correlation of electrocardiographic and pathologic findings in healed myocardial infarction

Correlation of Electrocardiographic and Pathologic Findings in

Healed Myocardial Infarction

WILLlAM SULLIVAN, BA

ZEEV VLODAVER, MD, FACC NAIP TUNA, MD, FACC LINDA LONG, MD JESSE E. EDWARDS, MD, FACC

St. Paul and Minneapolis, Minnesota

A correlative study in 50 cases of healed myocardial infarction compared the 12 lead electrocardiogram with pathologic observations. The electrocardiogram was interpreted according to established Minnesota codes with some modifications. The following conclusions were reached: (1) The electrocardiogram underestimates the extent of myocardial infarction. (2) When a healed myocardial infarct at a specific location is recognized with electrocardiographic criteria, it is likely that there are unrecognized infarcts involving other areas of the left ventricle. (3) Infarctions involving the lateral and inferobasal areas are frequently unrecognized. (4) The electrocardiogram is more likely to miss myocardial infarcts in patients with multiple, than in those with single, electrocardiographically diagnosed infarcts. (5) Apical myocardial infarction does not appear to have specific electrocardiographic findings, other than those related to general infarct localization by electrocardiogram, particularly in patients with anteroseptal or anterolateral infarction. (6) Abnormal 0 waves, generally thought to indicate transmural myocardial infarction, are frequently found in subendocardial infarction. (7) The simplified electrocardiographic classification of myocardial infarct site (anteroseptal, inferior, anterolateral) used in this study is preferable to more detailed classifications previously suggested by others.

From the Department of Pathology, United Hos- pitals-Miller Division, St. Paul, Minnesota and the Departments of Pathology and Medicine, Univer- sity of Minnesota, Minneapolis, Minnesota. This study was supported by Public Health Service Research Grant 5 RDl HL 05694 from the National Heart, Lung, and Blood Institute. National Institutes of Health, Bethesda, Maryland, and by the Saint Paul Foundation, St. Paul, Minnesota. Manuscript received May 25, 1978: revised manuscript received June 27, 1978, accepted June 28, 1978.

Address for reorints: Jesse E. Edwards, MD,

Most reports correlating electrocardiographic and pathologic findings in acute myocardial infarction agree that the electrocardiographic diagnosis is commonly correct.1 However, the electrocardiogram is generally considered less precise2 in the diagnosis and localization of healed myocardial infarction. Levine and Phillips,3 using the Wilson criteria for diagnosis of healed myocardial infarction, found in a study of 23 cases that only 20 percent of healed infarcts observed at autopsy were revealed in the electrocardiogram. In a correlative study of electrocardiographic and autopsy findings, Wood et al4 adopted the 1959 criteria of the World Health Organization Expert Committee on Cardiovascular Diseases and Hypertension for “very probable myocardial infarction.” Among 122 cases, they found that the accuracy rate of electrocardiographic diagnosis was 82 percent in acute infarction but only 27 percent when there was a single healed infarct. When multiple sites of old infarction were present, the accuracy rate increased to 58 percent, but the overall accuracy rate was only 48 percent.

The purpose of this study was to correlate in 50 cases of healed myocardial infarction the anatomic and electrocardiographic findings, interpreted with use of Minnesota Q and QS codes.

Material and Methods

Fifty consecutive patients with an autopsy-demonstrated healed myocardial infarct and at least one 12 lead electrocardiogram taken within 21 days of death

United Hospitals-Miller Division, Department of were studied. Ten of the 50 patients had an acute myocardial infarction in ad- Pathology, 125 West College Avenue, St. Paul, dition to the healed infarct. Thirty-three patients were men and 17 were women. Minnesota 55102. The age range was 32 to 89 years.

724 November 1978 The American Journal of CARDIOLOGY Volume 42

Pathologic Examination At the time of autopsy, the heart specimens had been sec-

tioned into five horizontal slices of approximately equal thickness from apex to base, each section measuring 0.8 to 1.3 cm in thickness. They were fixed in formaldehyde. By gross examination, the sites of infarction were indicated on di- agrams of cross sections of the ventricles. Slice 1 was apical and slice 5 was basal. Histologic examination was performed on at least three portions of the left ventricle, each repre- senting distribution of each of the three main coronary arte- ries.

Each myocardial infarct, whether acute or healed, was classified as subendocardial or transmural. All infarcts were further classified according to their location in the heart as a whole:

Pathologic identification of sites of infarction: Anter- obasal (anterior wall, including the anterior half of anterolateral papillary muscle-may include septum)-slices 4 and 5; anteroseptal (anterior wall and septum)-slices 1 to 3; anterolateral (anteroseptal and lateral)-slices 1 to 4; lateral (between the anterior edge of the posteromedial papillary muscle and the middle of the anterolateral papillary muscle) -slices 2 to 4; apical*-slices 1 and 2; inferior (involving the ventricular septum and inferior wall including the posteromedial papillary muscle)-slices 2 to 4; inferobasal-defined as inferior but restricted to slices 4 and 5; septal (strictly septal)-slices 2 to 4; inferolateral (confluence of inferior and lateral areas)-slices 2 to 4; inferolateral basal (confluence of lateral and inferobasal areas)-slices 4 and 5.

In Table I, infarcts are further classified according to amount and type of wall involved: transmural acute (TA); transmural healed (TH); subendocardial extensive acute (EA); subendocardial extensive healed (EH); subendocardial limited acute (ea); and subendocardial limited healed (eh).

Electrocardiographic Definitions

Serial I2 lead electrocardiograms were reviewed and the diagnosis of healed myocardial infarction was made when Minnesota Q or QS codes (l-l, l-2 and l-3) were present5 and there were no ST-T changes of acute myocardial infarction. When ST-T changes were present without diagnostic Q or QS codes, these were indicated as signs of either ischemia or acute infarction.

