J. ELECTROCARDIOLOGY 20(2), 1987, 98-109
Natural Course of Electrocardiographic Components and Stages in the First Twelve Hours of Acute Myocardial Infarction BY ELIEZER KLAINMAN,M.D., SAMUELSCLAROVSKY,M.D., RUBEN F. LEWIN, M.D., ON TOPAZ, M.D., HANAN FARBSTEIN, PH.D., AVRAHAMPINCHAS, M.D., LION FOHORILES, M.D. AND JACOB AGMON, M.D.
SUMMARY Time course evolution of R, Q, T and ST components of the electrocardiogram during the first 12 hours of an acute myocardial infarction was studied. A comparison between anteriorextensive and anteroseptal wall infarctions (anterior group), and inferior-extensive and inferior wall infarction (inferior group) showed appearance of significant Q waves within two hours in both groups. R wave loss was nearly a mirror image of Q wave development in both groups. T waves became negative and ST more isoelectric earlier in the inferior than in the anterior group. When combined variations of the four electrocardiographic components were analyzed, four stages of acute infarction were delineated. Stage I--tall R, no Q, ST elevation and positive T; Stage IIDsignificant Q wave appearance; Stage IIIDnegativlty of T waves; and Stage IV-ST isoelectric. The inferior group reached stages III-IV within 12 hours; the anterior group remained mostly in stage II. An early appearance of Q waves correlated well with rapid progression to stages III-IV within 12 hours in both infarction groups.
rately in four types of acute MI. We then classify the consecutive ECG changes at various stages and follow them in the different types of acute MI. We were interested only in the electrocardiographic course of the various types of MI, regardless of other factors such as enzymatic levels or hemodynamic factors.
The natural evolution of the electrocardiographic (ECG) changes occurring during the first hours of an acute myocardial infarction (MI) is of great importance, since the ECG recording may serve as a simple, non-invasive and inexpensive method of clinical follow-up. In addition, the dynamic ECG changes occurring during the development of MI may be of great importance in the study of its natural course and even of its prognosis. Previously authors have described the ECG changes occurring in the first hours of MI. 1-16 Generally, they have dealt with the natural evolution of the ST segment. Few authors have considered the components of the QRS complex separately or along with the ST segment, m.12,14,~6 In our study we follow the development of R waves, Q waves, ST segments and T waves sepa-
MATERIALS AND METHODS We studied 58 consecutive patients (47 men and 11 women, mean age 58 - 7.4 years) who were hospitalized from 1978-1982 in the Coronary Care Unit (CCU) with a first acute MI. The study was done in the hyperacute phase. It included ST elevation, Q waves of less than 2 mm in depth and high peaked T waves. The diagnosis of acute MI was established when the clinical course along with the typical enzymatic curve (creatine kinase, serum glutaminase, oxalic transaminase, lactic dehydrogenase) followed the development of Q waves. Patients with cardiomyopathy, valvular heart disease or previous conduction disturbances were excluded. Patients who demonstrated uncontrolled sinus tachycardia above 100 per minute or bradycardia under 60 per minute were also excluded in order to prevent the influence of those factors on ECG changes. All 58 patients'included in this study demonstrated the hyperacute phase (or Phase I) as defined further. They were classified into four types of AMI:
From the Israel and Ione Massada Center for Heart Diseases, Beilinson Medical Center, Petah Tikva and the Tel Aviv University Sackler School of Medicine, Tel Aviv, Israel, and the Department of Bio-Statistics,Hebrew University,Jerusalem. Reprint requests to: J. Agmon,M.D., MassadaCenter for Heart Diseases, BeilinsonMedicalCenter, Petah Tikva 49100, Israel. 98
NATURAL
ELECTROCARDIOGRAPHIC
COURSE
OF AMI
99
TABLE I Relationship of Q, R, ST, T and Q/R components to t (time) course in the four types of MI Type of MI Anterior Extensive AnteroSeptal Inferior Extensive
O(t) O = 7.3t °6
R(t)
ST(t)
R = 22.4t -°5
ST = 16.1t -°35
R2 = 0.9616
R2 = 0.9710
Q = 2 . 7 t °8 R2 = 0.9680
R = 14t -°s4 R2 = 0.9449
O=3t
°49
R=
R2 = 0.9123
1.3t+
21.7
T(t)
R2 = 0.9178 S T = 1 3 . 2 t -°4~ R2 = 0.8122 ST=16.6e
-°~7'
R2 = 0.9290
O/R(t)
T = 3 5 . 5 t -°42
O/R = 0.5t -
R2 = 0 . 8 2 3 1
0.5
R2 = 0.9463
T = 21t -°64 R2 = 0.9194
Q/R = O.5t - 0.3 R2 = 0.9469
T=-9.51nt+
22.5
R2 = 0.9075
O/R=O.lt-0.1 R2 = 0.8462
R2 = 0.9286 Infenor
Q=3.9t
°4,
R2 = 0.9626
R=-OAt+ 15.8 R2 = 0.8762 R = 1 6 e -°°3~ R2 = 0.8822
Abbreviations:
ST=O.3t+6.2
T=-6.51nt+
R2 = 0.7042
R2 = 0.7704
S T = 6 . 4 e -°86~ R2 = 0.5844
T = -1.8t
17.5
Q/R=O.lt+0.2 R2 = 0.9764
+
19
R2 = 0.9580
M I = ( a c u t e ) m y o c a r d i a l i n f a r c t i o n , (t) = t i m e .
