Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction

Incidence and Description Rhythm Complicating

Acute Myocardial

Ventricular Infarction

One hundred and nineteen episodes of accelerated ventricular rhythm (<125/min) were noted in 37 patients with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (> 12Wmin) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes, ectopic in 42 episodes and unknown in the remaining 12 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patients the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset -of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted.

EDGAR LICHSTEIN, M.D. CARLOS RIBAS-MENECLIER, M.D.” PREM K. GUPTA, M.D. KUL D. CHADDA,

of Accelerated

M.D.

Elmhurst, New York

It is co&zluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block. From the Department of Medicine, Division of Cardiology, Mount Sinai Hospital Services, City Hospital Center at Elmhurst. Mount Sinai School of Medicine of the City University of New York, Elmhurst. New York. Requests for reprints should be addressed to Dr. Edgar Lichstein, Division of Cardiology, Mount Sinai Hospital Services, City Hospital Center at Elmhurst, 79-01 Broadway, Elmhurst, New York 11373. Manuscript accepted June 4. 1974. * Present address: Mt. Sinai Hospital, 4300 Alton Road, Miami Beach, Florida 33140.

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February

1975

The American

ectopic rhythms frequently occur after acute myocarinfarction and are associated with an increased incidence of

Ventricular dial

ventricular

fibrillation

and

have

separated

according

been

increased

mortality

to their

rate

[ I].

These

and thought

rhythms to have

a

benign prognosis when the ventricular rate is less than lOO/min and a poorer prognosis when the rate exceeds iOO/min. The slow ventricular rhythm has been termed paroxysmal ventricular tachycardia [2], nonparoxysmal ventricular tachycardia [3], idioventricular rhythm [4], idioventricular tachycardia [ 51 and slow ventricular tachycardia [ 61.

Journal of Medicine

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ACCELERATED VENTRICULAR RHYTHM IN MYOCARDIAL INFARCTION-LICHSTEIN

We have chosen to use the term accelerated ventricular rhythm and, based on the experimental work of Logic et al. [7], have included all ventricular rhythm with a rate up to 125/min in this category. We report the incidence of this arrhythmia in a group of patients with acute myocardial infarction and describe the various characteristics of this arrhythmia.

rhythmia

was given as judged necessary

ET

AL.

by the medical

staff and usually consisted of a 50 mg bolus of lidocaine. This additional therapy was employed during prolonged episodes

of arrhythmia

or when

episodes

minutes of each other. The patients’

recurred

course

within

was followed

throughout the length of their hospital stay which averaged 21 days. Mortality figures refer to hospiial mortality only.

RESULTS METHOD All patients in the study group were admitted to our coronary care unit where they stayed an average of 4.5 days. The diagnosis of acute myocardial

(1) presence

of ischemic

trocardiographic

infarction was based on

chest pain, (2) typical serial elec-

changes

which

included

waves

and serial ST-T wave changes,

serum

glutamic

oxaloacetic

abnormal

Q

and (3) elevation

transaminase,

serum

of

lactic

dehydrogenase and creatinine phosphokinase levels. Electrolytes, including magnesium, were determined at the time of admission. All

patients

were

monitored

their stay in the coronary sion display*

and a Vl

continuously

throughout

care unit using a nonfade

monitor lead. Arrhythmias

televi-

were de-

tected by one or more of the following technics. (1) An ectopic beat detector.7 (2) routine hourly rhythm strips, (3) a rate

dependent

alarm

minus 20 beats/min rect observation the medical sweep

which

was

usually

and (4) di-

television

and may be “frozen”

19

on the screen

ventricular

125 beats/min. if they were differed terval

rhythm

21

A

as 3 or

23

Ia * LB.DC

with a rate of 55 to

24

q

as ventricular

25

An

their morphology

b 26

[9*

= 27

q

defined

The beats were designated

not preceded

by a P wave,

from the basic sinus morphology was 0.12

second

or greater.

