel electrocardiographic recorder (Siemens Elema). Samples of venous blood were obtained on admission and every 8 hours thereafter for determining plasma levels of creatinine phosMethods phokinase (upper value of normal 105 U/liter], serum Patients: Patients admitted to the coronary care unit glutamic oxaloacetic transferase (upper value of norbecause of ischemic chest pain were studied prospec- mal 40 U/liter) and lactic dehydrogenase (upper value tively when they fulfilled the following criteria: (11 of normal 400 U/liter] until the maximal plasma levels persistent chest pain was accompanied by ST-T seg were reached. Statistical analysis: Differences between means of ment changesindicating beginning of acute myocardial infarction; (2)streptokinase was administered intra- 2 groups were tested with the chi-square test and the venously or intracoronary within 3 hours after the unpaired t test. P values of
v2>
FIGURE 1. Simultaneous 124ead electrocardiogram of an acceierated idioventricuiar rhythm. Two runs of accelerated idioventricuiar rhythm are shown. Note the long coupling interval between the last sinus beat and the first QRS complex of accelerated idioventricuiar rhythm. The accelerated idioventricuiar rhythm is regular. The runs terminate because the sinus rhythm captures the ventricle. The infarct is located in the inferior wail. The accelerated ldioventricuiar rhythm also originates in that area.
FIGURE 2. Simultaneous B-lead electrocardiogram of a “slow ventricular tachycardia.” Note the short coupling interval, the irreguiarity and the abrupt cessation of ventricular rhythm.
February 1, 1988
TABLE I Divlslon of Patients According to the Presence of Myocardial Necrosis, Reperfuslon and Accelerated ldioventrlcular Rhythm (AIVR)
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 61
233
TABLE II Characteristics of Patients With Necrosis and Reperfusion With and Without Accelerated ldioventricular Rhythm (AIVR)
Pts
With AIVR
Without AIVR
57f 10 23:3 12:14
58f 10 24~8 14:17
Necrosis Reperfusion AIVR + = with; - = without.
AIVR occurred in 27 patients, 26 of whom had both myocardial necrosis and reperfusion of the infarct artery. Therefore, in patients with both necrosis and reperfusion, AIVR was seen in 26 of 58 (46%], in contrast to 1 of 29 patients in whom neither necrosis nor reperfusion was present (p
Electrocardiographic characteristics of accelerated idioventricular rhythm: Rhythm: An example of AIVR is shown in Figure 1. It characteristically starts after a long pause resulting in a long interval between the last sinus beat and the first QRS complex of AIVR. AIVR is regular and terminates because the sinus rhythm captures the ventricle. The infarct is located in the inferior wall. The AIVR also originates in this area. The relation between the last QRS interval during sinus rhythm and the interval to the first QRS complex could be measured in 24 patients. Data of different AIVRs that started during regular sinus rhythm were analyzed (n = 43). The remaining AIVRs started after a premature beat or the one configuration changed into another one without interrupting sinus beats. A linear relation was found between the last sinus beat interval and the coupling interval between the sinus beat to AIVR (y = 0.91x + 84) [r = 0.91). The mean and standard deviation of the cycle lengths of AIVRs studied were measured from a maximum of 10 consecutive intervals during a single run of AIVR. The majority (50 episodes) had a cycle length between 600 and 800 ms. Of the remaining runs of AIVR, 20 were between 800 and 1,000 ms, 5 between 1,000 and 1,100 and 9 between 500 and 600. The stan-
Age b-4 Male/female Anterior/inferior infarct location Killip class 1 CPK maximum (U/liter) SGOT maximum (U/liter) Potassium (mmol/liter) Creatinine (~mollliter) Lidocaine AP rep time (hrs) Sinus rate (beatslmin)
4 f 1,363 i 160 f 0.51 f 23 16 3.45 f 1.30 79% 14
2,466 273 3.92 101
3 i 1,307 f 117 4~ 0.81 f 36 11 4.08 f 2.30 85i 13
2,142 201 3.72 105
AP = onset of chest pain: AP rep time = time from the start of chest pain to moment of reperfusion; CPK = creatinine phosphokinase; SGDT = serum glutanic oxaloacetic transferase.
dard deviations of the measured intervals were small: in 55 runs between 0 and 40 ms and in the remaining runs between 40 and 80. From these findings it can be concluded that the AIVR occurring during the reperfusion phase of acute myocardial infarction is generally a regular rhythm. Configuration of accelerated idioventricular rhythm: During the reperfusion phase of myocardial infarction, an AIVR with different configurations could be observed. These QRS configurations always suggested an origin in the infarcted and reperfused area. This is illustrated by the example in Figure 3. In that case reperfusion of a large obtuse marginal branch was obtained. A continuous AIVR was recorded during 18 minutes showing 8 different configurations, which changed gradually from a right’ bundle branch block-like pattern with intermediate axis, to a right bundle branch block-like pattern with right axis. The polarity of the QRS complex became completely inverted in leads I, aVL and V, through Vg. These electrocardiographic changes indicate that during reperfusion of the obtuse marginal branch, impulse formation initially started in the posterobasal part of the left ventricle and gradually changed to a more inferolateral location. Table III shows different aspects of the QRS configuration of AIVR in relation to the infarct artery. It was found that the greatest number of AIVR configurations per patient occurred in patiknts with reperfusion of the left anterior descending branch with a maximum of 8. Left and right bundle branch block-like patterns occurred during reperfusion of both the left anterior descending branch and the right coronary artery. In contrast restoration of flow through the circumflex branch only caused AIVR with a right bundle branch block morphology. The frontal axis could point in all directions in either circumflex or left anterior descending branch reperfusion. Right coronary artery reperfusion, however, caused only a superior axis. Concerning QRS width, lactic dehydrogenase reperfusion of the
234
ACCELERATED
IDIOVENTRICULAR
TABLE III Artery
RHYTHM
ORB Configuration
of Accelerated
AlVRlFl
ldioventrlcular
Configuration
Rhythm (AIVR) in Relation to Infarct
Electrical
QRS Width
artery
Rts
(no)
1 2 3 4 5 6 7 8 LBBB RBBB 0 to 90° 90 to 190° 0 to -90’
LAD LC Right
12 7 7
49 10 17
5 24 15
2 2 2 1 1 1
19 0 7
30 18 10
17 3
14 4
LAD = left anterior descending branch: LBBB = left bundle branch block-like branch; RBBB = right bundle branch block-like configuration.