1) Anterior-Extensive MI (ST elevation in VI-V~, Ll and avL)--13 patients, 12 men, one woman--mean age 61 _ 8.3 years. 2) Antero-Septal MI (ST elevation in VI-V4, or at least in V2-V3)--11 patients, 10 men and one woman--mean age 58 - 10.2 years. 3) Inferior MI (ST elevation in L2, L3 and avF)--17 patients, 11 men and six women--mean age 56 - 7.8 years. 4) Inferior-Extensive MI (ST elevation in L2, L3, avF and Vs-V6)--17 patients, 14 men and three women--mean age 59 - 9.5 years. A continuous 12-lead electrocardiographic follow-up during the first 12 hours post admission to the CCU was carried out by a three-channel electrocardiograph. During the first three hours recordings were taken every 1530 minutes, and then hourly. We started our recordings during the hyperacute phase, before Q waves were noted, and not more than two hours after onset of pain. The amplitudes of Q and R waves were measured in mm (1 mV = 10 mm) from the isoelectric line (=TP segment, arbitrarily). The height of the ST segment was measured 0.06 seconds after the end of the QRS complex. The height of the T waves was measured at the highest point if the T wave was positive or at the lowest point if negative. When the T waves were biphasic, we measured both the highest point of the positive part of the T wave, mentioned in a positive value, and the lowest point of the negative part of it, mentioned in a negative value, and the sum of both measurements was calculated. Those measurements were taken from the chest leads V1-Vs in the patients who had Anterior-Extensive MI; from leads V2-V3 in patients with Antero-Septal MI; from L2, L3 and avF for Inferior and Inferior-Extensive MI. We define the quantities Rm, Qm, STm and Tm as the mean sum of each component in each type of MI, according to the specific leads which reflected the damaged area. As an example of calculation:
J. E L E C T R O C A R D I O L O G Y
20(2), 1 9 8 7
2; Q m =
2; qp, + 2; Qp2 + ... 2; Qp. n
where 2; Qpl means the sum of Q waves in all the leads reflecting the damaged area in patient one according to the type of MI; 2; Qp2 for patient two, and so on. According to the development of the four components (Q, R and T waves and S T segment) we divided the electrocardiographic evolution into consecutive stages of the AMIStage I) Hyperacute phase---increaseof R waves' height, S T segment elevation and positive T waves, with Q waves not deeper than 2 ram. Stage II) The appearance of Q waves deeper than 2 m m while S T segments are stillelevated and the T waves are stillpositive. Stage III)T waves become biphasic or negative,Q waves become deeper, and S T segments are stillelevated. Stage IV) S T segments return to the isoelectriclevel and the T waves remain negative. This division was based also upon our former clinical experience. Statistical Analysis
For each of the four functions, Q(t), R(t), ST(t) and T(t) and the relationship o f ~ (t) we used the least squares method to input the appropriate mathematical function. This was done for each type of infarct separately. Several functions were examined in order to get good results as judged by both high values of R 2 and minimal number of different functions, thus enabling comparison between different infarcts. The results are summarized in Table I. (For the sake of comparison we fit two functions to the inferior infarct). Note that most of the R ~ values are higher than 0.9. In order to compare the four infarcts by the stages data (refer to the former paragraph) we grouped the four stages
100
KLAINMAN
ET AL
TABLE II Relationship of Q, R, ST and T components to t (time} course in the two unified subgroups of MI Subgroup of MI
Q(t)
R(t)
ST(t)
T(t)
Anterior
Q = 2.0t + 4 R2 = 0 . 9 8 2 6
R = - 1 . 3 t + 17.5 R2 = 0 . 7 7 0 3
ST = - 0 . 8 t + 12.1 R2 = 0 . 8 6 6 6
T = 1.9t + 27.1 R2 = 0 . 8 4 8 3
(Extensive & Septal)
Q = 5.1 t ° 7 R~ = 0 . 9 8 2 9
R = 18.3t -° s R2 = 0 . 9 7 4 4
ST = 1 2 . 4 t - ° 4 R2 = 0 . 9 2 5 5
T = 28.2t -° s R2 = 0 . 8 9 3 2
Inferior
Q = O.7t + 3 . 5 R~ = 0 . 9 0 3 3
R = -O.8t + 6 R2 = 0 . 9 6 5 6
ST = - 0 . 8 t + 10.3 R2 = 0 . 8 7 6 4
T = - 2 . 1 t + 21.1 R2 = 0 . 9 6 6 7
(Inferior & Inferior-Extensive)
Q = 3 . 5 t °5 R2 = 0 . 9 7 7 1
R = 1 9 . 6 e -°°6' R2 = 0 . 9 4 8 7
ST = 11.3e - ° 13, R2 = 0 . 9 1 1 0
T = 3 7 . 9 e - ° 27, R2 = 0 . 9 0 0 1
those 12 hours post admission, we used the Fisher exact test.