Location of healed myocardial infarction: The electrocardiographic localization of healed myocardial infarcts was made according to the following criteria? Anterosep- tal-Q, QS codes in leads Vi to V.5; Anterolateral-Q, QS codes in leads I, aVL and Ve; Inferior-Q, QS codes in leads II, III and aVF.

Of the anatomic locations given, the Minnesota codes are defined only for anteroseptal, anterolateral and inferior healed myocardial infarction. We added an electrocardiographic diagnosis of inferobasal myocardial infarction and also criteria for the diagnosis of healed myocardial infarction in the presence of “atypical left bundle branch block.” In the absence of either right bundle branch block or right ventricular hypertrophy, the electrocardiographic diagnosis of inferobasal healed infarction was based on an R/S ratio in lead Vs greater than 1, absence of a Q wave in lead Vz and an R wave duration

+ Apical infarction may be anterior, lateral, inferior or circumferential. As indicated, the apical segment may be part of a larger segment, such as anteroseptal or inferior; in such cases, apical involvement will not be mentioned separately. If apical involvement is in one or more areas other than that of the “large segment,” then it is indicated separately (for example, anteroseptal and apical lateral). In identifying sites of infarction, the majority rule was always applied (if slices 4 and 5 were involved but the lesion included part of slice 3, the final diagnosis was anterobasal).

in lead Vz of 0.4 second or greater. A diagnosis of myocardial infarction was also considered in the presence of “atypical left bundle branch block” when abnormal Q waves were present or abnormal Q or Q-equivalent (M-shaped or rsR’) waves were present in leads I, aVL, V5 or Vae7 A QRS duration of 0.09 second or less was considered normal, and individual values were not indicated separately in the table. A QRS duration of 0.10 second or greater was indicated individually in each case. Intraventricular conduction delay was diagnosed when the QRS duration was 0.11 second or greater.

“Abnormal” Q waves in leads V5 and Vg: To correlate Q waves in leads Vs and Vs with apical involvement, the Q wave in lead V5 was arbitrarily called “abnormal” when it had a minimal duration of 0.02 second and a Q/R amplitude ratio of at least 0.05. In 16 of 50 patients there was an abnormal Q wave in lead Vr,, the mean Q duration being 0.03 second (range 0.02 to 0.06) and the mean Q/R amplitude ratio 0.19 (range 0.04 to 0.5).

An “abnormal” Q wave in lead V, was arbitrarily diagnosed when the Q wave duration was at least 0.02 second and the Q/R amplitude ratio was at least 0.053. In 17 patients with an abnormal Q wave in lead Va, the mean Q wave duration was 0.036 second (range 0.02 to 0.05) and the mean Q/R amplitude ratio was 0.173 (range 0.053 to 0.33). In 13 patients with a “normal” Q wave in lead Vs the mean Q wave duration was 0.015 second (range 0.01 to 0.02), whereas in 13 patients with a “normal” Q wave in lead Va the mean duration was 0.016 second (range 0.01 to 0.02). The mean Q/R amplitude ratio in patients with a “normal” Q wave was 0.037 (range 0.004 to 0.091), and 0.06 (range 0.005 to 0.111) for leads V5 and Vs, respectively.

Ischemia or subendocardial myocardial infarction: A diagnosis of ischemia or acute subendocardial myocardial infarction was considered when Q or QS code criteria were absent and there was horizontal S-T depression of 2 mm or greater or “ischemic T wave inversions” of 5 mm or more with or without S-T segment shifts in the absence of (1) electrolyte abnormalities, (2) left ventricular hypertrophy with strain, (3) intraventricular conduction abnormalities, (4) intracranial disease, or (5) digitalis, quinidine or procainamide adminis- tration. The diagnosis of electrocardiographic abnormalities other than myocardial infarction was made according to New York Heart Assoc;ation criteria.6

The electrocardiograms were first read for diagnosis of specific areas of infarction; then the diagnosis was compared with the pathologic findings. Table I is averaged according to the various electrocardiographic diagnoses, listing the pathologic findings within each diagnostic category.

Results

General Observations

Multiple sites of healed infarction were common. Six patients had one healed infarct, 18 had two healed infarcts, 19 had three healed infarcts and 7 had four or more separate sites of healed infarction. Ten of the 50 patients had an acute or healing infarct in addition to one or more healed infarcts. The healed myocardial infarcts were of the following types: transmural only (10 patients); subendocardial only (23 patients); and transmural and subendocardial(l7 patients).

In order of decreasing frequency, the sites of healed myocardial infarction were anteroseptal (17), apical (16), inferobasal (15), inferior (ll), anterolateral (ll), lateral (3), anterobasal (3) and septal (2). There was apical involvement in 33 percent of patients (2 of 6) with a single infarct, in 78 percent of patients (14 of 18) with

ELECTROCARDIOGRAM IN HEALED MYOCARDIAL INFARCTION-SULLIVAN ET AL.

November 1978 The American Journal of CARDIOLOGY Volume 42 725

ELECTROCARDIOGRAM IN HEALED MYOCARDIAL INFARCTION-SULLIVAN ET AL

two areas involved, in 89 percent of patients (17 of 19) with three areas involved and in 100 percent of patients (7 of 7) with four or more sites involved.

of infarction. These findings are listed, related to the pathologic findings and discussed in relation to a par- titular electrocardiographic grouping.

Inferior infarction (six cases. Table IA): Among.