A L0.E

22

was

beats in succession

A*

20

ogram was also obtained. Accelerated

and the QRS in-

Agonal

rhythms

were

; 2

28

El*

as 3 or more

29

A*

ventricular beats in succession whose rate was greater than 125/min. The ventricular origin was defined as de-

30

A

not included. Fast ventricular

scribed.

tachycardia

We will use the term ectopic

coupling interval between first ventricular terval,

was defined

and the term

is greater

heart

failure

of respiratory

tachycardia

beat

care

whenever

P-P in-

the interval

distress

defined

as a syndrome

associated rales severe

with

continuous

intravenous

sion of lidocaine at 2 mg/min unless the evidence of sinus bradycardia or advanced (A-V) block. All but two of the patients in received the lidocaine infusion. Additional

in the infu-

patient showed atrioventricular the study group therapy for ar-

* American Optical Memory Display System. Optical Model 264100 Cardio-Care Ectopic Beat Detector.

1 American

v-

i

LB

LB

q 9r

32

A

33

q*

34

Q*

35

A+.n

36 37

kl*

sinus

enough to

dlgitalis or both. Routine treatment unit included

beat

P-P interval. was

and basilar pulmonary

require diuretics, coronary

escape

the

31

sinus beat and the

than the preceding

sinus beat to the first ventricular

than the preceding

Congestive consisting

the preceding

beat is shorter

from the preceding

beat whenever

3___

18

has a

allowing for a delayed write-out). Whenever the length of the arrhythmia permitted, a complete 12-lead electrocardi-

more ventricular

2

I

17

at the central station by

or nursing staff (the nonfade

of 4.2 seconds

DAY

set to plus or

of the basic sinus rhythm,

of an arrhythmia

From December 1, 1972, through November 30, 1973, 119 episodes of accelerated ventricular rhythm were noted in 37 patients with acute myocardial infarction. In patients with multiple episodes of accelerated ventricular rhythm, the interval between episodes varied from minutes to hours. In none did the interval exceed 24 hours. The incidence of this arrhythmia was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia were noted in 16 of these 37 patients. This group consisted of 30 males and 7 females with an average age of 59.2 years (42 to 85 years). Eighteen patients had anterior wall infarction and 19 patients had inferior wall infarction.

Figure 1. Summary of significant crlnical features of 16 patients with both accelerated ventricular rhythm and fast ventricular tachycardia. S = accelerated (slow) ventricular rhythm. F = fast ventricular tachycardia. A = inferior wall myocardial infarction. Cl = anterior wall myocardial infarction. = ventricular premature beats were present with morphology similar to accelerated ventricular rhythm or fast ventricular tachycardia. + = accelerated ventricular rhythm with morphology similar to fast ventricular tachycardia. LB = Mocaine bolus. DC = direct current cardioversion. A = atropine. P = pronestyl. E = expired.

February 1975

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ACCELERATED VENTRKXJLAR RHYTHM IN MYOCARDIAL INFARCTION-LICHSTEIN

DAY

I

2

5

4

3

ET AL.

A*+

I

A*+Le

q *+ q *+LB

2

ISI*

3

[DDC ISI*

4 X”

5

Arc

E

6 A$;+ it

*+ * + LB ii *+

A++DC

A*+ A*+LB lsl*+

lEl*+DC El*+

q *+Le

13 14 15

0:

DC

El*+ El*+ l3*+

Figure 2. Summary of significant clinical features in 2 1 patients with acceferated ventricular rhythm alone. Symbols are the same as Figure 1.

I6

The onset of accelerated ventricular rhythm was classified as escape in 65 episodes occurring in 15 patients and as ectopic in 42 episodes occurring in 15 patients. In one patient both were noted in two separate instances. The onset of the arrhythmia was not available for analysis in 10 episodes. Ventricular premature beats were noted either immediately before or immediately after an episode of accelerated ventricular rhythm in 31 patients and im-