into two categories; the first two stages comprising the first category, the last two, the second category. The resulting frequencies for the three time points, 4 hours, 6 hours and 12 hours, are presented in Tables IIIa and IIIb. In each time point we used the Fisher exact test to compare and to stress similarity between the two anterior and the two inferior infarcts. The results of the same test and the relevant frequencies for comparison between the combined groups of anterior MI and inferior MI are shown in Table IV. In order to measure the dependence between stages in the first period of the MI (first one or two hours) and
RESULTS Figs. 1-8 show the d e v e l o p m e n t of Z Qm, 2; Rm, S T m , and 2; T m for the four types of AMI investigated. Extensive Anterior MI Evolution Q waves evolved rapidly during the first two hours and became deeper during the n e x t ten hours at a
TABLE Ilia Comparison of Anterior-Extensive MI with Antero-Septal MI by the stages data Time Point t=4h Stage of MI
t=6h
I-II
Ill-IV
I-II
11 (84.6%)
2 (15.4%)
12 (92.3%)
10 (90.9%)
1 (9.1%)
9 (81.8%)
t= Ill-IV
12h
I-II
Ill-IV
Total
1 (7.7%)
9 (69.2%)
4 (30.8%)
13 pts
2 (18.2%)
8 (72.7%)
3 (27.3%)
11 pts
Type of MI Anterior Extensive AnteroSeptal Pvalue
1.0
0.5761
1.0
TABLE IIIb Comparison of Postero-Lateral MI with Inferior MI by stages data Time Point t=4h Stage of MI
t=6h
t=
12h
I-II
Ill-IV
I-II
Ill-IV
I-II
Ill-IV
Total
13 (76.5%)
4 (23.5%)
11 (64.7%)
6 (35.3%)
4 (23.5%)
13 (76.5%)
17 pts
11 (64.7%)
6 (35.3%)
9 (52.9%)
8 (47.1%)
6 (35.3%)
11 (64.7%)
17 pts
Type of MI Infenor Extensive Inferior P value
0.7080
0.7283
0.7080
J. ELECTROCARDIOLOGY 20(2), 1987
NATURAL ELECTROCARDIOGRAPHIC COURSE OF AMI
101
mm
40
Ant. Ext. MI (V I - V 6)
50-
A n t . - Ext.Ml (V 1 - V 6)
=ERmI.SD
30-t
~EQm'-
=ETm
,~-STmJ ±SD
/ 40-
==Tm 30.
20-
2010-
~ =EQm 0 'i
10-
:2 ~1 ~ 5 6 "/ ~ ~ 101~1l~ZHours
Fig. 1. Time course evolution of R and Q waves in anterior extensive (Ant. Ext.) acute myocardial infarction (MI) in millimeters (ram). Note the mirror image between the two line drawings. Between bars _+standard deviation (SD). fairly rapid rate (Fig. 1). R waves show a sharp decrease in amplitude within the first five hours and then decline more gradually until they reach a minimal level at the end of 12 hours (Fig. 1). A sharp decline in the height of the T waves and a more gradual decline of the ST segments are observed in the first five hours. (Fig. 2. Consider also the magnitude of the corresponding exponents in Table I, first line.) Then, a secondary elevation of those components is noted, followed by a further slighter decline. At the end of 12 hours the T waves remained positive and the ST segments were still elevated above the isoelectric level (Fig. 2). Anteroseptal MI Evolution A fast development of Q waves is seen during the first hour. Q waves progress less rapidly during the next five hours, after which their development tends to stabilize (Fig. 3). Also the decline in R wave height is rapid during the first five hours, and then tends to stabilize by the 12th hour (Fig. 3). The T waves show a sharp decline in their amplitude during the first five hours while the ST segments show a slower decline (Fig. 4). Following this, both the T waves and ST segments decrease more gradually; however, the T waves continue to remain positive and ST segments are still elevated (Fig. 4).
J. ELECTROCARDIOLOGY20(2), 1987
0' ,~ ~ ~ ~ ~ ~ ~ ~ ~ 1~)1a11~Hours Fig. 2. Time course evolution of T and ST segment in anterior extensive (Ant. Ext.) acute myocardial infarction (MI) in millimeters (mm). Between bars + standard deviation (SD). Extensive-inferior MI Evolution Q waves evolve more slowly than in anterior infarctions during the first five hours and then stabilize to a plateau (Fig. 5). The relevant exponents of t for the two infarcts are 0.8 for anteroseptal and 0.5 for posterolateral (Table I). Changes in R waves mm 2018-
Ant.- Sept. MI ( V 2 - V 3) ~ERm
1412- R m ~ 108. 60 i 2 ~ 4 g g 7 ~ ~ 101~1 1~' Hours Fig. 3. Time course evolution of R and Q waves in anteroseptal (Ant. Sept:) acute myocardial infarction (MI) in millimeters (ram). Note the mirror image between the two line drawings. Between bars _ standard deviation (SD).
102
KLAINMAN ET AL
mm ~
Ant.-Sept.
26.
MI
(V 2 -V3)
\+
=ETm =ESTm)- SD
22-
mm 24-
Inf. E x t .
MI
22- r l 20- V=\T
(T[,1T[, avF) ~ERm/+
18161412108.
18" 14-
,o.
6 jA
6-
I-'I
4. 2.