left anterior descending branch induced AIVR with a less wide QRS compared with reperfusion of the circumflex and the right coronary artery (130vs 150ms, p
Discussion In the setting of acute ischemic heart disease the occurrence of ventricular arrhythmias, varying from premature beats and accelerated rhythms to ventricular tachycardia and fibrillation, is well known. Ac-
A
Axis
AIVR
Coronary
B I
3
-9Oto-180’
10 7 15 configuration:
8 4 2
W-4 131 f 25 148 f 23 150 f 20
LC = left circumflex
cording to studies before thrombolytic therapy for acute myocardial infarction was available, the incidence of AIVR varies between 8 and 46%. This figure is affected by the differences in accepted upper rate for AIVR. This arrhythmia has intrigued cardiologists for a long time in respect to its pathophysiology and, prognostic significance. For instance, AIVR has been considered to be a ventricular tachycardia with 2 or 3:1 exit block5J1J3g24 and also a marker for the risk of more severe ventricular arrhythmias.3*6*7JlJ4
4
5
6
7
8
avr
FtGURE 3. A, simultaneous 12-lead electrocardiograms from a patient with an Inferolateral infarction caused by an obtuse marglnal branch occlusion recorded during sfnus rhythm. 6, shows 8 different accelerated ldloventrlculai rhythms recorded during reperfuslon. The GRB configuration shows a right bundle branch block pattern with a gradual shift toward right axis devlatlon In the frontal plane and development of left lateral negativity In the horlrontal plane. This suggests that impulse formatlon started In the posterobasal part and gradually changed to an inferolateral location. This Is compatible with gradual reperfuslon of the myocardlum along the obtuse marginal branch. V, we8 not recorded in E, 4 through 8, to allow visualization of the maln stem of the left coronary artery during angiography.
February 1, 1988
Since the introduction of thrombolytic therapy, more insight has been gained in the pathophysiologic mechanism of AIVR. It was recognized that AIVR especially occurred during restoration of blood flow during acute myocardial infarction.16 This finding is supported by our study although the group of patients without reperfusion was small. Further, we found that the occurrence of an AIVR was always accompanied by an enzyme increase indicative of myocardial necrosis. Apparently, both reperfusion and necrosis are necessary to induce AIVR. This finding is of practical clinical importance. It may help to recognize reperfusion after administration of thrombolytic agents when coronary angiography is not performed. It might also be useful to diagnose spontaneous reperfusion when no thrombolytic agents are administered. The configuration of AIVR, although not highly specific, may be of help in the noninvasive identification of the infarct vessel. For instance multiple configurations and narrow QRS width point to the left anterior descending branch. A left bundle branch blocklike configuration virtually excludes the circumflex branch as the occluded artery: AIVR with an electrical axis between 0 and 180’ in the frontal plane makes the right coronary artery unlikely to be the infarct vessel, a finding in agreement with other studies.17 AIVR always started with a long coupling interval. This finding is of interest because it is in agreement with one of the criteria advanced for triggered activity based on delayed after-depolarizations as the underlying arrhythmogenic mechanism.25 In the isolated tissue preparation delayed after-depolarizations and triggered rhythms have been demonstrated during conditions mimicking reperfusion after an ischemic episode.26The possibility that AIVR is caused by triggered activity is not supported by our observation that AIVR was seen equally often in patients with and without the administration of lidocaine. Lidocaine is well known to suppress triggered activity induced by delayed after-depolarization.27 As previously noted, ventricular arrhythmias with intermediate rates have been divided into “accelerated idiov&tricular rhythms” in the restricted sense and “slow ventricular tachycardias.” Our study demonstrates that during the reperfusion phase of acute myocardial infarction especially, the accelerated idioventricular rhythm in the restricted sense is observed. In our (preliminary] experience “slow ventricular tachycardia” also occurs frequently during the first 24 hours of infarction but after the direct phase of reperfusion. The pathophysiologic significance of slow ventricular tachycardia is still a matter of investigation. No variables could be found to predict the all or none occurrence of AIVR in patients with reperfusion and myocardial necrosis (Table II). Although there was a trend for a higher enzyme increase to occur more often in the presence of AIVR, this relation did not achieve statistical significance. Indeed, we have observed that
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even very small infarcts could be accompanied by long-lasting sustained AIVR. Acknowledgment: J. Haenen is acknowledged for his assistance in collecting patient data and Arno Muytjens for his statistical advice.
References
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