Of the 37 patients with accelerated ventricular rhythm, 32 had this arrhythmia on the 1st day, 1 on the 2nd day, 3 on the 3rd day and 1 on the 4th day. Of the 16 patients who also had episodes of fast ventricular tachycardia, 10 patients had the accelerated ventricular rhythm first and 6 patients had the fast ventricular tachycardia first (Figures 1 and 2). The mean rate of accelerated ventricular rhythm was 81.4 beats/min (range 55 to 125 beats/min). The mean sinus rate preceding the episode of accelerated ventricular rhythm was 78 beatsfmin (range 40 to 120 beats/min) (Figure 3). The mean rate of fast ventricular tachycardia was 181 beats/min (range 136 to 250 beatsimin). The mean sinus rate preceding fast ventricular tachycardia was 83.1 beats/min (range 65 to 120 beatsimin).

mediately before or after fast ventricular tachycardia in 14 patients. The morphology of the accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients. The morphology of fast ventricular tachycardia was similar to the ventricular premature beats in 12 patients. In 11 patients, the morphology of the ventricular premature beats, the

1301 120

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February 1975

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VENT. TACHYCARDIA

194

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(8wts/mln)

The American Journal of Medicine

Volume 58

120

Figure 3. Relationship of rate of accelerated ventricular rhythm to preceding sinus rate.

ACCELERATED MNTRICULAR

accelerated ventricular rhythm and the fast ventricular tachycardia were all the same. In one patient, only the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same. In six patients, the coupling time between the preceding sinus beats and the onset of accelerated ventricular rhythm was the same as that for the ventricular premature beats. The accelerated ventricular rhythm in all six patients was classified as ectopic since the coupling time was shorter than the preceding P-P interval. In five patients, the coupling interval of the fast ventricular tachycardia was the same as the ventricular premature beats. In three patients, the coupling time of the ventricular premature beats, the accelerated ventricular rhythm and the fast ventricular tachycardia were the same. In another patient, who did not have ventricular premature beats, the coupling time of the accelerated ventricular rhythm and fast ventricular tachycardia was the same. In seven patients, not only was the morphology of the accelerated ventricular rhythm and the fast ventricular tachycardia the same, but, in addition, the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. In another patient with accelerated ventricular rhythm with varying rate, the rate varied by a multiple of a faster interval. Three patients had evidence of accelerated ventricular rhythm from more than one foci as manifested by different morphology and rate. Fusion beats were noted in 96 episodes of accelerated ventricular rhythm in 24 patients. In 13 of the 37 patients significant complications developed. Eight had congestive heart failure and six required treatment with digitalis. In all instances, accelerated ventricular rhythm preceded digitalis therapy: four with anterior infarction, and four with inferior infarction. Five of these patients had accelerated ventricular rhythm alone; three had both fast and accelerated ventricular rhythm. Two patients had cardiogenic shock: one with anterior wall infarction, and one inferior wall infarction. One patient had accelerated ventricular rhythm alone, whereas the other patient had both. In three patients pericarditis developed; all had anterior wall infarction. Two of these patients had accelerated ventricular rhythm alone and one had episodes of both accelerated ventricular rhythm and fast ventricular tachycardia. Three patients with both fast ventricular tachycardia and accelerated ventricular rhythm had episodes of ventricular fibrillation following fast ventricular tachycardia (Cases 4, 9 and 13). In addition to routine treatment consisting of lidoCaine infusion at 2 mg/min, the treatment of 27 episodes of fast ventricular tachycardia was as follows: 12 episodes in seven patients responded to a bolus

RHYTHM IN MYDCARDIAL INFARCTION-LlCHSlEIN

ET AL.

of lidocaine, whereas 6 episodes in three other patients required DC cardioversion. The three episodes of ventricular fibrillation were successfully cardioverted. Four episodes in three patients stopped spontaneously before any therapy could be initiated. Three patients in this group died; all had inferior wall myocardial infarction. One patient with both accelerated ventricular rhythm and fast ventricular tachycardia died of congestive heart failure on day 4. The two remaining patients had accelerated ventricular rhythm alone, and one died of cardiogenic shock on day 1 and the other in congestive heart failure on day 10. Several typical cases are described as follows: Case 6.

