New quantitative vectorcardiographic criteria for the detection of unsuspected myocardial infarction in diabetics

New quantitative vectorcardiagraphis detection of unsuspected myocardial infarction

T

#or the

in diabetics

he difficulty of establishing the diagnosis of myocardial infarction in the diabetic patient is well known.‘-’ In a study of autopsy-proved large myocardial infarcts, Rubin and Weiss” found that the electrocardiogram (ECG) was considerably less accurate in the diagnosis of myocardial infarction in the diabetic than in the nondiabetic patient. From these data and from the well-controlled series of Woods, Laurie, and Smith,” and Johnson, Achor, Burchell, and Edwards* it is clear that conventional ECG criteria diagnose definite infarction in nondiabetic subjects with about 50 to 60 per cent accuracy, and in diabetic patients with about 30 to 40 per cent accuracy. The complications observed in patients with diabetes mellitus are largely due to the vascular changes that occur in this disease. Seventy per cent of all deaths among diabetic patients in the United States are due to vascular disease.” Though the incidence of diabetes in the general population is 1 to 2 per cent, the record of patients From

criteria

with myocardial infarction indicate that between 3.0 and 20 per cent are diabetic.2,g*r0 Necropsy examination reveals that coronary-artery occlusion occurs in the diabetic group about five times as frequently as in the nondiabetic group,‘r and that in older diabetic persons, in whom the onset occurred after the age of 40, severe coronary arteriosclerosis occurs almost universally.2*12 It is not uncommon to find scars of old infarcts at autopsy of diabetic patients who died of other causes without a history of myocardial infarction.’ Furthermore, it has been observed that in older diabetic patients the incidence of myocardial infarction is unrelated to the duration or the degree of control of the diabetesL3er4 Consequently, in older patients, by the time a diagnosis of diabetes is made clinically, one can expect that severe coronary artery disease and ischemic fibrosis and/or infarction of the myocardium has occurred. Vectorcardiographic criteria for myocardial infarction have been described by

the Medical Science Service, Rancho Los Amigos Hospital, Downey; the Cardiopulmonary Laboratory at White Memorial Hospital, Los Angeles; and the Department of Internal Medicine, Loma Linda University at Los Angeles, Calif. This investigation ma supported in part by grants in aid from the Los Angeles County Heart Association and the Imperial County Heart Association, and a United States Public Nealth Service Research Grant No. HE 10722.01, Received for publication April 26, 1967.

335

336

sc1vester et ill.

various authors.15-17 These criteria involve dramatic change in the vectorcardiographic loop and usually mirror a large area of infarction. In addition, these changes usually involve the initial portion of this loop. Burch and associates18-20 describe smaller changes occurring in the mid or terminal portions of the loop and relate them to small areas of fibrosis. However, \?-e could find no specific criteria in the literature to determine which of these smaller deviations were normal or abnormal. With these observations in mind, the purpose of this study was twofold: (1) to establish vectorcardiographic criteria for small scars and/or infarction, and (2) to determine whether the vectorcardiogram (VCG) is more sensitive than the ECG in the diagnosis of myocardial infarction in the diabetic patient. Methods

and

materials

The records of 96 patients treated for diabetes mellitus since 1956 v,?-ere selected for use in this study. These records were obtained from the White I\Iemorial Hospital, Ranch0 Los Amigos Hospital, and the Los Angeles County General Hospital. The selection was based on two criteria: (1) the records must contain both an ECG and a VCG taken at the same time; and (2) the age of the patient at the time diabetes was diagnosed must have been 15 years or less, or 40 years or more. The second criterion served the purpose of clearly separating diabetic patients with juvenile onset from those with maturity onset. The two groups consisted of 32 with juvenile onset, ranging in age from 6 to 51 years, and 64 with maturity onset, ranging in age from 47 to 84 vears. Most of the ECG’s used ;n this study were recorded at the cardiopulmonary laboratory of the White I\‘Iemorial Hospital where for some years the V leads were routinely recorded at half standard. The adult and juvenile types were subdivided into three groups according to the duration of the disease: 0 to 10 years, 11 to 20 \-ears, and 21 y-ears and over. The fact that electrocardiographic records had been made on individual patients did not necessarily imply clinically suspected cardiac disease, but rather was

7'c~Dle

1.