•
l
I
I
I
I
(SD). are more prominent during the first four hours, then tend to stabilize for the next two hours. We observed further descent in R wave height until the last two hours of the follow-up period. Their level remains quite low at this time (Fig. 5). The T wave decline was sharp during the first eight hours of follow-up and then became negative. The magnitude of the ST segments decreased very slightly during the first three hours, and then decreased quite drastically until the seventh hour and stabilized near the isoelectric line at 12 hours of evolution (Fig. 6). Inferior MI
O
I
1 ;3 + ' + ' 12 Hours Fig. 4. Time course evolution of T and ST segments in anteroseptal (Ant. Sept.) acute myocardial infarction (MI) in millimeters (mm). Between bars _+ standard deviation
Evolution
The evolution of Q waves in the first two hours is fast, becoming more gradual later, and stabilizing during the last two hours of follow-up. The decline in R-wave height is moderate and very gradual during the first ten hours, and then tends to stabilize at the same level. R-waves remained high at the end of 12 hours of follow-up (Fig. 7), in contrast to patients with anterior MI. To stress this point, we note the rate of decrease for the anterior MI estimated as e -°-5 as opposed to e -°'°3 for the inferior MI. T waves remained positive during the first three hours, decreasing rapidly afterwards and becoming negative by the ninth hour (Fig. 8). ST segments stay at the same level during the first three hours and then decrease gradually until they almost reach the isoelectric level at about the ninth hour. They become somewhat more elevated towards the 12th hour of follow-up (Fig. 8).
I
I
I
'
I
1 2
5
7
9 1 11 12 Hours
Fig. 5. Time course evolution of R and Q waves in inferior-extensive (Inf.-Ext.) acute myocardial infarction (MI) in millimeters (mm). Between bars - standard deviation (SD). Stages of Evolution in the Four Groups Among the 13 patients with Anterior-Extensive MI only one reached the fourth stage during the 12-hour observation. Three patients reached stage III, and the others remained in lower stages. One patient died after seven hours, while in stage I (Fig.
9). mrrl
~~Trn
2624- ~ 5:Trn 2220-
Inf. Ext. MI (]].,lit, avF) =ESTm} +-SD
1816-
141210-
86-
42'
=
'
'
Fig. 6. Time course evolution of T and ST segment in inferior-extensive'(InL-Ext.) acute myocardial infarction (MI) in millimeters (ms). Between bars _+ standard deviation (SD). J. ELECTROCARDIOLOGY 20(2), 1987
NATURAL ELECTROCARDIOGRAPHIC COURSE OF AMI
Stage .1~
mm
20 T_ :ER m 16 [ ~ ~ _
1 2 3 4 5 6 7 8 9 1()li 12Hours Fig. 7. Time course evolution of R and Q waves in inferior (Inf.) acute myocardial infarction (MI) in millimeters (mm). Between bars _ standard deviation (SD). Among the 11 patients with Antero-Septal MI most (seven patients) remained in stage II. Three patients reached stages III and IV during the 12hour observation, and one patient died after nine hours while in stage I (Fig. 10). In Table IIIa we present the frequencies of stages at three time points for easy comparison between the last two infarcts. Among the 17 patients with Inferior-Extensive MI four patients remained at stage II and all others (13 patients) reached stages III and IV within the 12-hour observation. No patient died (Fig. 11). Consider also Table IIIb. Among 17 patients with Inferior MI only four remained in stage II at the end of the follow-up:
Inf. MI
20 T
(IT, m-, vF)
16
Ant.-Ext. MI
Inf. MI (I],111 ,avF) =ERm~ + S D
4 (=EQm
mm
103
STm - SD
Fig. 9. Time course evolution of acute myocardial infarction (MI) stages in patients with extensive anterior (Ant. Ext.) MI. six patients reached stage IV and the rest, stage III. No patient died (Fig. 12). Comparison of Infarcts Types Comparison between the four types of infarcts is based on the two sets of data which were analyzed, namely the functions Q(t), R(t), ST(t), T(t) and the data on stages. Thus, our conclusions are based on two different methods of analysis. For the Q waves, a power function was fitted in all four infarcts and examination of the estimated curves in Table I shows a faster rate of change in time (as measured by b) in both anterior infarcts as compared to inferior ones. The R waves revealed different patterns of evolution in time, a power function for the two anterior infarcts and a linear function for the two inferior infarcts. The rate of change in time (as measured by b) was similar for the two anterior infarcts. Examination of the results from the T waves also showed the same pattern in both anterior infarcts Stage
w'-
Ant.- Sept. MI (11 Pts.)
12 =ETrn 11[8. ]I-
4.
I-
0 ,;
~ ~ ~ ~ ~ 7 8. . 9 . . ~
.e
Hours 1~2
Fig. 8. Time course evolution of T and ST segment in inferior (Inf.) acute myocardial infarction (MI) in millimeters (mm). Between bars __ standard deviation (SD). J. ELECTROCARDIOLOGY20(2), 1987
3 ,~ 5
6
7
~
~ lb 1~ 12Hr.
Fig. 10. Time course evolution of acute myocardial infarction (MI) stages in patients with anteroseptal (Ant. Sept.) MI.
