Ventricular Fibrillation Complicating Acute Myocardial Infarction

Ventricular Fibrillation Complicating Acute Myocardial Infarction

Ventricular Fibrillation Complicating Acute Myocardiallnfarction* lWo Distinct Clinical and Electrocardiographic Features Eldad Rechavia, M.D.; Samuel...

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Ventricular Fibrillation Complicating Acute Myocardiallnfarction* lWo Distinct Clinical and Electrocardiographic Features Eldad Rechavia, M.D.; Samuel Sclarovsky, M.D.; Boris Strasberg, M.D.; Alex Sagie, M.D.; On Topaz, M.D.; and]acob Agmon, M.D.

1\vo distinct electrocardiographic patterns of ventricular 6brillation (VF) complicating acute myocardial infarction (AMI) were observed in 34 patients during the 6rst 24 hours from initial symptoms. Type 1 (seven patients) was charac-

Type 2 (27 patients) was defined as multiform QRS con6guration (>300/min) with marked changes in the amplitude (polymorphous VF~ Type 1 rhythm was seen mostly during the hyperacute ischemic phase, probably associated with total coronary vessel occlusion; type 2 was observed when Q waves were already present in the electrocardiogram.

Ventricular fibrillation (VF) is the major cause of cardiac death within the early hours of evolving infarction or ischemia. A number of clinical studies have attempted so far to evaluate the prognostic significance of primary VF complicating acute myocardial infarction (AMI), 1 the role of sympathetic activity,2 the tendency for recurrence," and prophylactic treatment. 4 Numerous studies have been designed in an attempt to define the predictive values of predisposing factors, such as the infarct's site and size,5.6 abnormalities of heart rate and conduction, 7 prolonged corrected Q-T interval (Q-T c),8 R-on-T phenomenon," warning arrhythmias," and metabolic disorders." None of these studies has commented on significant variability of fibrillation amplitude and configuration and their interpretation in relation to various stages of infarction. Primary VF has been defined when occurring without evidence of hypotension or heart failure during the first day of AMI or as primary electrical failure not associated with AMI. The purpose of this study was to characterize two distinct electrocardiographic patterns of primary VF complicating AMI and to correlate their course of appearance with specific electrocardiographic stages of evolving infarction. Different underlying mechanisms might be responsible for these two electrocardiographic patterns of primary VE

from initial cardiac symptoms. The criteria for the diagnosis of infarction were severe retrosternal chest pain of more than 30 minutes' duration, characteristic evolving electrocardiographic changes with the development of new pathologic Q waves, and typical elevation of serum cardiac enzymes compatible with AMI. A 12-leadelectrocardiogram was recorded on the patient's presentation to the emergency department and on arrival in the coronary care unit. Repeated ECGs taken consecutively at least every hour until two hours after the onset of VF were available. All patients had continuous electrocardiographic monitoring and the presence ofVF defined as irregular, fast ventricular activity (>300/min) associated with total pump failure demonstrated by automatically recorded rhythm strips with identical positions of the electrodes in all patients. The electrocardiographic evolution of AMI was divided as follows into four stages." (1)stage 1 consists ofST-segment elevation, peaked positive T waves, and Qwaves ofless than 2 mm; (2) stage 2 consists of Q wavesof more than 2 mm with decrease in the size of R waves; ST segment is still elevated with positive T waves; (3) stage 3 consists of inversion of the previously positive T waves and still with STsegment elevation; and (4) stage 4 consists of the ST segments return to the isoelectric baseline. A patient's stage of AMI was defined by two observers who were blinded, using the ECG prior to the onset of VR

terized by fast disorganized ventricular activity, small voltage, and no clear identmable QRS complexes (fine VF~


A retrospective study was done of 69 consecutive patients admitted to our coronary care unit within two hours after the onset of symptoms, who developed VF in the setting of AMI within 24 hours *From the Israel and lone Massada Center for Heart Diseases, Beilinson Medical Center, Petah Twa, and Tel Aviv University Sadder School of Medicine, Tel Aviv, Israel. Manuscript received January 16; revision accepted August 3. Reprint requests: Dr. Sclaroosky, Massada Center for Heart Disease, Beilinson Medical Center, Petah 7ilwa 49100, Israel

Selection of Patients

From the initial population studied, 35 were excluded because of the presence of other factors known to predispose or to be associated with ventricular arrhythmias. The criteria for exclusion that were applied (developed prior to the examination of the patient's data) were as follows: (a) patients treated with group 1 antiarrhythmic drugs, digoxin, amiodarone, or sympathomimetic drugs prior to the onset of VF, with or without prolonged Q-T, interval; (b) patients with previously known ischemic cardiomyopathy, ventricular arrhythmias, congestive heart failure, or left ventricular aneurysm; (c) patients with serum potassium concentration of less than 3.5 mmoVL or more than 5.5 mmollL (samples of blood were taken on admission); (d) patients with severe hypotension or cardiogenic shock; (3) patients with catheter-induced VF; and (f)patients in whom stages of AMI could not be recognized (complete left bundle-branch block, etc). The remaining 34 patients who fulfilled the criteria for entry into the study were divided to two groups: (1) group 1 consisted of seven patients with fast disorganized ventricular activity, small voltage CHEST I 93 I 3 I MARCH, 1988