Correlations of Electrocardiographic and Pathologic Findings

the six patients with an kectrocarkographic diagnosis of healed infarction restricted to the inferior wall, the uatholonic examination confirmed this findine: in onlv L - one. In two other patients, although the inferior wall was involved, there was additional involvement (inferobasal

The sections under this heading indicate the electrocardiographic categorization of each case by location

TABLE I

Electrocardiographic and Pathologic Findings in 50 Cases of Healed Myocardial Infarction

Age Associated QRS Q Wave Heart Myocardial Infarction

Case (yr) Minn. Electrocardio- Duration in Weight ECG Apex no. & Sex Code graphic Findings (seconds) v5-v6 (9) Confirmed Other Involved

A. Inferior Myocardial Infarction by Electrocardiogram (6 cases)

1 53 M l-l-4 LVH, LAD Normal Abnormal 650 No Apical circum- Yes ferential EH; anterolateral EH; inferolateral basal TH

: 58M l-l-4 . Normal Abnormal 560 Yes, eh None Yes 72M l-l-4 LVH with strain, Normal Normal 560 Yes, TH lnferobasal TH; No

ST-T changes lateral ea 4 56 F l-l-4 Anterior ischemia Normal Normal 350 Yes, EH Anteroseptal EH; Yes

or subendocar- inferobasal EH dial infarction

5 50 M l-2-4 Anterolateral Normal Normal 570 No Lateral EH No ischemia?

6 88 M l-l-4 IVCD. LVH, LAD 0.11 NoQ 400 No Apical circum- Yes ferential EH; anterolateral EH; inferolateral basal TH

B. Inferior and lnferobasal Myocardial Infarction by Electrocardiogram (3 cases)

7 63 F l-l-4 i-\/H with strain

Normal Abnormal 380 Yes, TH Lateral TH No 8 81 F l-l-4 Normal Normal 500 Yes, TH Lateral TH; apical Yes

circumferential EH 9 61 M l-2-4 Normal Normal 340 No, inferior; yes, eh No

inferobasal-

C. lnferobasal Myocardial Infarction by Electrocardiogram (1 case)

10 70M . . . Normal NoQ 450 Yes, EH None No

D. Anteroseptal Myocardial Infarction by Electrocardiogram (10 cases)

11 73 M l-2-8 Normal Normal 510 Yes, EH

72 F l-l-2 65 M l-l-l

Normal 0.11

LVH with strain IVCD, lateral

ischemia or subendocardial

L! LAD, 1” A-V blo’ck

Normal 500 Yes, eh Abnormal in Vg; 370 Yes, EA

no Q in V6

Apical anterior ea; apical circumferential eh; inferobasal eh

lnferobasal eh Inferior eh

Yes

Yes Yes

14 72 M l-l-7 0.10 No Q in V6 550 Yes, EH

15 80 M 1-3-1 IVCD (atypical LBBB), 1” A-V block

Anterolateral ischemia or subendocardial MI. lo A-V block

LVH with strain LVH with strain

0.14 No Q 480 Yes, eh

Anterolateral EH; Yes inferolateral EH; lnferolateral basal EH

Anterobasal eh No

16 80 F l-2-8 Normal No 0 560 Yes, EA, EH lnferolateral EA; anterolateral EH

Yes

::

19

20

66 M l-l-l 75 F l-2-8

32 F l-2-8

Normal Normal

LVH Normal

NoQ 450 Yes, eh Normal 460 Yes, EH

Normal 320 Yes, TH

60 F l-2-8 IVCD, marked LAD 0.11

Lateral eh lnferobasal eh;

anterolateral EH Apical anterolateral

TH; apical inferolateral ea .-..

Yes Yes

Yes

No Q 495 Yes, TH lnferobasal tH Yes

E. Inferior and Anteroseptal Myocardial Infarction by Electrocardiogram (11 cases)

21 66 M 1-2-4; Atrial fibrillation, 0.10 No 0 500 Yes, anteroseptal lnferobasal TA; Yes l-2-8 nonspecific ST-T TH; No, inferior anterobasal TH

changes



TABLE I (continued)

Age Associated QRS Q Wave Heart Electrocardio- Duration in

graphic Findings (seconds) Weight

VSV6 (9)

Myocardial Infarction ECG Apex

Confirmed Other Involved

22 59 M

23 70 M

24 46 M

25 73 M

26 45 M

27 75 F

28 73 F

29 52 M

30 81 M

31 55 F

l-l-l; l-l-2

l-l-4; l-2-7

l-2-4; l-2-7

l-l-4; l-2-8

l-l-4; l-l-7

l-l-4; l-2-8

l-l-4; l-2-8

l-2-4; l-l-l

l-l-4; l-2-8

l-2-5; l-2-8

Normal

IVCD 0.11

. Normal

IVCD, PVCs. atrial 0.11 fibrillation

IVCD 0.11

LVH Normal

PVCs, LVH, LAD Normal

0.10

. . Normal

. . . Normal

Abnormal 570

Normal 430

Abnormal 480

Abnormal 810

Abnormal in Vs 330

NoQ 400

No Q in V6

Abnormal

No Q

Normal

450

360

350

340

Yes, TH

Yes, TH

Yes, anteroseptal EH; no, inferior

Yes, anteroseptal TH; inferior EH

Yes, EH

Yes, EH

Yes, EH

Yes, inferior eh; anteroseptal TH

Yes, eh

Yes, inferior eh; anteroseotal EH

Anterobasal TH; lateral EH

lnferobasal TH; inferplateral basal TA

Anterobasal TH; inferolateral basal EH

Apical circumferential EA

Apical inferolateral EH; inferolateral basal EH

lnferobasal EH

None

lnferobasal eh; anterolateral eh

None

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

F. Anterolateral Myocardial Infarction by Electrocardiogram (6 cases)

;3 59 M l-l-l Atypical LBBB 0.14 Abnormal 510 Yes, EH 63M . . . Atypical LBBB 0.14 No Q 460 Yes, TH; EA

