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Body surface isopotential maps in old inferior myocardial infarction undetectable by 12 lead electrocardiogram
J. ELECTROCARDIOLOGY 17 (1), 1984, 55-62
Body Surface Isopotential Maps in Old Inferior Myocardial Infarction Undetectable by 12 Lead Electrocardiogram BY JUNICIII OSUGI, M.D., TOSIIIKI OHTA,M.D., JUNJI TOYAMA,M.D., FUMIMARO TAKATSU, M.D., TERUO NAGAYA, M.D. AND KAZUO YAMADA, M.D.
SUMMARY The purpose of this study is to examine the value of body surface isopotential maps in the diagnosis of old inferior myocardial infarction t h a t can not be diagnosed by 12 lead ECG. Forty-three patients with a Q wave of at least 0.02 sec but less than 0.04 sec in width and also less than 25% of the R wave in depth in lead aVF of the 12 lead ECG were selected for this study. The patients were divided into infarction and noninfarction groups based on their clinical histories and cardiac catheterization data. The infarction group showed characteristic surface maps with a minimum which moved from the left posterior chest to the lower back or from the lower back to the right anterior lower chest in the early phase of QRS. The noninfarction group exhibited a minimum which shifted from the back to the right upper chest or from the left anterior chest to the lower back in the same phase. Thus, both groups were clearly distinguishable from each other by the positional change of the minimum in the early phase of QRS. This study suggested that body surface maps contain diagnostic information concerning the presence or absence of inferior myocardial infarction which is not easily available from the 12 lead ECG. Inferior myocardial infarction is diagnosed by the appearance of new Q waves and ST elevation in leads II, I I I and aVF of the 12 lead ECG in the early stage of infarction. However, diagnosis of inferior infarction is often difficult or impossible in its late stages because of the disappearance of abnormal Q waves. In addition, Q waves suggestive of infarction are occasionally observed in leads II, I I I and aVF in cases with no history of myocardial infarction. Thus, one of the major problems of the 12 lead ECG is g e t t i n g an accurate diagnosis of the presence or absence of old inferior myocardial infarction.
On the other hand, it has been reported t h a t body surface isopotential maps are useful in the diagnosis of myocardial infarction. 1~ Recent clinical studies reported t h a t body surface isopotential maps contain useful information for the diagnosis of old inferior myocardial infarction which is not easily obtainable from the 12 lead ECG. In this study, we a t t e m p t e d to clarify whether or not it is possible to differentiate relatively inconspicuous Q waves of old inferior myocardial infarction from Q waves in cases without infarction by comparing body surface isopotential maps of cases with angiographically proven inferior myocardial infarction and of cases without left ventricular asynergy.
From the Department of Respiration and Circulation, Research Institute of Environmental Medicine, Nagoya University, Furo-Cho, Chikusa-Ku, Nagoya 464, and Anjo Kosei Hospital, Anjo 446, Japan. This work was supported by Research Grant for Cardiovascular Diseases 56 C-9 from the Ministry of Itealth and Welfare and Grant-in-Aid for ScientificResearch (56480178) from the Ministry of Education of Japan. The costs of publication of this article were defrayed in part by.the payment of page charges. This article must therefore be hereby marked "Advertisement" in accordance with 18 U.S.C. w1734 solely to indicate this fact. Reprint requests to: Toshiki Ohta, M.D., Division of Respiration and Circulation, Research Institute of Environmental Medicine,Nagoya University, Fur~Cho, Chikusa-Ku, Nagoya 464, Japan.
MATERIALS AND METHODS Among 500 consecutive cases who had undergone both selective coronary arteriography and left ventriculography, the following two groups of patients were selected for this study. The infarction group was composed of 24 patients (20 male and four female; mean age 59.6}. The time elapsed from the onset of infarction ranged from three months to 3.5 years. These patients satisfied all of the following criteria: (D Right coronary artery {RCA) and/or left circumflex
55
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Body surface isopotential maps were recorded no more than 24 hours prior to angiography. Since we have already reported the details concerning the method of data acquisition and processing 9, it will be described only briefly in the present report. Unipolar ECGs were recorded simultaneously from 87 lead points on the chest surface (59 points on the anterior and 28 on the posterior chest) with reference to Wilson's central terminal. These electrocardiographic data were scanned by a multiplexer, digitized by an A/D converter at a rate of 1,000 samples/sec and processed by a microcomputer to make maps every one msec throughout ventricular activation. The onset of QRS was defined as the first of five successive increases in the root mean square value of the 87 surface ECGs. The 12 lead ECG was also recorded simultaneously with the maps. Fig. 1 shows the 87 lead points used for body surface isopotential mapping in a grated system. The grated system is composed of 13 columns (A -- M) and seven rows. Column A indicates the right midaxillary line, column E the midsternal line and column I the left midaxillary line. Columns B -- D, F -- H, J and M are determined at an equal distance between the adjacent columns. Columns K and L are determined so that the distance between columns J and M is divided equally into three sections. Thus, horizontal interelectrode distance on the back is twice that on the anterior chest. To transfer the anatomical position of each column into a digital form, columns are numbered i through 16. On the other hand, rows 4 and 6 indicate the 5th and 2nd intercostral spaces on the midsternal line, respectively. Row 5 is fixed at the center of the two rows. Other rows are determined so as to equalize the adjacent inter-row distance. The number of each row was also used as digital data for quantitative analysis of maps. Map data were presented as mean _+_ SD for each subgroup and were analyzed with a t test. Table I summarizes 12 lead electrocardiographic, coronary arteriographic and left ventriculographic
artery (LCX) had a diameter narrowing of more than 75%; (2) Asynergies could be seen on the inferior segment of the left ventriculogram; (3) There was a definite history of an acute inferior myocardial infarction (prolonged chest pain, transient elevation of cardiac enzymes and serial ST-T changes in leads II, I I I and aVF of the 12 lead ECG); (4) In lead aVF of the 12 lead ECG, there was a Q wave of at least 0.02 sec but less than 0.04 sec in width and also less than one fourth in ratio to the succeeding R wave in depth when the R wave was 5 mm or moreJ The T wave in lead aVF was normal or showed nonspecific findings. The noninfarction group included 19 patients (13 male, six female; mean age 54.6) satisfying all of the following criteria: (1) None of the major coronary arteries had a diameter narrowing of more than 50%; (2) No asynergies could be observed in the left ventriculogram; (3) There was no clinical history suggestive of an acute myocardial infarction; (4) In lead aVF, the Q wave was 0.02 sec or more but less than 0.04 sec in width and also less than one fourth in ratio to the succeeding R wave in depth when the R wave was 5 mm or more. Those cases with a prominent deformity of the thorax or whose ECG showed any intraventricular conduction disturbance {right bundle branch block, left bundle branch block or hemiblock) were excluded from this study. Left ventriculography was performed in the 30 ~ right anterior oblique projection after an administration of nitroglycerin and was recorded at 30 frames per second using 35 mm cine film. Left ventricular asynergies were analysed qualitatively by observers, who had no knowledge of map data, following the committee reporting system of the American Heart Association s.