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FIGURE1. Example of type 1 VF in patient with inferior

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wall infarction (patient 1;Table 1).A. Electrocardiogram

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on admission (leads 2, 3, and aVF), demonstrating stage 1 of inferior wall infarction with minimal Q waves «2 mm). B. Type 1 VF (fine VF). C. Two hours later. Stage 3 of inferior wall infarction is observed.



the two groups. A level less than 0.05 was considered statistically significant.

«10 mm), an irregular, nonuniform undulated tracing, and no clear identifiable QRS complex (fine VF) (Fig 1);and (2) group 2 consisted of 27 patients with fast ventricular activity (>300/min), multiform QRS configuration with marked changes in the amplitude, and twisting axis (polymorphous or coarse VF) (Fig 2). Rhythm strips of VF were analyzed by two observers at an identical time three seconds from the beginning of VE


Group 1 (Table 1) included seven male patients with ages ranging from 39 to 79 years (mean, 58 years). Two patients had had previous myocardial infarction, four had effort-induced or unstable angina, and two were free of cardiac symptoms. The AMI was anterior in three patients and inferior, inferolateral, extensive

Statistical Analysis All data are presented as the mean ± standard deviation. The Fischer test was used in order to find statistical differences between




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FIGURE 2. Three-channel ECG showing evolution of anterior wall myocardial infarction complicated by type 2 VF (patient 21; Table 3). A. Electrocardiogram on admission (leads VI' Vi' and V3), showing stage 1 of anterior wall infarction. B. Type 2 VF (polymorphous VF) during stage 2 of AMI (Q waves more than 2 mm are seen before onset ofVF). C. Two hours later. Stage 3 of anterior wall infarction is observed.


Ventricular Fibrillation Complicating Acute MI (Rechavia et 8/)

Table I-Clinical and Electrocardiographic Data on Seven Patien" with Type 1 VF Complicating AMI Patient, Sex, Age (yr) 1,M,79 2,M,53 3,M,58 4,M,39 5,M,50 6,M,66 7,M,58

Cardiac Risk Factors *

AH Smoking Smoking AH Smoking

Previous Cardiac Diseaset

Phase of AMI

Localization of AMIi


1 1 1 1 1 1 2



Onset ofVF, hours after admission§ OA 1.5


No. of Episodes

Total No. of DC Shocks

1 1 3 1 1

1 1 3 1 1




Complicationsll SVf; reinfarction SVf


CS; death VF (type 2)

*AH, Arterial hypertension. t~ Angina pectoris; and MI, myocardial infarction. iI~ Inferior wall; INILA, inferolateral; EX/AN, extensive anterior; AS~ anteroseptal wall; and EX/PO, extensive posterior. lOA, On admission. !ISVI: Supraventricular tachycardia; and CS, cardiogenic shock.

posterior, and anteroseptal wall in the remaining four patients, respectively. None of these was given diuretics prior to the onset of VR Six patients developed VF during stage 1 of infarction, and in the remaining patient, VF was documented following the appearance of pathologic Q waves (Table 2). The mean duration of time between admission and VF occurrence was 2.5 hours (range, 0 to 16hours). An exception is patient 7, where VF was observed 16 hours after admission. Of the seven patients, only one (patient 3) had recurrent episodes of VR Direct-current shocks were remarkably efficient in the restoration of sinus rhythm. One patient died from cardiogenic shock on the fifth day of hospitalization (in-hospital mortality, 14 percent). Additional complications in this group were reinfarction (one patient) and atrial arrhythmias (two patients). Group 2 (Table3) included 27 patients (22 men) with ages ranging from 42 to 84 years (mean, 62 years), (p>0.2; not statistically significant vs group 1). Previous cardiac disease was found in 15 patients (56 percent). Three of the patients were receiving diuretic treatment because of hypertension, with normal levels of electrolytes upon admission. The site of infarction was anterior (seven patients), inferior (seven patients), anteroseptal (six patients), and inferolateral and extensive posterior in the remaining seven patients. Type 2 VF appeared once pathologic Qwaves were already apparent (electrocardiographic stage 2), with the exception of patients 4 and 26, in whom the arrhythmia was documented in the setting of stage 1 (p = 0.00015; statistically significant vs group 1). The mean duration of time between admission and the onset of the arrhythmia was 5.7 hours (range, 30 minutes to 17 hours) (p>0.1; not statistically significant vs group 1). Fourteen patients (52 percent) had a single episode of VF which was responsive to one to five direct-current shocks. In the remaining 13 patients (48 percent), recurrent episodes appeared, with an average of four episodes per patient (range from 2 to 15 episodes)