34 64M l-l-2 IVCD (atypical 0.15 Abnormal 508 Yes, anterior TH; b;Fs). LAD, no, lateral

35 59 F l-l-2 RBBB 0.12 Abnormal 320 Yes, lateral EH; no, anterior

36 79 F l-l-2 0.10 i&B, LAD, PVCs, 0.14

Abnormal 450 Yes, eh 37 68 M l-l-3 NoQ 500 Yes, EH

I0 A-V block

lnferolateral EH Anterobasal EH;

inferobasal eh Inferior TH

Yes Yes

Yes

lnferolateral EH, No inferolateral basal EH

lnferobasal eh Yes lnferolateral EH Yes

G. Anteroseotal and Anterolateral Mvocardial Infarction bv Electrocardioaram 17 cases)

38 86 M l-l-2; IVCD 0.12 Abnormal 340 Yes, lateral TH; no, lnferolateral TH; Yes l-l-2 anteroseptal inferolateral basal TH

39 79 M l-l-6; . Normal Abnormal in Vs; 520 Yes, TH None Yes l-l-2 normal in V6

40 59 F l-l-2; . . . Normal Abnormal 610 Yes, anteroseptal lnferobasal EH; Yes l-l-2 TH; no, lateral inferior EH

41 60 M l-l-2; RBBB 0.13 QS in Vs 540 Yes, lateral TH; no, lnferolateral TH; Yes l-l-l anterior inferolateral basal TH

42 64 F l-2-8; IVCD, LVH, atrial 0.12 Abnormal in V6 590 Yes, lateral TH; no, None Yes l-l-3 fibrillation anterior

43 70 M l-2-8; Left anterior Normal Abnormal 490 Yes, anteroseptal Inferior eh Yes l-l-l hemiblock TH; no, lateral

44 71 M l-2-8 Atypical LBBB 0.14 NoQ 600 Yes, lateral eh; None Yes Yes, anterior TH

H. Inferior and Anterolateral Myocardfal Infarction by Electrocardiogram (3 cases)

45 57 M l-l-l; IVCD (atypical 0.14 Abnormal in V6 500 Yes, TH lnferobasal TH Yes l-l-l LBBB)

46 89 M l-l-4; RBBB, LVH, lo 0.12 Abnormal 720 Yes, lateral, EH; lnferobasal TH No l-l-l A-V block no, inferior

(P-R 0.52) 47 75 F l-l-4; IVCD (atypical 0.14 Abnormal 700 Yes, anterolateral lnferobasal TH Yes

l-l-2 LBBB) EH: no. inferior

I. Infarction Not Identified by Electrocardiogram (3 cases)

48 76M . . . Nonspecific ST-T Normal Normal 410 No Anteroseptal eh; Yes changes in infe- apical inferior eh; rior and antero- inferobasal ea ‘lateral leads (II. 111, aVF,V,-Vi)

49 6OF LVH with strain. Normal Normal 360 No Inferior EH; seotal No ischemic T (I, ‘II, EH; inferobasal EH V4-Vd

50 70M . Nonspecific ST-T Normal No Q 490 No lnferobasal eh No chanoes

A-V = atrioventricular; EA = subendocardial, extensive acute infarct; ea = subendocardial, limited acute infarct; ECG = electrocardiogram; EH = subendocardial. extensive healed infarct; eh = subendocardial, limited healed infarct; IVCD = intraventricular conduction defect; LAD = left axis deviation: LBBB = left bundle branch block; LVH = left ventricular hypertrophy; Ml = myocardial infarction; PVCs = premature ventricular complexes; RBBB = right bundle branch block; TA = transmural acute infarct: TH = transmural healed infarct.

November 1978 The American Journal of CARMOLOGY Volume 42 727


and lateral in one and inferobasal and anteroseptal in the other). In the remaining three cases, the inferior region was not involved. In two of these, healed infarction involved the apical, inferolateral basal and the anterolateral regions. In the last case, only the lateral wall was involved.

Comment: The pathologic finding of inferobasal or lateral involvement, or both, in light of the electrocardiographic finding indicating restriction to the inferior regions suggests that the electrocardiographic criteria for inferior infarction are too restrictive. These criteria may be shared by either basal involvement of the diaphragmatic aspect or by the lateral wall. It is possible that the apical circumferential involvement in two cases affected the electrocardiographic diagnosis of inferior wall myocardial infarction. The lack of identification of anterior involvement may be caused by dominance of involvement of one wall negating signs of involvement of the opposite wall.

Inferior and anteroseptal infarction (11 cases, Table IE): The electrocardiographic diagnosis of inferior and anteroseptal infarction was confirmed in 9 of 11 cases. In two cases pathologic study revealed an inferobasal rather than an inferior infarct. In four cases, an inferobasal infarct was present in addition to the confirmed inferior infarct. In 5 of the 11 cases, some involvement of the lateral wall was present pathologically although not identified from the electrocardiogram.

Comment: The observations indicate that anteroseptal infarction is reliably diagnosed with the electrocardiogram and that, in contrast to the immediately preceding cases, coinfarction of the anterior and inferior walls may be identified in some cases. The electrocardiographic criteria for distinguishing inferior from inferobasal infarction are clearly not reliable, and lateral infarction tends to be undetected with the electrocardiogram.

Inferior and inferobasal infarction (four cases, Table I, B and C): In three patients (Table IB), the electrocardiographic diagnosis was coexistent inferior and inferobasal healed myocardial infarction. This was confirmed at autopsy in two, but in both, lateral involvement evident in the pathologic studies had not been suspected from the electrocardiogram. In the third case, only the inferobasal aspect was involved; the inferior aspect, as defined, was devoid of lesions. In a fourth case (Table IC) the electrocardiographic diagnosis of inferobasal healed myocardial infarction was confirmed.