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1 A B I 2
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Fig. 1. Eighty-seven lead points for body surface isopotential mapping. The grated system is composed of 13 columns and seven rows.
J. ELECTROCARDIOLOGY 17 (1), 1984
S U R F A C E M A P S IN O L D I N F E R I O R I N F A R C T I O N
TABLE
57
I
Electrocardiographic, coronary arteriographic and left ventriculographic findings of the 4 3 patients.
Case
Age
Sex
ECG findings
CAG findings
Width (sec) of Q wave and depth of Q/R/(S) (mm) in lead aVF
Coronary arteries with stenosis greater than 7 5 %
The infarction group 1. 57 F 2. 70 M 3. 66 M 4. 66 M 5. 55 M 6. 54 M 7. 65 F 8. 67 F 9. 58 M 10. 54 M 11. 55 M 12. 61 M 13. 54 M 14. 49 M
0.02 0.02 0.02 0.03 O.O2 0.02 0.03 0.02 0.02 0.02 0.02 0.02 0.02 0.02
1/5 1.5/12.5 1/2/5(QRS) 4/30 1.5/7 1/4 1.5/12 1/12 1.5/8 1.5/6.5 I/I/5(QRS) 0.5/2.5 1/10 1/6
15.
54
M
0.03
3/13
16. 17. 18. 19. 20. 21. 22. 23. 24.
60 60 64 66 63 64 53 69 46
M M M F M M M M M
0.02 0.03 0.02 0.03 0.03 0.03 0.02 0.03 0.03
1/6 2/9 1/4 2.5/12 2/9 1/5 1/6 1/9 2/10
The noninfarction group 25. 33 F 26. 50 M 27. 53 F 28. 68 F 29. 45 M 30. 58 M 31. 56 F 32. 56 F 33. 62 M 34. 65 M 35. 69 M 36. 67 F 37. 66 M 38. 43 M 39. 69 M 40. 44 M 41. 58 M 42. 20 M 43. 55 M
0.03 0.02 0.03 0.03 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.03 0.02 0.02 0.03 0.03 0.03
2/10 1/6 2/9 1/6 1/7 1/8 O.5/3 1/8 2/10 2/10 1/4 2/10 2/10 1/17 2/9 2/9 2115 3/13 2/9
RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA None None None None None None None None None None None None None None None None None None None
Cx Cx Cx Cx Cx
Cx Cx
Cx
Cx
Cx Cx
LVG findings Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf.
Hypokinesis Hypokinesis Akinesis Akinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Akinesis Akinesis Akinesis Hypokinesis Akinesis Hypokinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis
HOCM LVH LVH Normal Normal Normal LVH LVH LVH Normal LVH LVH LVH LVH LVH Normal LVH Normal Normal
Abbreviations: CAG = Coronary arteriogram; Cx = Left circumflex coronary artery; ECG = Electrocardiogram; HOCM = Hypertrophic obstructive cardiomyopathy; Inf. = Inferior segment of the left ventricle; LVG = Left ventriculogram; LVH = Concentric hypertrophy of the left ventricle; RCA = Right coronary artery.
findings for the 43 p a t i e n t s . All 23 p a t i e n t s of the infarction group had a Q wave of 0.02 sec or more b u t less t h a n 0.04 sec in w i d t h and less t h a n 88 of the succeeding R wave in d e p t h when the R wave is 5 m m or more in lead aVF, although t h e y were known to have
J. E L E C T R O C A R D I O L O G Y
17 (1), 1984
inferior m y o c a r d i a l infarction clinically and angiographically. Left v e n t r i c u l o g r a m s for this group showed h y p o k i n e s i s or akinesis in their inferior s e g m e n t s . On the other hand, all 19 cases in the noninfarction g r o u p h a d a Q w a v e in lead a V F which could not be
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OSUGI ET AL
I1I_..~,/~
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ANTERIOR POSTERIOR
1
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--.~. V~
10
_ V~
Fig. 2. The 12 lead ECGs and the body surface isopotential maps of a typical case in the infarction group. The map pattern is called the "MI-I" pattern. Note that the minimum moved from the 20 mser left posterior chest to the lower back in the early phase of QRS. MI-I 15
A
v,I
v.
Fig. 2 shows 12 lead ECGs and body surface isopotential maps of a typical case (case 9) exhibiting the " M I - I " pattern. The 12 lead ECG of this case had a Q wave of 0.02 sec in lead aVF, which was t h o u g h t not to be indicative of inferior myocardial infarction. Body surface isopotential maps are shown for 10, 15 and 20 msec after the initiation of the QRS complex. The left and right halves of each map frame indicate the anterior and posterior chest, respectively. M a x i m u m is indicated by + and minimum by - . Isopotential lines are drawn at an interval of 0.2 mV. A t 10 msec from the onset of QRS, m a x i m u m was observed in the middle portion of the anterior chest and minimum in the left posterior chest. A t 15 and 20 msec the m a x i m u m remained in the middle portion of the anterior chest but the minimum moved into the lower back. Thus, the specific characteristics of the body surface isopotential
distinguished from the infarction group. In addition, 12 out of the 19 cases showed hypertrophy of the left ventricle. RESULTS The infarction group.
Body surface maps of the infarction group were characterized by a minimum which remained in the lower portion of the chest in the entire early phase of QRS. However, surface maps of the group were classified into two patterns based on the position of the minimum at 20 msec: The " M I - I " p a t t e r n showed the minimum on the back (Columns A and I, or more posterior) and the " M I - 2 " p a t t e r n showed the minimum on the anterior chest. A m o n g 24 cases of the infarction group, 17 cases had body surface maps classified into the " M I - I " p a t t e r n and seven cases had maps falling into the " M I - 2 " pattern.
i
I
I
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I1
ANTERIOR POSTERIOR
aV~
10
_.IX,, V, I .
V.
V~
V.
50msec
/@/ MI-2
15
0 mser
Fig. 3. Body surface maps are shown with 12 lead ECGs for another typical case in the infarction group. The map pattern is " M I - 2 " pattern. The minimum shifted from the lower back to the right lower chest. J. ELECTROCARDIOLOGY 17 (1), 1984
SURFACE MAPS IN OLD INFERIOR INFARCTION
I11
1!
59
ANTERIOR POSTERIOR
i%_
V i ave"
aVL
j,,. V,
V,
V~
V~
V,
I
Fig. 4. The 12 lead ECGs and the body i surface maps of a typical case in the noninfarction group. The map pattern is called the "Non MI-I" pattern. Note that the minimum moved from the mid- I dle back to the right upper chest.