(p = 0.4; not statistically significant vs group 1). Directcurrent shocks were given more frequently to patients in group 2 (1.27direct-eurrent shocks per VF attack in group 2 vs one direct-current shock in group 1); however, this difference was not statistically Significant (p = 0.5). In one instance, spontaneous conversion of tachyarrhythmia was observed. Three patients died (in-hospital mortality, 11 percent; not statistically significant vs type 1); deaths were related to reinfarction, pump failure, or both. Late morbidity included severe left-sided heart failure (two patients) and atrial arrhythmias (four patients). DISCUSSION Ventricular fibrillation has been defined by Surawiez" as chaotic, asynchronous fractionated activity of the cardiac ventricles. Two electrocardiographic patterns of VF were characterized by Friedberg" in the 1960s; the first was characterized by fairly uniform undulatory rhythm with amplitude of 8 to 10 mm and frequency of 130 to 300 beats per minute with no isoelectric interval, sometimes termed ventricular flutter. In the second type the main electrocardiographic features were irregular oscillations with continuous change in amplitude, width, and configuration, representing bizarre QRS complexes, where the ST segTable 2-ClinictJl Correlate, Data

Group 1

Group 2

p Value*

No. of patients Age, yr Phase of AMIt Stage 1 Stage 2 Onset of VF, hours after admission No. of episodes No. of DC shocks perVF

7 58±11

27 62±10


6 1 2.5±5

2 25 5.7±5

1.3±O.7 1.3±O.7

2.4±2.8 3.1±3.2

0.00015 NS


*NS, Not Significant. tData are numbers of patients. CHEST I 93 I 3 I MARCH. 1988


Table 3-ClinictJl and EiectroctJrdtograplaic Data on 27 PatientI witla 7yPe 2 VF Complicating AMI Patient, Sex, Age (yr) I,M,70 2,M,59 3,M,71 4,F,54 5,F,42 6,M,84 7,M,50 8,F,70 9,M,59 10,F,64 II,M,52 12,M,71 13,M,70 14,M,73 15,M,47 16,M,53 17,M,66 18,F,74 19,M,72 2O,M,59 21,M,62 22,M,67 23,M,47 24,M,60 25,M,60 26,M,66 27,M,49

Cardiac Risk Factors·

Previous Cardiac Diseaset AP






AH; SM SM; hyperlipidemia


Phase of AMI 2

2 2 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 2


Onset ofVF, hours after admission 1 0.5 0.5 1 1 8 0.75 3 2 10 17 4 11 3.5 14 3 12 10 4

2 3 17 10 2 2 1.5 9

No. of Episodes

Total No. of DC Shocks

2 7 1 1 3 1 5 1 4 2 1 1 2 1 3 1 1 1 2 1 1 2 3 2 1 15 1

3 7 1 1 3 1 7 SCI 4 2 3 1 2 3 3 3 1 1 2 2 1 2 5 5 1 17 2


IW AMI; death CHB; death PE

SVf SVf; reinfarction

CS; death Reinfarction PE;SVf


·AH, Arterial hypertension; SM, smoking; and OM, diabetes mellitus. t A~ Angina pectoris; and MI, myocardial infarction. *EXIAN, extensive anterior; AS~ anteroseptal wall; IW, inferior wall; IN/LA, inferolateral; and EX/PO, extensive posterior. Ise, Spontaneous conversion. II~ Inferior wall; CBB, complete heart block; PE, pulmonary edema; SVI: supraventricular tachycardia; and CS, cardiogenic shock.

ment and the T wave cannot be differentiated from the entire ventricular complex. In 1966, a French authors defined another distinct form of ventricular tachyarrhythmia using the term, "torsade de pointes," whose main characteristics consist of paroxysms of ventricular tachycardia in which the QRS axis undulates over runs of 5 to 20 beats around an imaginary isoelectric line. The clinical course of a given patient with AMI is difficult to predict regarding the appearance of electrical failure in various stages of the acute coronary event. Conventionally, VF during AMI is defined as primary and secondary, with predictive factors and predisposing causes related for each form. Ventricular fibrillation is classified as primary if it occurs within 24 hours of infarction in the absence of heart failure, hypotension, or shock." The amplitude of fibrillation may relate to dynamic changes of myocardial perfusion during coronary occlusion and reperfusion. When fibrillation results from acute ischemia, changes of the wave form and the pattern of electrical activity during VF have been attributed to ischemia caused by fibrillation itself: 17 Fine VF (low amplitude) has been considered by Weaver et allS as an ominous prognostic sign 488