This 46 year old woman had inferior wall myocardial infarction. Her rhythm strip, shown in Figure 4A,

demonstrates an episode of accelerated ventricular rhythm which appears as an escape phenomena and terminates with a fusion beat. A ventricular premature beat is also evident on the same strip which has a similar morphology to the accelerated ventricular rhythm but a different coupling time. Evidence of parasystole could not be found. Case 25. This 42 year old man had inferior wall myocardial infarction. Figure 48 demonstrates an episode of ac celerated ventricular rhythm starting with an ectopic ventricular beat. Case 30. This 45 year old man had inferior wall myocardial infarction. A brief episode of accelerated ventricular rhythm is shown in Figure 4C. It is postulated that the basic ectopic cycle is 0.28 second and that the shorter intervals are twice this multiple and the longer interval of 0.84 second is three times this multiple. Case 16. This 65 year old man had anterior wall myocardial infarction. Figure 4D illustrates two episodes of accelerated ventricular rhythm in succession. The morphology and the rate of each episode differ and the second episode terminated with a fusion beat. Case 9. This 52 year old man had inferior wall infarction. Figure 5A illustrates atrial fibrillation with an episode of fast ventricular tachycardia. Figure 58 is a rhythm strip obtained later on the same day after DC conversion to normal sinus rhythm. The episode of accelerated ventricular

rhythm noted has the same morphologyas the fast ventricular tachycardia and is exactly half the rate of the fast ventriculartachycardia. Case 7. This 40 year old man had inferior wall myocardiil infarction. Figure 5C shows an episode of fast ventricular tachycardia with spontaneous reversion to normal sinus rhythm. Figure 50, taken a half hour later, shows an episode of accelerated ventricular rhythm with the same morphology as the fast ventricular tachycardia. The rate of the accelerated ventricular rhythm is equal to one third the rate of the first episode of fast ventricular tachycardii shown in Figure 5C.

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ACCELERATED VENTRICULAR RHYTHM IN MYOCARDIAL INFARCTION-LICHSTEIN

ET AL.

Figure 4. Episodes of accelerated ventricular rhythm in Cases 6 (A), 25 (B), 30 (C) and 18 (D). See text for further details.

A

._

Figure 5. Rhythm strips from Cases 9 (A and B) and 7 (C and D). See text for further details.

Figure 6. Rhyihm strips from Case 14 (A B and C). See text for further

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ACCELERATED VENTRICULAR RHYTHM IN MYDCARDIAL INFARCTION-L.ICHSTEIN

ET AL.

Case 14. This 57 year old man had anterior wall infarction. Figure 6A shows an episode of accelerated ventricular rhythm starting and ending with a fusion beat. Figure 6B, taken 6 minutes later, shows a ventricular premature beat with the same morphology as the accelerated ventricular rhythm in Figure 6A. Following the ventricular premature beat is a ventricular escape beat which has the same morphology and same escape interval as the accelerated ventricular rhythm seen in Figure 6C. Case 15. This 57 year old man had inferior wall myocardial infarction. Figure 7A shows ventricular premature beats which are repetitive in one instance. Figure 78 shows an episode of accelerated ventricular rhythm with morphology similar to that of the ventricular beats seen in Figure 7A. Figure 7C shows ventricular premature beats again resembling those seen in Figure 7A and an episode of fast ventricular tachycardia which is exactly twice as fast as the accelerated ventricular rhythm in Figure 7B and has the same morphology. The coupling time of the ventricular premature beats seen in Figures 7A and 7C and the coupling time of the fast ventricular tachycardia are all identical. Figure 7D, taken later the same day, shows another episode of accelerated ventricular rhythm but with a different rate and morphology than that noted previously. Electrolytes including magnesium were normal. COMMENTS