104
KLAINMAN ET AL
Stage
Inf. Ext. Mi
I"
~i1~52
3 4
5
t~
"7
8
~)10
(power function) and a different pattern in the inferior group. Based on the above results we consider the anterior infarcts as one group and the inferior infarcts as another. In order to further validate the grouping, we analyzed the data Q of the ratio - ( t ) for the four infarcts, assuming that this ratio R is a meaningful parameter in itself. The results, which are presented in Table I, support our grouping: a linear function was fitted successfully (consider the high values of R 2 in Table I) to all four infarcts and the coefficient of t is similar in the two anterior infarcts (0.5) as well as in the two inferior infarcts (0.I). Based on the above results, we grouped the data and repeated the analysis for the two new groups. The new results are presented in Table II. The values of R2were generally higher than before the subgrouping was done for almost all functions in both groups. This fact is explained by a correct Stage
.]3Z-
1~1 12Hr.
Fig. 11. Time course evolution of acute myocardial infarction (MI)stages in patients with inferior-extensive (Inf.Ext.) MI.
grouping in which the larger numbers produced a better fit. We also give the linear fit of R(t), ST(t) or T(t) in the anterior infarction group for the sake of parametric comparison with the inferior groups. The other set of data we used for the comparison was that of the aforementioned four stages (Tables IIIa and IIIb). In each of the three points in time (4, 6, and 12 hours) the two anterior infarcts behaved very similarly (Table IIIa) as well as the two inferior infarcts (Table IIIb). The similarity is apparent on inspection and demonstrated by the high P-values of the Fisher exact test (last line in each table). In addition, Fig. 13 shows the mean evolution of stages in the four types of MI. The significant difference between the anterior infarcts and inferior infarcts is apparent. The resulting frequencies, together with the corresponding test of comparison, are presented in Table IV. The difference between the two groups (higher proportions of stages III and IV in the inferior
Inf. MI
(17 Pts.)
m_
I-
4
S 6
?
8
9 10 1"I 12Hr.
Fig. 12. Time course evolution of acute myocardial infarction (MI) stages in patients with inferior (Inf.) MI. J. ELECTROCARDIOLOGY 20(2), 1987
NATURAL ELECTROCARDIOGRAPHIC COURSE OF AMI
STAGE
105
sion for the anterior infarcts, and in the second hour for the inferior infarcts. For example, in Table Va we note that all eight patients who stayed at stage I after the first hour of follow-up remained at the low stages (I-II) after the 12th hour. Of the five patients who reached stage II after the first hour, only one remained at stage II, and all others reached stage III or IV. The electrocardiographic pattern of the other types of MI (Tables Vb, Via, b) is similar. This difference was found statistically significant in both groups.
/t I
/ /
DISCUSSION Development of Q waves and loss of R waves in the ECG recordings during the initial period of acute MI indicate myocardial necrosis, constituting an irreversible change in the infarcted myocardiurn. ls,2~.25The development of Q waves and reduction or loss of R waves occurs in the first hour after the onset of AMI. 19.26 According to the abovementioned findings in our study we can conclude that reversible injury, represented by ST segment elevation without Q waves, may change into irreversible injury indicated by the appearance of pathological Q waves and reduction of R waves. Such an event happens in the first hour after the onset of AMI. Therefore the hyperacute phase, in which no Q waves are present, is a quite accurate and well-established criterion for a starting point of follow-up, regardless of other subjective criteria such as onset of specific symptoms. In addition, according to Jennings ~° and Lefer, 27 we can expect an irreversible injury in all maximally ischemic cells up to 12 hours after occlusion of the coronary artery. Those reports support our 12-hour follow-up of AMI, though some authors demonstrated extension of myocardial necrosis in more than half of all patients after the first 12 hours from onset of AMI. 4,2s,29
///I / !
Fig. 13. Time course average development of stages of acute myocardial infarction in the four types: I = Inferior, P = Posterolateral, E = Anterior Extensive, S = Anteroseptal. Similarity is found for the two anterior (E and 8) and the two inferior (I and P) evolutions. subgroup) is significant at all time points. However, it is statistically significant at 6 and 12 hours (Pvalues of 0.02 and 0.003, respectively). Prediction of Electrocardiographic Course (Tables Va, b; Via, b) We studied the ability to predict the future course of ECG stages in a patient by his stage progression during the first one or two hours after admission. The stage of MI after 12 hours of admission may be inferred by the stage in the first hour of admis-
TABLE IV Comparison of Anterior MI (subgroup} to Posterior MI (subgroup} by stages data T~me Point t=4h Stages of MI Type of MI Anterior subgroup Inferior subgroup Pvalue
t=6h
t=12h
I-II
Ill-IV
I-II
Ill-IV
I-II
21 (87.5%)
3 (12.5%)
21 (87.5%)
3 (12.5%)
17 (70.8%)
7 (29.2%)
24 pts
24 (70.6%)
10 (29.4%)
20 (58.8%)
14 (41.2%)
10 (29.4%)
24 (70.6%)
34 pts
0.2019
J. ELECTROCARDIOLOGY 20(2), 1987
0.0216
Ill-IV
0.003
Total
106
K L A I N M A N ET AL
Tables V a - V l b : Dependence between stages in first or second hour and those after twelfth hour in the four types of M I TABLE Va Extensive Anterior Infarction