compared to "coarse" fibrillation (high amplitude), indicating that adequate circulation is being provided during resuscitation; however, when VF occurs in patients already monitored and defibrillation is immediately applied, it is not clear how much more information the VF amplitude would add to the risk stratification of patients who survived to leave the hospital. A unique aspect of our study consists of the characterization of two electrocardiographic patterns of primary VF, correlated with specific stages of AMI. As amplitude of wave form tends to decrease and to become more monomorphic after several minutes of fibrillation, rhythm strips ofVF were analyzed at an identical time, immediately following the onset of Vii: Our groups included patients developing VF during AMI. We separated them according to preestablished electrocardiographic criteria into two groups which were comparable in age, coronary risk factors, and previous cardiac diseases. Those two types of tachyarrhythmias could be correlated with specific phases of infarction based upon electrocardiographic natural evolution of AMI. Increased ventricular vulnerability to fibrillation can Ventricular Abrillation Complicating AcuteMI (Rechavla et III)

occur secondary to a complete coronary occlusive event. Investigations designed to assess the correlation between ST-segment alterations and coronary dynamics demonstrated that ST-segment elevation with a peaked positive T wave is an initial electrocardiographic expression of transmural myocardial ischemia, 19.10 resulting from sudden reduction of coronary blood flo~ The fact that less than 20 percent of the patients were found to have type 1 arrhythmia may suggest that in a substantial number of patients, it takes place during the so-called prehospital phase, whereas type 2, the multiform variety, was found to be the dominant pattern during the phase of hospitalization. The ischemic mechanism considered is well supported by clinical observations in patients with variant angina. 21-23 In these patients, coronary spasm and transmural myocardial ischemia may account for the development of ventricular arrhythmias noted during the period of ST-segment elevation" which represents the most prominent electrocardiographic finding of the vasospastic attack. Restoration of coronary blood flow is frequently associated with ventricular arrhythmias. Reentry or enhanced automaticity (or both) may playa role in the genesis of reperfusion arrhythmias during ischemia or infarction.15-18 Reestablishment of coronary blood How after relief of spasm may also be responsible for the development ofVF and sudden death in patients with vasospastic angina, even with no evidence of significant coronary artery disease. 14.18-31 Of the 27 patients with type 2 VF, 25 were found to develop VF during stage 2 of AMI, once pathologic Q waves were already recognized in the ECC. Rapid release of creatine kinase is a useful marker of early spontaneous recanalization. The appearance of Q waves, which used to be regarded as a marker of myocardial necrosis, was closely parallel to the "washout" of cardiac enzymes observed after reopening of an occluded coronary vessel. 31 Therefore, these data suggest that the likely substratum involves reperfusion changes of the ischemic myocardium. The destruction of cells which were damaged by ischemia and the release of myocardial metabolites accumulated during occlusion may account for the electrical instability during reestablishment of coronary artery patency.

Limitations of Study Selection of patients for this kind of study is extremely difficult. We have excluded patients with predisposing factors whose role and relevance to the clinical situation studied is not well determined and are of uncertain clinical connection; for example, this study may well be hampered by removal of patients with hypokalemia; however, we believe that in this way a clear distinction may be obtained between delayed

repolarization ventricular arrhythmias (a term adopted by Schweitzer and MarJ(33) and VF with the multiform QRS configuration. This concept could be further consolidated by the relative lack of spontaneous conversion, the unlimited course, and the relatively good response to cardioversion of the multiform variety of VF, in contrast to what would be expected, respectively, concerning the clinical course of "torsade de pointes.?" In our opinion, these observations may justify this approach to selection, which is particularly essential in patients with AMI. As mentioned before, patients included in this study were admitted to our coronary care unit within two hours of the onset of symptoms. Therefore, it is not inconceivable that the first group of patients in this study may not be representative of the larger number of individuals who died before the arrival of the mobile care unit or admittance to the hospital. One other limitation is the lack of coronary angiography in order to prove or disprove the occurrence of reperfusion. CONCLUSIONS

Based on electrocardiographic criteria, two patterns of VF were recognized during AMI. They were well correlated with preestablished electrocardiographic stages of AMI and differed in their propensity for early recurrence. The basis of this electrocardiographic and clinical distinction is explained most probably by different pathophysiologic mechanisms and electrophysiologic properties of the myocardium. These suggestions remain speculative for the present time. Further correlated clinical-electrocardiographic studies should be considered to work towards a better understanding of the mechanisms involved and their clinical implications. ACKNOWLEDGMENT: We thank Gill Sher and Sasdi Yehudit for their assistance in the preparation of this manuscript. REFERENCES

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ventricular Rbrtllation Complicating Acute MI (Rechavla et 81)