Anterolateral infarction (six cases, Table IF): The electrocardiographic diagnosis of anterolateral myocardial infarction was made in six cases and confirmed in four. In one of the two remaining cases the lateral wall was not involved; in the other the anterior wall was not involved. In each of the six cases additional involvement of either the inferior or the inferobasal aspect was not detected with the electrocardiogram. In one of the latter cases, the nonidentified infarct was inferior and transmural. The diagnosed anterolateral infarct was also transmural.

Comment: The main point of disagreement between the autopsy and electrocardiographic findings was that involvement of the lateral wall by transmural infarction was not suspected when present. This finding may re- flect either stronger forces related to the inferobasal lesion or a general tendency for lateral involvement to be relatively silent. The findings also indicate that the electrocardiogram may identify a lesion of the diaphragmatic aspect but lacks specificity in distinguishing the basal from the more apical aspect of this wall.

Comment: The pattern of correlation in this subset conforms to that observed with anteroseptal myocardial infarction and probably indicates that the electrocardiogram responds to a resolution of forces in which the signs of involvement of the anterior wall dominate those of involvement of other sites. In all but one case, there was intraventricular conduction delay (right bundle branch block in one and atypical left bundle branch block in four). All four patients with atypical left bundle branch block had three or more sites involved by healed infarction.

Anteroseptal infarction (10 cases, Table ID): The electrocardiographic diagnosis of anteroseptal myocardial infarction was confirmed pathologically in all 10 cases. However, the involvement was more extensive than suggested by the electrocardiogram. The most common infarct sites that were not detected were lateral and inferior. With one exception, the lateral and inferior healed infarcts were subendocardial in distribution. The exception involved a transmural apical anterolateral infarct.

Comment: The electrocardiographic criteria for anteroseptal infarction appear to be reliable but in the presence of such infarction signs of other infarcted areas tend to be less dominant and may not be apparent. All but one of the nondiagnosed infarcts were subendocardial; it is not known whether these infarcts would have been apparent if they had been transmural. The one unidentified transmural infarct occupied an anterolateral position.

Anteroseptal and anterolateral infarction (seven cases, Table IG): In seven cases, the electrocardiogram indicated both anteroseptal and anterolateral involvement; pathologic findings substantiated this combination in only two cases. In the five remaining cases there was some involvement in the broad zone covered, but the pathologic process was less extensive than suggested by the electrocardiogram. In three of these cases the infarction was primarily lateral and in two primarily anteroseptal. Four specimens showed additional involvement of the inferior or inferobasal walls that was not suggested in the electrocardiogram. Two of these infarcts were transmural.

Comment: Failure of the electrocardiogram to identify a lesion in the inferior wall when there are lesions in some other part of the free wall of the left ventricle was observed in other subsets of this study. The lack of clear correlation with pathologic findings when the electrocardiogram indicates both anteroseptal and an-


terolateral involvement suggests that the electrocardiographic criteria for distinguishing the anterior from the lateral wall are too rigid. Intraventricular conduction delay occurred in four cases.

Inferior and anterolateral infarction (three cases, Table IH): The electrocardiographic diagnosis of inferior and anterolateral infarction was confirmed at autopsy in one case. In the other two cases the inferobasal aspect rather than the inferior region was involved. Additionally, in the one case with pathologic confirmation inferobasal infarction was also present.

Comment: Involvement of the lateral wall does not mask signs of infarction of the diaphragmatic aspect of the left ventricle but, as in previous cases, the electrocardiographic criteria for distinction between the inferior and inferobasal aspects as defined are not reliable.

Nonspecific changes (Table II): In three cases, the electrocardiogram was abnormal but did not indicate a specific zone of infarction. The healed infarction was limited and subendocardial in two cases, anteroseptal in one and inferobasal in the other. In the third case there was extensive subendocardial infarction in the inferior, inferobasal and septal regions.

Comment: The finding that only 3 of 50 cases of pathologically identified healed infarction had a non- diagnostic electrocardiogram suggests that the electrocardiogram is fairly reliable in identifying old infarction whatever its shortcomings are in identifying all specific areas of infarction.

Apical infarction: Of 13 patients with anteroseptal or anterolateral myocardial infarction, or both, and apical circumferential infarction, 3 had left bundle branch block. Two of these had abnormal Q waves. Of the remaining 10, only 3 had “abnormal” Q waves, 3 had no Q wave and 4 had “normal” Q waves. Two subjects, each with a single infarct and apical involvement, had “abnormal” Q waves in leads Vs and Vs. Of 14 patients with an infarct in two areas and also apical involvement, 9 (64 percent) had an “abnormal” Q wave in leads Vg and Vs. Of 17 patients with apical involvement and infarction in three areas, 24 percent (4 of 17) showed “abnormal” Q waves in leads Vs and Vs, whereas of 7 patients with apical involvement and infarction in four areas, 29 percent (2 of 7) had “abnormal” Q waves in these leads. The Q wave was absent in leads Vs and Vs in 14 percent of patients (2 of 14) with apical involvement and two areas of infarction, in 41 percent of patients (7 of 17) with apical involvement and three areas of infarction and in 43 percent of patients (3 of 7) with apical involvement and four areas of infarction. Thus, 45 percent of 40 patients (18 of 40) with apical involvement showed “abnormal” Q waves in leads Vs and Vs, 25 percent (10 of 40) had normal Q waves in these leads and 30 percent (12 of 40) had no Q wave in these leads.