Age

disiributions

of

$opdations

studied

Onset

of diabetes

Jmmile

Muturifv

4 8 8 6 5 1 0 0 0

0 0 0 0 2 11 26 20 5

Age (YY.1

O-10 1 l-20 21-30 31-40 41-50 5 l-60 61-70 71-80 SO+ Totals

1 Normal

32

1

-1

Raxdonz I

21 18 34 14 9 7 3 0 0

0 4 34 14 23 19 2 2 0

106

98

done only as a matter of routine in this study. All of the patients were ambulatory and none was suspected of having clinically acute heart problems. The vectorcardiographic tracings were taken with the cube system of electrode placement and consisted of timed VCC’s and spatial VCG’s recorded in horizontal, frontal, and right sagittal projections. We also studied a random sample of 9X hospital employees ranging in age from 15 to 75 years, none of whom were known to have diabetes. In addition, we studied 106 normal people ranging in age from 2M weeks to 66 years who had no clinical, x-ray, or electrocardiographic evidence of heart disease. This group was used as a basis for establishing new vectorcardiographic criteria for small or medium-sized destructive my-ocardial lesions. The age distributions of the populations studied are summarized in Table 1. VCG’s from the 106 normal subjects were examined to determine the degree of variation in the loop that could be considered compatible with “normalcy.” These variations presenting as “scallops” or “bulges” \\:ere measured in terms of voltage and duration of change. This \vas done by projecting a line across the “scallop” in the path that the loop would have taken had it not deviated from a smooth progression, and then measuring the deviation in millivolts and milliseconds (Fig. 1).

New qunntitutive

0.08

vectorcrrrdiog~aphic

criteria

337

mv

fb b / t

SIZED

bW-4)

INFARCT

L

Fig. 1. A medium-sized and a small infarct by the criteria proposed is shown on a horizontal plane cube vectorcardiogram. The medium-sized infarct shows the displacement from a smoothly transcribed loop of 0.18 mv. maximum magnitude for a duration of 10 msec. The small infarct shows a displacement of 0.08 mv. for 4 msec.

Table

II.

l/CG

criteria

jov inJ-iLrction*

Magnitude

Normal Possible Small Medium

0.07-0.09 0.10~).20 0.21-0.30

0.04 or less 0.05-0.06 0.07-0.14

2-6

0.15-0.21

7-14

Large

0.31 or more

0.22 or more

*The

0.06 or

less

15 or more

abnormality had to meet the above criteria either in magnitude or duration to be called abnormal to that degree (see text).

The criteria thus established were based on a voltage alteration of sufficient duration or extent to distort the smooth progression of the vectorcardiographic loop beyond that seen in the series of normal tracings. These criteria are described in Table II. Examination of the normal series indicated that there was greater voltage variation in any one segment of the tracing consistent with “normalcy” in the individuals under ten years of age than there was in those older than ten years. The voltage criteria therefore varies with the

patient’s age. We have also classified the size of the lesions as small, medium, or large, depending on the extent of voltage change or the time duration over which the change occurred (Table II). The large lesions by these criteria correspond to the classical criteria for larger infarctions described by various autllors,15-1i and represent a large displacement from a smooth loop or from an average loop for that age group. Based on vectorcardiographic changes, we also classified these lesions as to location into the following areas: (1) anteroseptal, lower half, (2) basal-septal, (3) apex or lateral, (4) free ventricular wall, posterior, (5) superior, including basal left ventricle, (6) free wall posterobasal, and (7) inferior or diaphragmatic, including basal left ventricle (Fig. 2). The vector changes of location were interpreted on the basis of the model of the VCG previously reported.21 This model assumes the human activation sequence to be similar to that reported by Scher and Young”” and confirmed in dogs by our group, and more recently confirmed in human subjects by Durrer and associates.23 The conventional 13-lead ECG’s were read independently by three qualified cardiologists. They did not have the benefit