TABLE Vb Antero-Septal Infarction
Stages after 12th hour I-II Stage after 1st hour I 8(100%) II or more 1 (20%)
Ill-IV
0(0%)
Stages after 12th hour Total
I-II
8 P = 0.007
4 (80%)
5
The various findings regarding the time curve evolution of the R and Q waves and ST segment in AMI are controversial. Wikswo et al? ~ concluded that the rate of changes of QRS approached zero after 48 hours. Selwyn et al2 ,3t and Zymslinski et al? 2 have reported a rapid loss of R waves and development of Q waves, including completion of these processes in six hours. Selwyn et al. a also mentioned the complex relations between the development of Q waves and the natural history of ST segment elevation in the anterior MI. However, Askenazi 32and Henning et al? 3 provided data suggesting that in many patients a loss of R wave and Q wave changes proceeded for longer than 12 hours and were only completed at 24 hours. Inoue et al24 showed that in patients with inferior infarction, Q wave changes continued for as long as three days even in the absence of reinfarction. Poliwoda 35found that only 25% of his patients with AMI demonstrated maximal amplitude of the Q waves within one week. On the contrary, Thygesen et al. t have demonstrated that the development of Q waves begins within two hours of the onset of symptoms, and their average depth increases linearly up to 12 hours. The natural course of R wave loss fell almost linearly from three to 15 hours in an inferior MI. Thygesen ~ observed a significant correlation between the average amplitudes of the Q and R waves even after that "linear period" up to 48 hours of follow-up. However, his conclusion was that for evaluating the course of the infarction process, the loss of R waves during the first 24 hours is more significant than the Q waves' evolution. Some controversy also exists regarding the time course of ST segment elevation. Maroko et al. 2~and Madias and Wood, 22as well as Flaherty et al. 23have reported that ST segment elevation is stable and changes little in the first 24 hours. Thygesen et al.) Selwyn et al., 2 Zymslinski et al., 12 and Essen et al. 4
Stage after 1st hour I 8(100%) I1 or more 0 (0%)
Ill-IV
Total
0(0%)
8
3 (100%)
3
P = 0.0061
have shown that ST elevation is maximal in the first few hours and then rapidly declines considerably by 6 to 12 hours. They emphasized that the maximal ST elevation in inferior MI appears approximately two hours later than in the anterior MP (three hours versus one hour after onset of MI). Yusuf et al2 support both points of view. Their main conclusion was that infarct evolution is variable and was completed in some patients within four hours while in others it took as long as 48 hours, regardless of whether it was anterior or inferior MI. Furthermore, Yusuf and others 17,a~ reported that maximal ST elevation correlates well with final Q or R waves' amplitude. Since ST-elevation usually
TABLE Via Inferior-Extensive Infarction Stages after 12th hour I-II Stage after 2nd hour I 4 (50%) II or more 0 (0%)
Ill-IV
Total
4 (50%)
8
9 (100%)
9
P = 0.0294
TABLE Vlb Inferior Infarction Stages after 12th hour I-II Stage after 2nd hour I 6 (75%) II or more 0 (0%)
Ill-IV
Total
2 (25%)
8
9 (100%)
9
P = 0.0023
J. ELECTROCARDIOLOGY 20(2), 1987
NATURAL ELECTROCARDIOGRAPHIC COURSE OF AMI
reaches a maximum well before R wave loss and Q wave development are completed, maximum ST elevation may be used as a predictor of final R wave or A wave development. We divided our follow-up into two parts. Firstly, we studied for 12 hours the evolution of separate components--R, Q and T waves and ST segm e n t s - i n each type of AMI separately. Secondly, we followed the progression of the four stages of AMI from the combined evolution of the above four components in the same 12 hours. In general, we observed the appearance of significant Q waves (according to stage II definition) at the average time of the first two hours of onset of MI. The rate of deepening of the Q waves was faster in the anterior than in the posterior group, b u t the tendency towards stability was stronger in the posterior group. We can make no conclusion about the termination of the evolution of Q waves within the 12 hours of follow-up in any type of MI. Another interesting finding was that the earlier the Q waves appeared, the earlier the progression toward stages III and IV occurred. In other words, an early appearance of Q waves may indicate blood reperfusion in the infarcted area, supporting the study of Blumenthal et al27 who observed that significant Q waves appeared 15-30 minutes after release of occlusion of the coronary artery. In our clinical follow-up of the patients admitted to the CCU we observed a better early prognosis in those patients who progressed more rapidly to the late stages of III and IV. This was especially observed in patients with inferior MI and in some patients with anterior MI. However, this subject needs further and more intensive investigation. Regarding the decline of R waves, we observed an almost mirror image in the Q waves deepening in all types of MI. Here also we cannot come to a conclusion about termination of the R waves' decline, even though there is some stabilization in the last hours of follow-up. The decline of R waves in the anterior MI group was sharper and of much smaller size than in the inferior MI group at the end of follow-up. It seems that there is no difference regarding electrocardiographic stabilization of the R versus Q wave components within the first 12 hours of onset of MI. The function Q (t), shown in Table I, supports this conclusion and also emphasizes the difference between anterior and inferior MI's. We can observe the similarity in development of the two anterior infarcts as well as the two inferior MI's (a -- 0.5 in J. ELECTROCARDIOLOGY 20(2), 1987