Discussion

General considerations: Numerous studies have correlated electrocardiographic and pathologic findings

in instances of healed myocardial infarction.g-27 The methods used to evaluate the electrocardiograms and pathologic specimens have varied considerably. The electrocardiographic diagnosis of myocardial infarction has been based on abnormal Q waves defined as either a deep Q (Q/R amplitude ratio greater than 25 percent)2s or a Q wave duration greater than 0.03 or 0.04 second7J3-1s~2s,2g or the combination of a Q/R ratio greater than 25 percent and a Q wave duration from onset to nadir greater than 0.02 or 0.03 second, de- pending on the lead.ls-ls We have used the Minnesota codes in interpreting the 12 lead electrocardiograms. These codes have been used extensively in large scale epidemiologic studies for the diagnosis and localization of myocardial infarction. They include a spectrum of electrocardiographic abnormalities based on degrees of Q wave duration and Q/R amplitude ratio in various leads and provide criteria for myocardial infarction that range from strong (codes l-l) to somewhat weak (codes l-3).

The pathologic approaches to examination of the heart also vary considerably. The studies based on multiple gross cross sections of the ventricles generally provide accurate information about the extent and location of myocardial infarcts. Recently, attempts have been made to quantitate the size of myocardial infarcts by subjecting the margins of infarcts to planimetry after obtaining photographs of sections of the heart.27

Inferior and inferobasal infarction: Our correlative findings concerning inferior and inferobasal myocardial infarcts diagnosed with the electrocardiogram are in general agreement with those of others.17Jsp2s-27 When the electrocardiographic diagnosis is inferior myocardial infarction, the pathologic specimen often shows involvement of the inferobasal and adjacent lateral sites in addition. There is also frequent apical involvement. Our findings suggest that the terms inferior, diaphragmatic and inferoposterior (posterobasal, strictly posterior) are too restrictive, because they imply that the electrocardiogram can distinguish between involvement of one of these areas and involvement of other areas. No electrocardiographic findings were identified in this study that would aid in recognizing involvement of inferobasal, apical and adjacent lateral sites when they are associated with inferior involvement.

The pathologic findings in our hearts with an electrocardiographic diagnosis of inferior infarction are similar to those reported by others.2e>2s-27 Inferior myocardial infarction as defined pathologically is rarely found as an isolated lesion. A review of 12 “typical” cases with posterior myocardial infarction reported by Savage et a1.27 showed basal and medial involvement in all cases and apical involvement in 10 cases.

Anterior infarction: In cases with anteroseptal myocardial infarction, the apex was involved in all but one case. In the exceptional case, the infarct involved the anterobasal sites and related ventricular septum. The areas mainly involved in anteroseptal myocardial infarction were the middle and the apical portions of the




anterior left ventricular wall and septum. Additional involvement of anterolateral sites seen pathologically was not revealed in the electrocardiogram. We found no electrocardiographic clues for identifying apical involvement in the presence of anteroseptal myocardial infarction. Apical involvement is common in anteroseptal myocardial infarction and its presence can be assumed in nearly every case with a diagnosis of anteroseptal myocardial infarction.

markers to identify apical involvement. In 8 of 11 cases in this group, the diagnosis of anteroseptal infarction was based on relatively weak (l-2-8 or l-2-7) codes.

In 5 of 10 cases the diagnosis of anteroseptal myocardial infarction was based on a relatively weak Min- nesota code (l-2-8). This code is characterized by a decreased R wave amplitude in the precordial leads. Our findings in anteroseptal myocardial infarction are in agreement with those reported previ- ou~ly.1~-~3~~0~~~~24~25~27~29~30 The reported cases are comparable with ours and frequently have lateral, inferior or anteroseptal involvement in addition to the anteroseptal infarct, as in 10 of 12 cases reported by Savage et a1.27

In each of the three cases with an electrocardiographic diagnosis of inferior and anterolateral myocardial infarction, the QRS duration was prolonged. Two cases had an atypical left bundle branch block and one a right bundle branch block pattern. There was inferior involvement in the form of inferior or inferobasal infarct in all three cases. Anterolateral or lateral involvement was present in two cases, and apical circumferential involvement in the third.

Intraventricular conduction delay in the form of atypical left bundle branch block occurred frequently in cases with a diagnosis of anterolateral myocardial infarction alone or in combination with other infarcts. Such cases exhibit Q waves in leads I and aVL, and sometimes in leads Vs and Vs.

In the six cases with electrocardiographically diagnosed anterolateral myocardial infarction, the QRS complex was wide except in one case with a QRS duration of 0.10 second. Apical involvement was present in all four patients with atypical left bundle branch block and anterolateral myocardial infarction. Our findings agree with those of Horan et a1.,7 who have reported extensive apical and anteroseptal infarction in the presence of left bundle branch block with Q waves in leads I, aVL, V5 and Vs. Except for one case, lateral involvement was part either of anterolateral or inferolateral involvement.

Acute myocardial infarction: Acute myocardial infarction alone or in combination with healed infarcts was present in 10 cases. The acute myocardial infarction was transmural in two and subendocardial in the remaining eight cases (four limited, four extensive). There was S-T segment elevation corresponding to the area involved in three cases, S-T depression and T wave in- version in six cases and only flat T waves in one case. In the latter case there was a limited acute apical anterior subendocardial infarct.

When the electrocardiographic diagnosis of combined anteroseptal and anterolateral myocardial infarction was made, four of seven cases had a prolonged QRS duration. Three exhibited an atypical left bundle branch block and one a right bundle branch block pattern. Apical involvement was present in each of the seven cases. Pathologically, lateral involvement was present in five cases. In two cases, there was no lateral involvement. Anterior left ventricular wall involvement in the form of anteroseptal, anterobasal and apical was present in five cases. In two cases with an electrocardiographic diagnosis of anteroseptal myocardial infarction, only the inferolateral or apical inferolateral portions of the left ventricle were involved.