The incidence of accelerated ventricular rhythm after acute myocardial infarction varies considerably. The highest incidence (48 per cent) was found by Logic et al. [7] in the experimental animal. The incidence reported in other clinical studies varies from 36 per cent to 8 per cent [3,6,8,9]. Our incidence of 12.7 per cent is at the lower end of this spectrum and may be explained by the lack of constant tape monitoring and our policy of routine lidocaine infusion. The reported location of myocardial infarction in patients with accelerated ventricular rhythm varies. Most of the patients reported by Bashour et al. [6] and Raftery et al. [9] had anterior wall myocardial infarction, whereas in the reports by Castellanos et al. [lo] and Rothfield et al. [4] inferior wall infarction predominated. There was no significant difference in our series between the location of the infarction and the occurrence of accelerated ventricular rhythm, with an equal number of inferior and anterior wall infarctions. Sixteen of the 37 patients with accelerated ventricular rhythm also had fast ventricular tachycardia. The incidence of fast ventricular tachycardia during our study period was 11 per cent. Of these 50 per cent were in patients with accelerated ventricular rhythm. The incidence of fast ventricular tachycardia alone varies with the type of monitoring. Lown et al. [I] reported a 29 per cent incidence whereas Norris and his associates [ 1 l] found an incidence of only 11 per cent. Of interest is that in 53 per cent of Nor-

.I -

‘Jo ~~~~~~

j

.I

,i.

akin

;:tiiNI/~t~

,/I,>(

Figure 7. Rhythm strips from Case 15 (A through 0). See text for further details.

ris’s patients, fast ventricular tachycardia progressed to ventricular fibrillation, whereas similar progression occurred in only 19 per cent of our patients. The 50 per cent incidence of fast ventricular tachycardia in our group of patients with accelerated ventricular rhythm is significantly greater than expected and is at present unexplained. The low incidence of ventricular fibrillation in this group may be explained by careful monitoring which allowed for prompt administration of additional doses of lidocaine in addition to the

maintenance intravenous infusion given to all patients. The similarity between morphology of the ventricular premature beats and the accelerated ventricular rhythm in most of our patients and the similarity in coupling intervals in some instances suggest that both the ventricular premature beat and the accelerated ventricular rhythm were similar in origin. Ventricular premature beats with similar morphology to accelerated ventricular rhythm were noted by Castellanos et al. [lo]. They suggested that they were not actually ventricular premature beats but rather an accelerated ventricular rhythm with exit block. Although we found other evidence of exit block, we could not explain any of the ventricular premature beats occurring in close proximity to accelerated ventricular rhythm in this manner. Since these beats had a shorter coupling interval than the preceding P-P cycle, a constant coupling interval and no evidence of exit block, we conclude that they are ectopic in nature. This is consistent with Castellanos’s concept of active and passive discharge from the same ectopic focus [ lo]. Ectopic activity after myocardial infarction results from changes in the degree of diastolic depolarization and variations in the threshold potential of injured fibers [ 121. For example, if the

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ACCELERATED VENTRICULARRHYTHM IN MYOCARDIAL INFARCTION-LICHSTEIN ET AL

ectopic focus is very active, it may discharge prior to the sinus impulse and therefore have all the characteristics of an ectopic beat or an ectopic rhythm. If the focus is less active, it may appear only as an escape phenomenon. Characteristics of accelerated ventricular rhythm include intermittency and variation in rate. The intermittent nature of the arrhythmia may be explained by subtle changes in the extent of diastolic depolarization in an unstable condition such as acute myocardial infarction [ 131. The intermittent arrhythmia is not parasystolic due to absence of protection of the automatic center which allows the arrhythmia to be suppressed by the sinus pacemaker [ lo]. The variation in rate may be sudden or progressive and may be due to several factors. A progressive increase in rate may be due to true intermittency or variable conduction delays surrounding the ectopic focus [lo]. If the variations in rate are a multiple of a fixed interval, exit block is thought to be present. Examples of accelerated ventricular rhythm with exit block were seen in our series and have also been described by Lown [ 11, Schamroth [ 121 and Castellanos [lo] and their associates. Our observation that 7 of 16 patients with both accelerated ventricular rhythm and fast ventricular tachycardia had rates which were multiples of each other support this hypothesis. A progressive decrease in rate can be explained by intermittency or the Munk-Gaskell phenomena, which is thought to be an extinction of the automatic properties of a pacemaker [ 141. The mortality in our group of patients was less than that usually seen with acute myocardial infarction. All three patients who died had inferior wall infarction, and none had ventricular fibrillation. This benign prognosis has been reported by others [4,5,6,10]. In contrast to this is the report by Raftery