AT--__/L_ 50reset
Non MI-I
maps of the " M I - I " pattern were the appearance of the minimum in the left posterior chest at 10 msec after the initiation of the QRS complex and its movement toward the lower back during the following 10 msec. Another typical pattern of the body surface isopotential maps of the infarction group is given in Fig. 3 and called " M I - 2 " pattern. The ECG in this case (case 19) showed a nonspecific Q wave of 0.03 sec in lead a VF. In the body surface isopotential map for this case, the minimum was observed in the lower back area at 10 msec and 15 msec and moved into right lower chest by 20 msec after the initiation of the QRS complex. Thus, the specific surface characteristics of the " M I - 2 " p a t t e r n were the appearance of a minim u m mostly in the lower back at 10 msec and its
gradual movement into the right anterior lower chest by 20 msec after QRS initiation. Noninfarction
group.
Body surface maps of the noninfarction group were also classified into two patterns based on the position of the m i n i m u m at 20 msec: The " N o n M I - I " pattern showed the minimum on the upper chest (row 4 or upper) and the " N o n MI-2" pattern showed it on the lower chest. A m o n g the 19 cases of the noninfarction group, 13 exhibited the " N o n M I - I " pattern and six the " N o n MI-2" pattern. Fig. 4 shows 12 lead E C G s and body surface isopotential maps of a typical case (case 27) exhibiting the "Non M I - I " pattern. A Q wave of 0.03 sec was recorded in lead aVF of this case, but his coronary arteriogram and left ventriculogram
ANTERIOR POSTERIOR I
i
aV"I
V,[
aVL
aV~
V,
V~
15 Fig. 5. Body surface maps are shown with 12 lead ECGs for another typical case in the noninfarctien group. The map pattern is "Non MI-2" pattern. The minimum shifted from the left anterior chest to the lower back.
J. ELECTROCARDIOLOGY 17 (1), 1984
~.
:
~
V~ ~
V,
0 rnsec
Non M I-2
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OSUGI ET A L
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.
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Fig. 6. The positional changes of the minimum in the "MI-I" and "'MI-2" patterns.
I
.
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MI-2 showed no abnormal findings except for concentric hypertrophy of the left ventricle. In this case, as shown in Fig. 4, a minimum appeared in the middle back and moved into the right upper chest during the early phase of the QRS complex. The map pattern was quite similar to that for normal subjects previously reported 1~except for the high voltage on the chest surface. Thus, the specific finding of this pattern is the minimum at 10 msec mostly on the back and its movement up to the right upper chest b y 20 msec. The position of the minimum at 20 msec was quite different from
that of the " M I - I " and " M I - 2 " patterns in the vertical direction. Another typical pattern of the body surface isopotential map of the noninfarction group is exhibited in Fig. 5 and called " N o n MI-2" pattern. In the ECG of this case {case 39) a Q wave of 0.02 sec was present in lead aVF. Coronary arteriography showed no abnormal findings and the left ventriculogram revealed concentric hypertrophy of the left ventricle. As shown in Fig. 5, a minimum appeared in the left anterior chest at 10 msec after the initiation of the QRS complex and
MIN T
N O N M l- 1
. • "~..T,, MIN 1 0
T
MIN 15
~M1N
20
NONMI-2
Fig. 7. The positional changes of the minimum in the "Non MI-I" and "Non MI-2" patterns.
J. E L E C T R O C A R D I O L O G Y 17 (1), 1984
SURFACE MAPS IN OLD INFERIOR INFARCTION
it gradually moved into the lower back during the succeeding 10 msec. It was an additional interesting feature of the " N o n MI-2" pattern that the maximum and the minimum at 10 msec were located very close together. Thus, specific finding of the " N o n MI-2" pattern is the appearance of the minimum at 10 msec on the left anterior chest and its gradual movement to the lower chest by 20 msec. The minimum at 20 msec was located in a similar position to the " M I - I " and " M I - 2 " patterns. However the minimum at 10 msec was located in a different position from the infarction group. Fig. 6 summarizes the positional changes of the minimum in the " M I - I " and " M I - 2 " patterns. The mean position and standard deviation of the minimum are shown at 10, 15 and 20 msec for each pattern. The most characteristic finding commonly appearing in both patterns was the presence of a minimum at 20 msec in the lower portion of the chest. Fig. 7 summarizes the positional changes of the minimum in the " N o n M I - I " and " N o n MI-2" patterns. The " N o n M I - I " was characterized b y the minimum at 20 msec in the upper portion of the chest and the position of the minimum at 20 msec was significantly different from both the " M I - I " and " M I - 2 " patterns in the vertical direction. The minimum was located at the level of 5.1 _+ 1.1 in the " N o n M I - I " pattern, b u t 2.7 __ 0.6 in the " M I - I " pattern (p < 0.001) and 2.6 _+ 1.4 in the " M I - 2 " pattern (p < 0.001). The " N o n MI-2" pattern showed a minimum at 20 msec in the lower portion of the chest and this finding was similar to that of the infarction group. However, this " N o n MI-2" pattern was also characterized b y the minimum at 10 msec located on the left anterior chest. This position was significantly different from the " M I - I " pattern in the horizontal direction and from the " M I - 2 " pattern in the vertical direction. The minimum was located in the column of 8.2 _ 0.5 in the " N o n MI-2" pattern b u t 10.3 ___ 1.7 in the " M I - I " pattern (p < 0.001), and at the level of 3.8 ___ 0.05 in the " N o n MI-2" pattern b u t 1.3 _+ 0.8 in the " M I - 2 " pattern (p < 0.001). B a s e d on these findings, we proposed the following surface map criteria for the diagnosis of the presence of the old inferior myocardial infarction: The minimum at 20 msec is located in the lower portion of the chest (lower than row 4) and also the minimum at 10 msec is not located on the left anterior chest (more anterior than column I and also higher than row 2). These criteria showed a sensitivity of 83% and a specificity of 95% for d. ELECTROCARDIOLOGY 17 (1), 1984
61
all the materials in this study.