C) the function of ~ (t) in both anterior MI's, and
107
a
0.1 in both posterior MI's). Regarding T wave dynamics during the natural course of AMI, reports in the literature are scarce. We observed here a significant difference in the evolution of this component in the anterior versus the inferior group of infarctions. A sharp decline of T waves' height is demonstrated in the first five hours in the two anterior MI's. There is then a more gradual decline, but at the end of the 12 hours of follow-up the T waves still remain positive in their mean value, unlike those in the two inferior MI groups in which they become negative in the eighth or ninth hour from onset of MI. The importance of the T-component is that its negativity defines a later new stage of the acute MI development, while T waves almost always become negative after the appearance of Q waves, defining the third stage of AMI. Differences between the anterior and inferior group regarding T waves' development still exists, while the similarity of the two anterior MI's as well as the two inferior MI's is also demonstrated. The two inferior infarctions tend to progress towards the third stage of MI (and even more) during the 12 hours of follow-up, while anterior infarctions remain in stage II, in most cases (significant Q waves with positive T waves). The dynamics of ST segments is of great importance, since their elevation started in the very initial stage of AMI, and their return to the isoelectric level occurs at the final fourth stage of the AMI and defines this stage. Our observation indicates a significant dynamic of the ST segment in all four types of AMI, even within the first 12 hours. It should be noted that in the inferior MI, ST segment stability was seen together with its gradual return almost to the isoelectric level; then it re-elevated towards the end of the follow-up. The other types of MI showed a sharp decline of the ST segment, with a relatively greater decline in the inferior-extensive MI, in which this segment became very close to the isoelectric level, i.e., reached stage IV of AMI. In the anterior MI's, the level of ST remained at a higher level than in the inferior MI's. Though a significant decline in the ST segment is demonstrated, there were no returns to the isoelectric level in any individual case before the T waves became negative. Therefore, the return of ST to the isoelectric level can define a later stage of AMI than inverted T waves. We followed the evolution of the four stages of MI as defined above, in the first 12 hours in each
108
KLAINMAN ET AL
type of MI. Once more a significant difference was found between the anterior and the inferior infarctions, while the evolution of stages in both anterior extensive MI as well as antero-septal MI are similar. When the two anterior infarctions remained in the second stage, the inferior infarctions demonstrated progression to the third and even fourth stage within the 12 hours of follow-up. In conclusion, anterior and inferior infarcts behave differently regarding the time course of R, Q, T and S T components of the ECG during the first 12 hours of evolution. Arrangement of the ECG components' evolution according to stages was found helpful in differentiating between anterior and inferior groups. REFERENCES I. TRYGESEN, K, HORDER M, NIELSEN, B L AND PETERSEN, P H-" Evolution of S T segment and Q and R waves during early phase of inferior myocardial infarction. Acta M e d Scand 205:25, 1979 2. SELWYN,A P, OGUNRO,E A ANDSHILLINGFORDJ P: Natural historyand evaluationof ST segmentchanges and MB-CK release in acute myocardial infarction. Br Heart J 39:988, 1977 3. SELWYN,A P, Fox, K, "~VELMAN,E ANDSHILLINGFORD, J P: Natural history and evaluationof Q wavesduring acute myocardialinfarction. Br Heart J 40:383, 1978 4. ESSEN,R V, MERX, ~,VAND EFFERT, S: Spontaneous course of ST segment evaluation in acute anterior myocardial infarction. Circulation 59:105, 1979 5. YUSUF, S, LOPEZ,R, MADDISON,A AND SLEIGHT,P: Variability of electrocardiographic and enzyme evolution of myocardial infarction in man. Br Heart J 45:271, 1981 6. NIELSEN,B L: ST segment elevation in acute myocardial infarction: prognostic importance. Circulation 48:338, 1973 7. WILSON, C AND PANTRIDGE, J F: ST segment displacement and early hospital discharge in acute myocardial infarction. The Lancet 2:1284, 1973 8. BRAUNWALD,E ED: Protection of the ischemic myocardium. Circulation 53(suppl I):I-1, 1976 9. THYGESEN,K, HORDER,M, NIELSEN,B L AND PETERSEN, P H: The variability of ST segment in the early phase of acute myocardialinfarction. Acta Med Scand (supp) 623:61, 1979 I0. MAROKO,R R, LIBBY,P, COVELL,J W, SOBEL,B E, ROSS, J ANDBRAUNWALD,E" Precordial ST segment elevation mapping: an atraumatic method for assessing alterations in the extent of myocardial ischemic injury. Am J Cardiol 29:223, 1972
11. REID,P R, TAYLOR,D R, KELLY,D T, ~VEISFELDT, M L, HUMPHRIES,J O, Ross, R S ANDPITT,B: Myocardial infarction extension detected by precordial ST segment mapping. N Engl J Med 290:123, 1974 12. ZMYSLINSKI,R W, AKIYAMA,T, BIDDLE, T L AND
13.
14.
15.
16.