and associates [9] describing a 30 per cent mortality in a small group of patients with accelerated ventricular rhythm. All of their 11 patients with accelerated ventricular rhythm had anterior wall infarction; in 6 of these ventricular fibrillation developed, and 4 of these died. Of interest is that nonparoxysmal junctional tachycardia, which is a rhythm thought to be analogous to accelerated ventricular rhythm, has recently been reported to have an unfavorable prognosis when complicating acute anterior wall myocardial infarction [ 151. This rhythm may be seen with digitalis intoxication in a manner similar to nonparoxysmal junctional tachycardia. Therefore, discontinuing digitalis therapy should always be considered when this rhythm is observed. On occasion the loss of the atrial contraction becomes clinically significant: /n these instances, acceleration of the sinus rate with atropine may prove helpful [ 161. If the patient’s cardiovascular status is precarious, an electrical pacemaker may also be considered for overdrive [lo]. Lidocaine may be used when the ectopic rhythm cannot be overdriven as in any rapid ventricular tachycardia. It is concluded that accelerated ventricular rhythm is a relatively common and benign complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time and the instances of two arrhythmias having common rate multiples suggest that accelerated ventricular rhythm may not always represent an escape phenomena but, at least in some instances, more likely an ectopic focus with varying degrees of exit block. ACKNOWLEDGMENT We thank

Mr. Manuel

Beckerman

for his art work.

REFERENCES 1.

2. 3. 4.

5.

6.

7.

a.

199

Lown B, Fakhro AM, Hood WB Jr, Thorn GW: The coronary care unit-new perspectives and directions. JAMA 199: 156, 1967. Katz LN, Pick A: Clinical Electrocardiography. I. The Arrhythmias, Philadelphia, Lea & Febiger, 1956. Rothfeld EL, Zucker IR: Non-paroxysmal ventricular tachycardia. Clin Res 15: 220. 1967. Rothfeld EL, Zucker IR, Parsonnet V, Alinsonorin CA: Idioventricular rhythm in acute myocardial infarction. Circulation 37: 203, 1968. Schamroth L: ldioventricular tachycardia. J Electrocardiol 1: 205, 1968. Bashour FA, Jones E, Edmondson R: Cardiac arrhythmias in acute myocardial infarction. II. Incidence of common arrhythmias with special references to ventricular tachycardia. Dis Chest 51: 520. 1967. Logic JR, Morrow DH, Gatz RN: ldioventricular tachycardia complfcating experimental myocardial infarction. Dis Chest 56: 477, 1969. Spawn JF, Moellering RC, Haber E, Wheeler EO: Arrhythmias in acute myocardial infarction. N Engl J Med 271: 427, 1964.

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Raftery EB, Rehman MF. Banks DC, Oram S: Incidence in management of ventricular arrhythmias after acute myocardial infarction. Br Heart J 31: 273, 1969. Castellanos A Jr, Lemberg L, Arcebal AG: Mechanism of slow ventricular tachycardia in acute myocardial infarction. Dis Chest 56: 470, 1969. Norris RM, Mercer CJ, Yeates SE: ldioventricular rhythm complicating acute myocardial infarction. Br Heart J 32: 617, 1970. Schamroth L: Genesis and evolution of ectopic ventricular rhythm. Br Heart J 28: 244, 1966. Singer DH, Lazzara R, Hoffman BF: Interrelationships between automaticity and conduction in Purkinje fibers. Circ Res 21: 537, 1967. Scherf D, Cohen J: The Atrioventricular Node and Selected Cardiac Arrhythmias, New York, Grune & Stratton, 1964, p 198. Konecke LL, Knoebel SB: Non-paroxysmal junctional tachycardia complicating acute myocardial infarction. Circulation 45: 367, 1972. Schamroth L: ldioventricular tachycardia. Dis Chest 56: 466, 1969.