DISCUSSION Although various electrocardiographic criteria for the diagnosis of old inferior myocardial infarctions have been reported, 1113 their sensitivities are rather insufficient, ranging from 34% to 43% when they are compared with angiographic findings. 14,1~ On the other hand, the usefulness of body surface isopotential maps in the diagnosis of myocardial infarction has been reported, although there have been few reports in which presence or absence of old inferior myocardial infarction was examined with body surface isopotential maps. Vincent et al. analysed the body surface isopotential maps of 28 patients with a clinical history of inferior myocardial infarction. 3 They detected a minimum with negative area in the lower chest or in the right chest in all 28 cases, and 12 out of the 28 cases showed a nonspecific Q wave in lead aVF of the 12 lead ECG. These reports suggested that body surface maps contain useful information for the diagnosis of inferior infarction which is not available from 12 lead ECGs. In the p r e s e n t study, we e x t e n d e d these previous studies and examined whether or not it is possible to differentiate inconspicious Q waves of old inferior infarction from Q waves in cases without infarction using consecutive cases which had had coronary arteriography and left ventriculography. In addition, the electrophysiological mechanisms of these cases were speculated upon using angiographic and surface map findings. In the majority of cases whose diagnosis of inferior myocardial infarction was supported both b y clinical history and b y angiographic findings, body surface isopotential maps showed a minim u m which moved from the left posterior chest to the lower back ( " M I - I " pattern) or from the lower back to the right lower chest ("MI-2" pattern) in the early portion of the QRS complex. These map findings coincided with those reported b y Vincent e t al. 3 The minimum and negative areas in the lower thorax were considered to reflect a loss of electromotive forces of the diaphragmatic aspects of the left ventricle caused b y inferior myocardial infarction. On the other hand, body surface isopotential maps of the noninfarction group were classified into two patterns. Cases of this group showed a shallow and narrow b u t obvious Q wave in lead aVF, b u t had neither any clinical history suggestive of infarction nor significant coronary artery narrowings on angiography. In the " N o n
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M I - I " pattern, the minimum moved from the back to the right upper chest and in the "Non MI-2" pattern from the left anterior chest to the lower back. Cases showing the " N o n M I - I " or " N o n MI-2" p a t t e r n did not appear in the report b y Vincent et al. Explaining the electrophysiological mechanisms of the noninfarction group m a y be quite difficult. As shown in Table I, however, 12 of the 19 cases in the noninfarction group {seven of the 13 "Non M I - I " and five of the six " N o n MI-2" cases) exhibited hypertrophy of the left ventricle in the left ventriculograms. This indicates that surface map findings were closely related to this hypertrophy in the majority of cases in the noninfarction group. On the other hand, in an experimental s t u d y using a torso model in which a single dipole model was set parallel to and nearly at the anterior surface, we observed that the minimum was located near the maximum. 16 The surface map findings of the " N o n MI-2" pattern somewhat resembled the experimental model. Accordingly, it is possible that in cases with " N o n MI-2" pattern the early excitation front in the myocardium m a y be present relatively close to the precordial surface. Thus, the positions of the minimum at 10 and 20 msec played a significant role in clarifying the presence or absence of old inferior infarction in patients with a shallow and narrow b u t obvious Q wave in lead aVF. The maximum and minimum are findings available only with body surface isopotential maps. These facts suggest that body surface m a p s contain diagnostic information relating to the presence or absence of old inferior infarction which is not easily available from the 12 lead ECG. Further examination using a larger number of subjects will be required to establish surface map criteria for the diagnosis of inferior myocardial infarction.
REFERENCES I. FLOWERS, N C, HORAN, L G, SOLI, ~ S, HAND, R C AND JOHNSON, J C: N e w evidefice for inferoposterior myocardial infarction on surface potential maps. A m J Cardiol 38:576, 1976 2. FLOWERS, N C, HORAN, L G AND \ JOIINSON, J C: Anterior infarction changes occuring during mid and late ventricular activation detectable by surface mapping techniques. Circulation 54:906, 1976 3. VINCENT, G M, ABILDSKOV, J A, BURGESS, M J, MILLER, K, Lux, R L AND WYATT,R F: Diagnosis
of old inferior myocardial infarction by body surface isopotential mapping. Am J Cardiol 39:510, 1977
4. YAMADA, K, TOYAMA, J, SUGENOYA, J, WADA, M AND SUGIYAMA, S: Body surface isopotentialmaps: Clinical application to the diagnosis of myocardial infarction.Jpn Heart J 19:28, 1978 5. OIITA, T, TOYAMA, J, OIISUGI, J, KINOSIIIT, A, ISOMURA, S, TAKATSU, F, ISIlIKAWA, H, NAGAYA, T ANn YAMADA, K: Correlation between body surface isopotential maps and leftventriculograms in patients with old anterior myocardial infarction.Jpn Heart J 22:747, 1981 6. OnTA, T, K1NOSIIITA, A, OIISUGI, J, ISOMURA, S,
TAKATSU, F, ISIIIKAWA,H, TOYAMA,J, NAGAYA,T ANDYAMADA,K: Correlation between body surface isopotential maps and left ventriculograms in patients with old inferioposterior myocardial infarction. Am Heart J 104:1262, 1982 7. GOLnMAN, M J: Principles of Clinical Electrocardiography. Lange Medical Publications Los Altos, 1976 8. AUSTIN,W G, EDWARD,J E, FRYE, R L, GENSINI,G G, GOTT, V L, GRIFFITII, L S C, McGooN, D C, MURPIIY, M L AND ROSE, B B: AHA Committee Report: A reporting system on patients evaluated for coronary artery disease. Circulation 51: 5, 1975 9. WATANABE, T, TOYAMA, J, TOYOSIIIMA, H, OGURI, H, OUNO, M, OtlTA, T, OKAJIMA, M, NAITO, Y AND YAMADA, K: A practical microcomputer-based mapping system for body surface, precordium and epicardium. Comput Biomed Res 14:341, 1981 10. TACCARDI, B: Distribution of heart potentials on the thoracic surface of normal human subjects. Circ Res 12: 341, 1963 Ii. MYERS, G B, KLEIN, H A AND HIRATZKA, TV: Correlation of electrocardiographic and pathologic findings in posterior infarction. A m Heart J 38:547, 1949 12. WALSn, T J, TIONGSON,P M, STODDARD,E A AND MASSIE, E: The vectorcardiographic QRSsE-loop findings in inferoposterior myocardial infarction. Am Heart J 63:516, 1962 13. TIIE CRITERIA COMMITTEE OF TIlE N E W YORK HEART ASSOCIATION: Nomenclature and Criteria for Diagnosis of Disease of the Heart and Heart Vessels. Little, Brown Company, Boston, 1979, p.91 14. SHETTIGAR, U R, HULTGREN, H N, PFEIFER, J F AND LIPTON, M J: Diagnostic value of Q-wave in inferior myocardial infarction. A m Heart J 88:170, 1974 15. HURD, H P, STARLING, M R, CRAWFORt), M H, DLABAL, P W AND O'RouRKE, R A: Comparative accuracy of electrocardiographicand vectorcardiographic criteriafor inferiormyocardial infarction. Circulation 63:1025, 1981 16. YAMADA, K, TOYAMA, J, OKAJIblA, M, ISnIKAWA, T ANn NIIMI, N: Relationship between the cardiac wave-fronts and the m a x i m u m and minimum on the body surface isopotential map. Ann Rep Environ M e d Nagoya Univ 27:99, 1976
J. ELECTROCARDIOLOGY 17 (1), 1984
Body Surface Isopotential Maps in Old Inferior Myocardial Infarction Undetectable by 12 Lead Electrocardiogram BY JUNICIII OSUGI, M.D., TOSIIIKI OHTA,M.D., JUNJI TOYAMA,M.D., FUMIMARO TAKATSU, M.D., TERUO NAGAYA, M.D. AND KAZUO YAMADA, M.D.