SHAN, P M: Natural course of the ST segment and QRS complex in patients with acute anterior myocardial infarction. Am J Cardiol 43:29, 1979 CAPONE, R J AND MOST, A S: The single precordial lead for ST segment monitoring: comparison with the multiple lead map. Am Heart J 97:753, 1979 MIRVlS,D M: Electrocardiographic QRS changes induced by acute coronary ligation in the isolated rabbit heart. J Electrocardiol 12:141, 1979 MAROKO,P R, KJEKSHUS,J K, SOBEL,B E, WATANABE, T, COVELL,J W, Ross, J, JR AND BRAUNWALD, E: Factors influencing infarct size following experimental coronary artery occlusion. Circulation 43:67, 1971 RAKITA, L, BORDUAS, J L, ROTHMAN, S AND PRINZMETAL,M: Studies on the mechanism of ventricular activity. XII. Early changes in the RS-T segment and QRS complex following acute coronary artery occlusion. Experimental study and clinical applications. A Heart J 49:351, 1954
17. YusuF, S, LOPEZ,R, MADDISON,A, MAW,P, RAY,N, McMILLAN,S AND SLEIGHT,P: Value of electrocardiogram in predicting and estimating infarct size in man. Br Heart J 42:286, 1979 18. HILLIS,L D, ASKENAZI,J, BRAUNWALD,E, RADVANY, P, MULLER,J E, FISHBEIN,M C AND MAROKO,P R: Use of changes in the epicardial QRS complex to assess interventions which modify the extent of myocardial necrosis following coronary artery occlusion. Circulation 54:591, 1976 19. ESSEN,R V, MERX,W, DOERER,R, EFFERT,S, SILNY, J ANDRAU, G: QRS mapping in the elevation of acute anterior myocardial infarction. Circulation 62:266, 1980 20. JENNINGS,R B: Early phase of myocardial ischemia and infarction. Am J Cardiol 24:753, 1969 21. MAROKO,P R, DAVIDSON,D M, LIBBY,P, HAGAN,A D AND BRAUNWALD,E: Effects of hyaluronidase administration on myocardial ischemic injury in acute infarction. Ann Intern Med 82:516, 1975 22. MADIAS, J E AND WOOD, W B, JR: Precordial ST segment mapping. 3. Stability of maps in the early phase of acute myocardial infarction. Am Heart J 93: 603, 1977 23. FLAHERTY,J T, REID, P R, KELLY,D T, TAYLOR,D R, WEISFELDT,M L ANDPITT, B: Intravenous nitroglycerin in acute myocardial infarction. Circulation 51:132, 1975 24. MULLER,E J, MAROKO,P R AND BRAUNWALD,E: Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemie injury. Circulation 52:16, 1975 25. SAVAGE, R M, WAGNER, G S, IDEKER, R E, PODOLSKY, S A AND HACKEL, D B: Correlation of postmortem anatomic findings with electrocardiographicchanges in patients with"myocardial infarction:retrospective study of patients with typical anterior and posterior infarcts.Circulation 55:279, 1977 J. ELECTROCARDIOLOGY 20(2), 1987
NATURAL ELECTROCARDIOGRAPHIC COURSE OF AMI
26. SELWYN,A P, Fox, K M, WELMAN,E, JONATHAN,A AND SHILLINGFORD, J P: Electrocardiographicprecordial mapping in anterior myocardial infarction. The critical period for interventions as exemplified by methylprednisolone. Circulation 58:892, 1978 27. LEFER, A M: Physiologic mechanisms in acute myocardial infarction. In Cardiovascular clinics 7/2 innovations in the diagnosis and management of acute myocardial infarction. A N Brest, ed. F A Davis, Philadelphia, 1975, pp 25-37 28. FLAHERTY,J T: Clinical uses of precordial ST segment mapping and the pathophysiology of ST segment voltage changes. Circulation 53(suppl I):l, 1976 29. HOOD, W B: ST segment mapping in ischemia and infarction. Circulation 53(suppl I):l, 1976 30. WIKSWO,J P, GUNDERSEN,S C, MURPHY,W, DAWSON, A K AND SMITH, R F: Segmental QRS vector subtractions in acute myocardial infarction in humans. Circulation Research 49:1055, 1981 31. SELWYN, A P, OOUNRO, E AND SHILLINGFORD,J P: Loss of electrically active myocardium during anterior infarction in man. Br Heart J 39:1186, 1977
J. ELECTROCARDIOLOGY 20(2), 1987
109
32. ASKENAZl,J, MAROKO,P R, LESCH,M ANDBRAUNWALD,E: Usefulnessof ST segmentelevationsas predictors of electrocardiographic signs of necrosis in patients with acute myocardial infarction. Br Heart J 39:764, 1977 33. HENNINO,H, HARDARSON,T, FRANCIS,G, O'ROUKE, R A, RYAN, IV, ROSS, J, JR: Approach to the estimation of myocardialinfarct size by analysis of precordial ST-segmentand T wave maps. Am J Cardiol 41:1, 1978 34. INOUE,M, HORI,M, FUKUI,S, ABE,H, MINAMINO,T, KODAMA,K ANDOHGITANI,N" Evaluation of evolution of myocardialinfarctionby serial determinations of serum creatine kinase activity. Br Heart J 39:485, 1977 35. POLIWODA, H" The thrombolytic therapy of acute myocardial infarction. Angiology17:528, 1966 36. BLUMENTHAL,~VR, WANG,H ANDLIU,M P: Experimental coronary arterial occlusion and release: effects on enzymes, electrocardiograms, myocardial contractility and reactive hyperemia.Am J Cardiol 56:225, 1975