Combined inferior and anterior infarction: When an electrocardiographic diagnosis of both inferior and anteroseptal myocardial infarction is made, there is usually extensive involvement of anterior and inferior walls of the left ventricular wall. Observations related to the electrocardiographic identification of isolated anteroseptal and inferior infarction also apply to their combination. In two cases, inferior myocardial infarction was diagnosed with the electrocardiogram, but pathologic studies revealed apical circumferential without inferior involvement. Furthermore, there was apical involvement in all cases with an electrocardiographic diagnosis of combined inferior and anteroseptal myocardial infarction. In contrast to previous claims,14,20,22,27,31 we found no electrocardiographic

Intraventricular conduction defects: Forty percent of patients (16 of 40) with apical involvement had

,increased QRS duration (15 had “atypical” or “typical” left bundle branch block, whereas 1 had right bundle branch block). Thirty percent of patients (3 of 10) with no apical involvement had increased QRS duration (1 patient had intraventricular conduction delay, and 2 had right bundle branch block). Thus, 38 percent of patients (19 of 50) in this study had increased QRS duration. The incidence of increased QRS duration was 6 percent (1 of 16) in single infarcts, 44 percent (8 of 18) in patients with two areas involved, 37 percent (7 of 19) in patients with three areas involved and 43 percent (3 of 7) in patients with four areas involved. Thus, there were three subjects with right bundle branch block, nine with left bundle branch block and seven with intraventricular conduction delay. The septum and parts of the septum closely related to the conduction system were involved in every case except one with intraventricular conduction delay and apical lateral infarction. These observations support previous findings of septal and apical infarction when the electrocardiogram shows a left bundle branch block pattern with abnormal Q waves.26 Although both electrocardiographic and vectorcardiographic criteria for the diagnosis of myocardial infarction in the presence of left bundle branch block have been described, these should be used with caution because of many false positive results.7,26,32-3g

Q waves in subendocardial infarction: Our findings regarding the incidence of abnormal Q waves in subendocardial infarction agree with previous data.11J2J4,25-27 The majority of our cases had subendocardial myocardial infarction. Although it has been



repeatedly shown that subendocardial infarcts, even very small ones, can produce abnormal Q waves40 the electrocardiographers have traditionally ascribed abnormal Q waves to transmural myocardial infarction.

Implications: The electrocardiographic localization of myocardial infarction based on Minnesota codes (inferior, anteroseptal, anterolateral) appears more reasonable than the numerous localizations suggested in previous reports (septal, anteroseptal, anterior, lateral, high lateral, inferior, true posterior, apical, and so forth). The 12 lead electrocardiogram does not provide adequate information for such detailed and exact classification.

Our study indicates that, in general, the electrocardiographic recognition of myocardial infarction (Min- nesota codes l-l, l-2,1-3) is reasonably good. The recognition of general localization is fair. However, as previously reported,18,25-27 the recognition of the exact extent of myocardial involvement is poor. There is frequently extension of the infarct into areas adjacent to the main infarct. Such extensions usually are not recognized in the electrocardiogram. Although the sensi- tivity (percent of cases with myocardial infarction

diagnosed as myocardial infarction) of electrocardiographic criteria used in this study appears to be good, the specificity (percent of noninfarct cases diagnosed as nonmyocardial infarction) is not known.

It has been suggested that in the presence of anterior myocardial infarction, a normal R wave in leads V4 to Ve represents anterior apical, a markedly diminished R wave implies intermediate apical and an abnormal Q wave represents apical circumferential involvement. Our studies do not justify such a conclusion. In the presence of anteroseptal myocardial infarction or combined anteroseptal and anterolateral myocardial infarction, one can assume with high probability that there is apical involvement.

Whether other methods of recording the electrical potentials of the heart, such as vectorcardiography or body surface mapping, will provide information regarding the location and extent of myocardial infarction superior to that provided by the 12 lead electrocardiogram is not known. There are limitations to the use of various electrocardiographic terms related to the location and extent of myocardial infarcts. These need to be recognized.

References

1.

2.

3.

4.

5.

6.

7.

a.

9.

10.

11.

12.

13.

14.

Merrill SL, Pearce ML: An autopsy study of the accuracy of the electrocardiogram in the diagnosis of recurrent myocardial infarction. Am Heart J 81:48-54, 1971 Achor RWP, Futch WD, Burchell HB, Edwards JE: The fate of patients surviving acute myocardial infarction. Arch Intern Med 98:162-174, 1956 Levine HD, Phillips E: An appraisal of the newer electrocardiog- raphy: correlations in one hundred and fifty consecutive autopsied cases. New Engl J Med 245:833-842. 1951 Woods JD, Laurie W, Smith WG: The reliability of the electrocardiogram in myocardial infarction. Lancet 2:265-269. 1963 Blackburn H, Keys A, Simonson E, Rautaharju P, Punsar S: The electrocardiogram in population studies. A classification system. Circulation 21:1160-1175, 1960 Coronary Drug Project Research Group. The Coronary Drug Project: Design, Methods, and Baseline Results. Circulation 47:Suppl I:I- l-I-50, 1973 Horan LG, Flowers NC, Tolleson WJ, Thomas JR: The significance of diagnostic Q waves in the presence of bundle branch block. Chest 58:214-221, 1970 The Criteria Committee of the New York Heart Association: No- menclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels, seventh edition. Boston, Little, Brown, 1973, p 347 Fenichel NM, Kugell VH: The large Q-wave of the electrocardiogram. A correlation with pathological observations. Am Heart J 71235-248, 1931 Wolferth CC, Wood FC: Acute cardiac infarction involving anterior and posterior surfaces of left ventricle. Electrocardiographic characteristics. Arch Intern Med 56:77-87. 1935 Kossmann CE, de la Chapelle CE: The precordial electrocardiogram in myocardial infarction. I. Observations on cases with infarction principally of the anterior wall of the left ventricle and adjacent septum. Am Heart J 15:700-720, 1938 Wilson FN, Johnston FD, Rosenbaum FF, Erlanger H, Kossmann CE, Hecht H: The precordial electrocardiogram. Am Heart J 27: 19-85,1944 Myers GB, Klein HA, Stofer BE: I. Correlation of electrocardiographic and pathologic findings in anteroseptal infarction. Am Heart J 36:535-575, 1948 Myers GB, Klein HA, Hiratzka T: II. Correlation of electrocardiographic and pathologic findings in large anterolateral infarcts. Am

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.