SUMMARY The purpose of this study is to examine the value of body surface isopotential maps in the diagnosis of old inferior myocardial infarction t h a t can not be diagnosed by 12 lead ECG. Forty-three patients with a Q wave of at least 0.02 sec but less than 0.04 sec in width and also less than 25% of the R wave in depth in lead aVF of the 12 lead ECG were selected for this study. The patients were divided into infarction and noninfarction groups based on their clinical histories and cardiac catheterization data. The infarction group showed characteristic surface maps with a minimum which moved from the left posterior chest to the lower back or from the lower back to the right anterior lower chest in the early phase of QRS. The noninfarction group exhibited a minimum which shifted from the back to the right upper chest or from the left anterior chest to the lower back in the same phase. Thus, both groups were clearly distinguishable from each other by the positional change of the minimum in the early phase of QRS. This study suggested that body surface maps contain diagnostic information concerning the presence or absence of inferior myocardial infarction which is not easily available from the 12 lead ECG. Inferior myocardial infarction is diagnosed by the appearance of new Q waves and ST elevation in leads II, I I I and aVF of the 12 lead ECG in the early stage of infarction. However, diagnosis of inferior infarction is often difficult or impossible in its late stages because of the disappearance of abnormal Q waves. In addition, Q waves suggestive of infarction are occasionally observed in leads II, I I I and aVF in cases with no history of myocardial infarction. Thus, one of the major problems of the 12 lead ECG is g e t t i n g an accurate diagnosis of the presence or absence of old inferior myocardial infarction.
On the other hand, it has been reported t h a t body surface isopotential maps are useful in the diagnosis of myocardial infarction. 1~ Recent clinical studies reported t h a t body surface isopotential maps contain useful information for the diagnosis of old inferior myocardial infarction which is not easily obtainable from the 12 lead ECG. In this study, we a t t e m p t e d to clarify whether or not it is possible to differentiate relatively inconspicuous Q waves of old inferior myocardial infarction from Q waves in cases without infarction by comparing body surface isopotential maps of cases with angiographically proven inferior myocardial infarction and of cases without left ventricular asynergy.
From the Department of Respiration and Circulation, Research Institute of Environmental Medicine, Nagoya University, Furo-Cho, Chikusa-Ku, Nagoya 464, and Anjo Kosei Hospital, Anjo 446, Japan. This work was supported by Research Grant for Cardiovascular Diseases 56 C-9 from the Ministry of Itealth and Welfare and Grant-in-Aid for ScientificResearch (56480178) from the Ministry of Education of Japan. The costs of publication of this article were defrayed in part by.the payment of page charges. This article must therefore be hereby marked "Advertisement" in accordance with 18 U.S.C. w1734 solely to indicate this fact. Reprint requests to: Toshiki Ohta, M.D., Division of Respiration and Circulation, Research Institute of Environmental Medicine,Nagoya University, Fur~Cho, Chikusa-Ku, Nagoya 464, Japan.
MATERIALS AND METHODS Among 500 consecutive cases who had undergone both selective coronary arteriography and left ventriculography, the following two groups of patients were selected for this study. The infarction group was composed of 24 patients (20 male and four female; mean age 59.6}. The time elapsed from the onset of infarction ranged from three months to 3.5 years. These patients satisfied all of the following criteria: (D Right coronary artery {RCA) and/or left circumflex
55
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OSUGI ET AL
Body surface isopotential maps were recorded no more than 24 hours prior to angiography. Since we have already reported the details concerning the method of data acquisition and processing 9, it will be described only briefly in the present report. Unipolar ECGs were recorded simultaneously from 87 lead points on the chest surface (59 points on the anterior and 28 on the posterior chest) with reference to Wilson's central terminal. These electrocardiographic data were scanned by a multiplexer, digitized by an A/D converter at a rate of 1,000 samples/sec and processed by a microcomputer to make maps every one msec throughout ventricular activation. The onset of QRS was defined as the first of five successive increases in the root mean square value of the 87 surface ECGs. The 12 lead ECG was also recorded simultaneously with the maps. Fig. 1 shows the 87 lead points used for body surface isopotential mapping in a grated system. The grated system is composed of 13 columns (A -- M) and seven rows. Column A indicates the right midaxillary line, column E the midsternal line and column I the left midaxillary line. Columns B -- D, F -- H, J and M are determined at an equal distance between the adjacent columns. Columns K and L are determined so that the distance between columns J and M is divided equally into three sections. Thus, horizontal interelectrode distance on the back is twice that on the anterior chest. To transfer the anatomical position of each column into a digital form, columns are numbered i through 16. On the other hand, rows 4 and 6 indicate the 5th and 2nd intercostral spaces on the midsternal line, respectively. Row 5 is fixed at the center of the two rows. Other rows are determined so as to equalize the adjacent inter-row distance. The number of each row was also used as digital data for quantitative analysis of maps. Map data were presented as mean _+_ SD for each subgroup and were analyzed with a t test. Table I summarizes 12 lead electrocardiographic, coronary arteriographic and left ventriculographic
artery (LCX) had a diameter narrowing of more than 75%; (2) Asynergies could be seen on the inferior segment of the left ventriculogram; (3) There was a definite history of an acute inferior myocardial infarction (prolonged chest pain, transient elevation of cardiac enzymes and serial ST-T changes in leads II, I I I and aVF of the 12 lead ECG); (4) In lead aVF of the 12 lead ECG, there was a Q wave of at least 0.02 sec but less than 0.04 sec in width and also less than one fourth in ratio to the succeeding R wave in depth when the R wave was 5 mm or moreJ The T wave in lead aVF was normal or showed nonspecific findings. The noninfarction group included 19 patients (13 male, six female; mean age 54.6) satisfying all of the following criteria: (1) None of the major coronary arteries had a diameter narrowing of more than 50%; (2) No asynergies could be observed in the left ventriculogram; (3) There was no clinical history suggestive of an acute myocardial infarction; (4) In lead aVF, the Q wave was 0.02 sec or more but less than 0.04 sec in width and also less than one fourth in ratio to the succeeding R wave in depth when the R wave was 5 mm or more. Those cases with a prominent deformity of the thorax or whose ECG showed any intraventricular conduction disturbance {right bundle branch block, left bundle branch block or hemiblock) were excluded from this study. Left ventriculography was performed in the 30 ~ right anterior oblique projection after an administration of nitroglycerin and was recorded at 30 frames per second using 35 mm cine film. Left ventricular asynergies were analysed qualitatively by observers, who had no knowledge of map data, following the committee reporting system of the American Heart Association s.
7 6
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1 A B I 2
C 3
D E 4 5
F 6
G H 7 8
I 9
J 10
K 12
L 14
M 16
Fig. 1. Eighty-seven lead points for body surface isopotential mapping. The grated system is composed of 13 columns and seven rows.
J. ELECTROCARDIOLOGY 17 (1), 1984
S U R F A C E M A P S IN O L D I N F E R I O R I N F A R C T I O N
TABLE
57
I
Electrocardiographic, coronary arteriographic and left ventriculographic findings of the 4 3 patients.
Case
Age
Sex
ECG findings
CAG findings
Width (sec) of Q wave and depth of Q/R/(S) (mm) in lead aVF
Coronary arteries with stenosis greater than 7 5 %
The infarction group 1. 57 F 2. 70 M 3. 66 M 4. 66 M 5. 55 M 6. 54 M 7. 65 F 8. 67 F 9. 58 M 10. 54 M 11. 55 M 12. 61 M 13. 54 M 14. 49 M
0.02 0.02 0.02 0.03 O.O2 0.02 0.03 0.02 0.02 0.02 0.02 0.02 0.02 0.02
1/5 1.5/12.5 1/2/5(QRS) 4/30 1.5/7 1/4 1.5/12 1/12 1.5/8 1.5/6.5 I/I/5(QRS) 0.5/2.5 1/10 1/6
15.
54
M
0.03
3/13
16. 17. 18. 19. 20. 21. 22. 23. 24.
60 60 64 66 63 64 53 69 46
M M M F M M M M M
0.02 0.03 0.02 0.03 0.03 0.03 0.02 0.03 0.03
1/6 2/9 1/4 2.5/12 2/9 1/5 1/6 1/9 2/10
The noninfarction group 25. 33 F 26. 50 M 27. 53 F 28. 68 F 29. 45 M 30. 58 M 31. 56 F 32. 56 F 33. 62 M 34. 65 M 35. 69 M 36. 67 F 37. 66 M 38. 43 M 39. 69 M 40. 44 M 41. 58 M 42. 20 M 43. 55 M
0.03 0.02 0.03 0.03 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.02 0.03 0.02 0.02 0.03 0.03 0.03
2/10 1/6 2/9 1/6 1/7 1/8 O.5/3 1/8 2/10 2/10 1/4 2/10 2/10 1/17 2/9 2/9 2115 3/13 2/9
RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA RCA None None None None None None None None None None None None None None None None None None None
Cx Cx Cx Cx Cx
Cx Cx
Cx
Cx
Cx Cx
LVG findings Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf. Inf.
Hypokinesis Hypokinesis Akinesis Akinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Hypokinesis Akinesis Akinesis Akinesis Hypokinesis Akinesis Hypokinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis Akinesis
HOCM LVH LVH Normal Normal Normal LVH LVH LVH Normal LVH LVH LVH LVH LVH Normal LVH Normal Normal
Abbreviations: CAG = Coronary arteriogram; Cx = Left circumflex coronary artery; ECG = Electrocardiogram; HOCM = Hypertrophic obstructive cardiomyopathy; Inf. = Inferior segment of the left ventricle; LVG = Left ventriculogram; LVH = Concentric hypertrophy of the left ventricle; RCA = Right coronary artery.
findings for the 43 p a t i e n t s . All 23 p a t i e n t s of the infarction group had a Q wave of 0.02 sec or more b u t less t h a n 0.04 sec in w i d t h and less t h a n 88 of the succeeding R wave in d e p t h when the R wave is 5 m m or more in lead aVF, although t h e y were known to have
J. E L E C T R O C A R D I O L O G Y
17 (1), 1984
inferior m y o c a r d i a l infarction clinically and angiographically. Left v e n t r i c u l o g r a m s for this group showed h y p o k i n e s i s or akinesis in their inferior s e g m e n t s . On the other hand, all 19 cases in the noninfarction g r o u p h a d a Q w a v e in lead a V F which could not be
58
OSUGI ET AL
I1I_..~,/~
aVL
111
ANTERIOR POSTERIOR
1
aV~"
--.~. V~
10
_ V~
Fig. 2. The 12 lead ECGs and the body surface isopotential maps of a typical case in the infarction group. The map pattern is called the "MI-I" pattern. Note that the minimum moved from the 20 mser left posterior chest to the lower back in the early phase of QRS. MI-I 15
A
v,I
v.
Fig. 2 shows 12 lead ECGs and body surface isopotential maps of a typical case (case 9) exhibiting the " M I - I " pattern. The 12 lead ECG of this case had a Q wave of 0.02 sec in lead aVF, which was t h o u g h t not to be indicative of inferior myocardial infarction. Body surface isopotential maps are shown for 10, 15 and 20 msec after the initiation of the QRS complex. The left and right halves of each map frame indicate the anterior and posterior chest, respectively. M a x i m u m is indicated by + and minimum by - . Isopotential lines are drawn at an interval of 0.2 mV. A t 10 msec from the onset of QRS, m a x i m u m was observed in the middle portion of the anterior chest and minimum in the left posterior chest. A t 15 and 20 msec the m a x i m u m remained in the middle portion of the anterior chest but the minimum moved into the lower back. Thus, the specific characteristics of the body surface isopotential
distinguished from the infarction group. In addition, 12 out of the 19 cases showed hypertrophy of the left ventricle. RESULTS The infarction group.
Body surface maps of the infarction group were characterized by a minimum which remained in the lower portion of the chest in the entire early phase of QRS. However, surface maps of the group were classified into two patterns based on the position of the minimum at 20 msec: The " M I - I " p a t t e r n showed the minimum on the back (Columns A and I, or more posterior) and the " M I - 2 " p a t t e r n showed the minimum on the anterior chest. A m o n g 24 cases of the infarction group, 17 cases had body surface maps classified into the " M I - I " p a t t e r n and seven cases had maps falling into the " M I - 2 " pattern.
i
I
I
111
I1
ANTERIOR POSTERIOR
aV~
10
_.IX,, V, I .
V.
V~
V.
50msec
/@/ MI-2
15
0 mser
Fig. 3. Body surface maps are shown with 12 lead ECGs for another typical case in the infarction group. The map pattern is " M I - 2 " pattern. The minimum shifted from the lower back to the right lower chest. J. ELECTROCARDIOLOGY 17 (1), 1984
SURFACE MAPS IN OLD INFERIOR INFARCTION
I11
1!