Heart J 36:838-881, 1948 Myers GB, Klein HA, Hiratzka T: Ill. Correlation of electrocardiographic and pathologic findings in anteroposterior infarction. Am Heart J 37:205-236, 1949, Myers GB, Klein HA, Hiratzka T: IV. Correlation of electrocardiographic and pathologic findings in infarction of the interven- tricular septum and right ventricle. Am Heart J 37:720-770, 1949 Myers GB, Klein HA, Hiratzka T: V. Correlation of electrocardiographic and pathologic findings in posterior infarction. Am Heart J 38:547-591.1949 Myers GB, Klein HA, Hiratzka T: VI. Correlation of electrocardiographic and pathologic findings in posterolateral infarction. Am Heart J 38:837-862, 1949 Myers GB, Klein HA, Stofer BE: VII. Correlation of electrocardiographic and pathologic findings in lateral infarction. Am Heart J 37:374-417,1949 Hoffman MS, Edwards JE, Pruitt RD: The Electrocardiogram in Acute and Healing Myocardial Infarction: Clinicopathologic Cor- relations. Rochester, Minnesota, The Mayo Clinic, 1952 Sayen JJ, Sheldon WF, Wolferth CC: The heart muscle and the electrocardiogram in coronary disease. Ill. A new classification of ventricular myocardial damage derived from the clinicopathologic findings in 100 patients. Circulation 12:321-337, 1955 Dunn WJ, Edwards JE, Pruitt RD: The electrocardiogram in infarction of the lateral wall of the left ventricle. A clinicopathologic study. Circulation 14:540-555, 1956 Cook RW, Edwards JE, Pruitt RD: Electrocardiographic changes in acute subendocardial infarction. I. Large subendocardial and large nontransmural infarcts. Circulation 18:603-612, 1958 Richman JL, Wolff L, Call R: The significance of QS deflections in the right-sided precordial leads: autopsy correlation. Am Heart J 541537-547, 1957 Wilkinson RS Jr, Schaefer JA, Abildskov JA: Electrocardiographic and pathologic features of myocardial infarction in man. Am J Cardiol 11:24-35, 1963 Horan LG, Flowers NC, Johnson JC: Significance of the diagnostic Q wave of myocardial infarction. Circulation 43:428-436, 1971 Savage RM, Wagner GS, ldeker RE, Podolsky SA, Hackel DB: Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction. Retro- spective study of patients with typical anterior and posterior in-


farcts. Circulation 55:279-285, 1977 28. Pardee HEB: The significance of an electrocardiogram with a large

Q in lead 3. Arch Intern Med 46:470-48 1, 1930 29. Goldberger E: The differentiation of normal from abnormal Q

waves. Am Heart J 30:341-365, 1945 30. Feil H, Cushing EH, Hardesiy JT: Accuracy in diagnosis and lo-

calization of myocardial infarction. Am Heart J 15:721-738, 1938

3 1. Barnes AR: Electrocardiogram in myocardial infarction. Review of one hundred and seven clinical cases and one hundred and eight cases proved at necropsy. Arch Intern Med 55:457-483, 1935

32. Chapman MG, Pearce ML: Electrocardiographic diagnosis of myocardial infarction in the presence of left bundle-branch block. Circulation 16:558-571, 1957

33. Rhoads DV, Edwards JE, Pruitt RD: The electrocardiogram in the presence of myocardial infarction and intraventricular block of the left bundle-branch type. A clinical pathologic study. Am Heart J 62:735-745, 1961

34. Sodi-Pallares D, Cisneros F, Medrano GA, Bisteni A, Testelli M, De Micheli A: Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block (right and left),

ventricular premature beats and Wolff-Parkinson-White syndrome. Prog Cardiovasc Dis 6:107-136. 1963

35. Besoain-Santander M, Gomez-Ebensperguer G: Electrocardio- graphic diagnosis of myocardial infarction in cases of complete left bundle branch block. Am Heart J 60:886-897, 1960

36. Doucet P, Walsh TJ, Massie E: A vectorcardiographic and electrocardiographic study of left bundle branch block with myocardial infarction. Am J Cardiol 17:171-179, 1966

37. DePasquale N, Burch GE: The spatial vectorcardiogram in left bundle branch block and myocardial infarction, with autopsy studies. Am J Med 29:633-639, 1960

38. Neuman J, Blackaller J, Tobin JR Jr, Szanto PB, Gunnar RM: The spatial vectorcardiogram in left bundle branch block. Am J Cardiol 16:352-358, 1965

39. Wallace AG, Estes EH Jr, McCall BW: The vectorcardiographic findings in left bundle branch block. A study using the Frank lead system. Am Heart J 63:508-515, 1962

40. Durrer D, Van Lier AAW, Buller J: Epicardial and intramural ex- citation in chronic myocardial infarction. Am Heart J 68:765-776, 1964


correlation of electrocardiographic and pathologic findings in healed myocardial infarction

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