59
ANTERIOR POSTERIOR
i%_
V i ave"
aVL
j,,. V,
V,
V~
V~
V,
I
Fig. 4. The 12 lead ECGs and the body i surface maps of a typical case in the noninfarction group. The map pattern is called the "Non MI-I" pattern. Note that the minimum moved from the mid- I dle back to the right upper chest.
AT--__/L_ 50reset
Non MI-I
maps of the " M I - I " pattern were the appearance of the minimum in the left posterior chest at 10 msec after the initiation of the QRS complex and its movement toward the lower back during the following 10 msec. Another typical pattern of the body surface isopotential maps of the infarction group is given in Fig. 3 and called " M I - 2 " pattern. The ECG in this case (case 19) showed a nonspecific Q wave of 0.03 sec in lead a VF. In the body surface isopotential map for this case, the minimum was observed in the lower back area at 10 msec and 15 msec and moved into right lower chest by 20 msec after the initiation of the QRS complex. Thus, the specific surface characteristics of the " M I - 2 " p a t t e r n were the appearance of a minim u m mostly in the lower back at 10 msec and its
gradual movement into the right anterior lower chest by 20 msec after QRS initiation. Noninfarction
group.
Body surface maps of the noninfarction group were also classified into two patterns based on the position of the m i n i m u m at 20 msec: The " N o n M I - I " pattern showed the minimum on the upper chest (row 4 or upper) and the " N o n MI-2" pattern showed it on the lower chest. A m o n g the 19 cases of the noninfarction group, 13 exhibited the " N o n M I - I " pattern and six the " N o n MI-2" pattern. Fig. 4 shows 12 lead E C G s and body surface isopotential maps of a typical case (case 27) exhibiting the "Non M I - I " pattern. A Q wave of 0.03 sec was recorded in lead aVF of this case, but his coronary arteriogram and left ventriculogram
ANTERIOR POSTERIOR I
i
aV"I
V,[
aVL
aV~
V,
V~
15 Fig. 5. Body surface maps are shown with 12 lead ECGs for another typical case in the noninfarctien group. The map pattern is "Non MI-2" pattern. The minimum shifted from the left anterior chest to the lower back.
J. ELECTROCARDIOLOGY 17 (1), 1984
~.
:
~
V~ ~
V,
0 rnsec
Non M I-2
60
OSUGI ET A L
I "~ ~MI'N20 MIN 15
MIN 10
i-1
20
MIN 10]" =
.
.
.
.
.
.
.
.
.
Fig. 6. The positional changes of the minimum in the "MI-I" and "'MI-2" patterns.
I
.
T
,
i
,
MI-2 showed no abnormal findings except for concentric hypertrophy of the left ventricle. In this case, as shown in Fig. 4, a minimum appeared in the middle back and moved into the right upper chest during the early phase of the QRS complex. The map pattern was quite similar to that for normal subjects previously reported 1~except for the high voltage on the chest surface. Thus, the specific finding of this pattern is the minimum at 10 msec mostly on the back and its movement up to the right upper chest b y 20 msec. The position of the minimum at 20 msec was quite different from
that of the " M I - I " and " M I - 2 " patterns in the vertical direction. Another typical pattern of the body surface isopotential map of the noninfarction group is exhibited in Fig. 5 and called " N o n MI-2" pattern. In the ECG of this case {case 39) a Q wave of 0.02 sec was present in lead aVF. Coronary arteriography showed no abnormal findings and the left ventriculogram revealed concentric hypertrophy of the left ventricle. As shown in Fig. 5, a minimum appeared in the left anterior chest at 10 msec after the initiation of the QRS complex and
MIN T
N O N M l- 1
. • "~..T,, MIN 1 0
T
MIN 15
~M1N
20
NONMI-2
Fig. 7. The positional changes of the minimum in the "Non MI-I" and "Non MI-2" patterns.
J. E L E C T R O C A R D I O L O G Y 17 (1), 1984
SURFACE MAPS IN OLD INFERIOR INFARCTION
it gradually moved into the lower back during the succeeding 10 msec. It was an additional interesting feature of the " N o n MI-2" pattern that the maximum and the minimum at 10 msec were located very close together. Thus, specific finding of the " N o n MI-2" pattern is the appearance of the minimum at 10 msec on the left anterior chest and its gradual movement to the lower chest by 20 msec. The minimum at 20 msec was located in a similar position to the " M I - I " and " M I - 2 " patterns. However the minimum at 10 msec was located in a different position from the infarction group. Fig. 6 summarizes the positional changes of the minimum in the " M I - I " and " M I - 2 " patterns. The mean position and standard deviation of the minimum are shown at 10, 15 and 20 msec for each pattern. The most characteristic finding commonly appearing in both patterns was the presence of a minimum at 20 msec in the lower portion of the chest. Fig. 7 summarizes the positional changes of the minimum in the " N o n M I - I " and " N o n MI-2" patterns. The " N o n M I - I " was characterized b y the minimum at 20 msec in the upper portion of the chest and the position of the minimum at 20 msec was significantly different from both the " M I - I " and " M I - 2 " patterns in the vertical direction. The minimum was located at the level of 5.1 _+ 1.1 in the " N o n M I - I " pattern, b u t 2.7 __ 0.6 in the " M I - I " pattern (p < 0.001) and 2.6 _+ 1.4 in the " M I - 2 " pattern (p < 0.001). The " N o n MI-2" pattern showed a minimum at 20 msec in the lower portion of the chest and this finding was similar to that of the infarction group. However, this " N o n MI-2" pattern was also characterized b y the minimum at 10 msec located on the left anterior chest. This position was significantly different from the " M I - I " pattern in the horizontal direction and from the " M I - 2 " pattern in the vertical direction. The minimum was located in the column of 8.2 _ 0.5 in the " N o n MI-2" pattern b u t 10.3 ___ 1.7 in the " M I - I " pattern (p < 0.001), and at the level of 3.8 ___ 0.05 in the " N o n MI-2" pattern b u t 1.3 _+ 0.8 in the " M I - 2 " pattern (p < 0.001). B a s e d on these findings, we proposed the following surface map criteria for the diagnosis of the presence of the old inferior myocardial infarction: The minimum at 20 msec is located in the lower portion of the chest (lower than row 4) and also the minimum at 10 msec is not located on the left anterior chest (more anterior than column I and also higher than row 2). These criteria showed a sensitivity of 83% and a specificity of 95% for d. ELECTROCARDIOLOGY 17 (1), 1984
61
all the materials in this study.
DISCUSSION Although various electrocardiographic criteria for the diagnosis of old inferior myocardial infarctions have been reported, 1113 their sensitivities are rather insufficient, ranging from 34% to 43% when they are compared with angiographic findings. 14,1~ On the other hand, the usefulness of body surface isopotential maps in the diagnosis of myocardial infarction has been reported, although there have been few reports in which presence or absence of old inferior myocardial infarction was examined with body surface isopotential maps. Vincent et al. analysed the body surface isopotential maps of 28 patients with a clinical history of inferior myocardial infarction. 3 They detected a minimum with negative area in the lower chest or in the right chest in all 28 cases, and 12 out of the 28 cases showed a nonspecific Q wave in lead aVF of the 12 lead ECG. These reports suggested that body surface maps contain useful information for the diagnosis of inferior infarction which is not available from 12 lead ECGs. In the p r e s e n t study, we e x t e n d e d these previous studies and examined whether or not it is possible to differentiate inconspicious Q waves of old inferior infarction from Q waves in cases without infarction using consecutive cases which had had coronary arteriography and left ventriculography. In addition, the electrophysiological mechanisms of these cases were speculated upon using angiographic and surface map findings. In the majority of cases whose diagnosis of inferior myocardial infarction was supported both b y clinical history and b y angiographic findings, body surface isopotential maps showed a minim u m which moved from the left posterior chest to the lower back ( " M I - I " pattern) or from the lower back to the right lower chest ("MI-2" pattern) in the early portion of the QRS complex. These map findings coincided with those reported b y Vincent e t al. 3 The minimum and negative areas in the lower thorax were considered to reflect a loss of electromotive forces of the diaphragmatic aspects of the left ventricle caused b y inferior myocardial infarction. On the other hand, body surface isopotential maps of the noninfarction group were classified into two patterns. Cases of this group showed a shallow and narrow b u t obvious Q wave in lead aVF, b u t had neither any clinical history suggestive of infarction nor significant coronary artery narrowings on angiography. In the " N o n
62
OSUGI ET AL
M I - I " pattern, the minimum moved from the back to the right upper chest and in the "Non MI-2" pattern from the left anterior chest to the lower back. Cases showing the " N o n M I - I " or " N o n MI-2" p a t t e r n did not appear in the report b y Vincent et al. Explaining the electrophysiological mechanisms of the noninfarction group m a y be quite difficult. As shown in Table I, however, 12 of the 19 cases in the noninfarction group {seven of the 13 "Non M I - I " and five of the six " N o n MI-2" cases) exhibited hypertrophy of the left ventricle in the left ventriculograms. This indicates that surface map findings were closely related to this hypertrophy in the majority of cases in the noninfarction group. On the other hand, in an experimental s t u d y using a torso model in which a single dipole model was set parallel to and nearly at the anterior surface, we observed that the minimum was located near the maximum. 16 The surface map findings of the " N o n MI-2" pattern somewhat resembled the experimental model. Accordingly, it is possible that in cases with " N o n MI-2" pattern the early excitation front in the myocardium m a y be present relatively close to the precordial surface. Thus, the positions of the minimum at 10 and 20 msec played a significant role in clarifying the presence or absence of old inferior infarction in patients with a shallow and narrow b u t obvious Q wave in lead aVF. The maximum and minimum are findings available only with body surface isopotential maps. These facts suggest that body surface m a p s contain diagnostic information relating to the presence or absence of old inferior infarction which is not easily available from the 12 lead ECG. Further examination using a larger number of subjects will be required to establish surface map criteria for the diagnosis of inferior myocardial infarction.
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of old inferior myocardial infarction by body surface isopotential mapping. Am J Cardiol 39:510, 1977
4. YAMADA, K, TOYAMA, J, SUGENOYA, J, WADA, M AND SUGIYAMA, S: Body surface isopotentialmaps: Clinical application to the diagnosis of myocardial infarction.Jpn Heart J 19:28, 1978 5. OIITA, T, TOYAMA, J, OIISUGI, J, KINOSIIIT, A, ISOMURA, S, TAKATSU, F, ISIlIKAWA, H, NAGAYA, T ANn YAMADA, K: Correlation between body surface isopotential maps and leftventriculograms in patients with old anterior myocardial infarction.Jpn Heart J 22:747, 1981 6. OnTA, T, K1NOSIIITA, A, OIISUGI, J, ISOMURA, S,
TAKATSU, F, ISIIIKAWA,H, TOYAMA,J, NAGAYA,T ANDYAMADA,K: Correlation between body surface isopotential maps and left ventriculograms in patients with old inferioposterior myocardial infarction. Am Heart J 104:1262, 1982 7. GOLnMAN, M J: Principles of Clinical Electrocardiography. Lange Medical Publications Los Altos, 1976 8. AUSTIN,W G, EDWARD,J E, FRYE, R L, GENSINI,G G, GOTT, V L, GRIFFITII, L S C, McGooN, D C, MURPIIY, M L AND ROSE, B B: AHA Committee Report: A reporting system on patients evaluated for coronary artery disease. Circulation 51: 5, 1975 9. WATANABE, T, TOYAMA, J, TOYOSIIIMA, H, OGURI, H, OUNO, M, OtlTA, T, OKAJIMA, M, NAITO, Y AND YAMADA, K: A practical microcomputer-based mapping system for body surface, precordium and epicardium. Comput Biomed Res 14:341, 1981 10. TACCARDI, B: Distribution of heart potentials on the thoracic surface of normal human subjects. Circ Res 12: 341, 1963 Ii. MYERS, G B, KLEIN, H A AND HIRATZKA, TV: Correlation of electrocardiographic and pathologic findings in posterior infarction. A m Heart J 38:547, 1949 12. WALSn, T J, TIONGSON,P M, STODDARD,E A AND MASSIE, E: The vectorcardiographic QRSsE-loop findings in inferoposterior myocardial infarction. Am Heart J 63:516, 1962 13. TIIE CRITERIA COMMITTEE OF TIlE N E W YORK HEART ASSOCIATION: Nomenclature and Criteria for Diagnosis of Disease of the Heart and Heart Vessels. Little, Brown Company, Boston, 1979, p.91 14. SHETTIGAR, U R, HULTGREN, H N, PFEIFER, J F AND LIPTON, M J: Diagnostic value of Q-wave in inferior myocardial infarction. A m Heart J 88:170, 1974 15. HURD, H P, STARLING, M R, CRAWFORt), M H, DLABAL, P W AND O'RouRKE, R A: Comparative accuracy of electrocardiographicand vectorcardiographic criteriafor inferiormyocardial infarction. Circulation 63:1025, 1981 16. YAMADA, K, TOYAMA, J, OKAJIblA, M, ISnIKAWA, T ANn NIIMI, N: Relationship between the cardiac wave-fronts and the m a x i m u m and minimum on the body surface isopotential map. Ann Rep Environ M e d Nagoya Univ 27:99, 1976
J. ELECTROCARDIOLOGY 17 (1), 1984