338

Am. Heart I. Mar&, 1968

Selvester et aE.

of clinical history on any patient in the series, except for age, sex, and cardiac drugs. The criteria used for selection of one interpretation from the three interpretations where there was a difference of opinion are found in Table III. Results

Fig. 2. An illustration into seven segments of infarction in this

Table III. I. II.

III.

*There

Definite Two

of the subdivision used for the purpose study.

Proposed vectorcardiographic criteria. In the examination of the VCG’s of 106 people in the normal series, we found three patients who had changes in potential consistent with infarction by our criteria. These were men of ages 26, 45, and 47 at the time the tracings were done. In addition to these three, there were three others whose tracings fell into the questionable category.

of the heart of location

Criteria for myocardial infarction myocardial infarction or more agreed

Possible myocardial infarction A. Two or more agreed B. One made the diagnosis of definite or possible myocardial infarction, plus one or more of the following: 1. Interventricular conduction defect 2. Left axis deviation of minus 30” or more in the frontal plane 3. Myocardial fibrosis No evidence of infarction A. n‘ormal ECG Two or more agreed, plus any diagnosis except definite myocardial infarction B. Possible normal ECG 1. Two or more agreed 2. One made the diagnosis of possible normal or borderline and the others a diagnosis of the following: a. Normal b. Incomplete right bundle branch block c. Questionable early hypertrophy d. Nonspecific ST-T change C. Interventricular conduction defect without other evidence of infarction 1. Two or more had to agree on one of the following: a. Complete or incomplete right bundle branch block b. Complete or incomplete left bundle branch block c. Interventricular conduction defect type, undertermined D. Left ventricular hypertrophy” without other evidence of infarction. Two or more had to agree E. Pulmonary disease without other evidence of infarction Two or more had to agree F. Nonspecific ST changes Two or more had to agree G. Digitalis effect Two or more had to agree were no cases of right

ventricular

hypertrophy

in this

series.

diagnosed

any

including

one

New quantitative vectorcardiographic

When the criteria were applied to the nondiabetic random sample, it was found that 11 of the 98 subjects had tracings indicative of infarction, and one had a questionable abnormality. The ages of those showing an abnormality ranged from 25 to 73 years. In the series of diabetic patients there were 32 with juvenile-onset diabetes (Table IV). Of these, 12 had definite vectorcardiographic changes suggestive of small infarction, and two others showed questionable abnormalities. In the maturity-onset group of 64 patients, 55 had vectorcardiographic evidence of infarction, usually multiple, with an additional five patients demonstrating questionable changes. Thus, it was found that 44 per cent of the juvenileonset diabetic group, and 94 per cent of the maturity-onset group, had tracings that were read as possible or definite infarction. From Tables IV and V, a comparison \?;as made of evidence for infarction by the proposed vectorcardiographic criteria in juvenile-onset and maturity-onset diabetes as compared to the random group of comparable age. The x” test indicated a significant increase in incidence of infarction (p < 0.05) in the total diabetic group. From Table IV a comparison was made of juvenile-onset with maturityonset diabetes. The increased incidence of

339

criteria

infarction in the maturity-onset group is significant (p < 0.05). This is confounded, however, by the difference in the ages of these two groups. An attempt was made to correct for the effect of aging, by comparing each diabetic group to an agecomparable group from the random population, and then evaluating the resultant differences, thus controlling for the effect of aging. A significant difference between juvenile-onset and maturity-onset groups controlled for age was found (p < 0.05). However, the age distribution in the random group versus the diabetic group was not entirely comparable in each of these age groups (Table I). The age confounding, therefore, between juvenile-onset and maturity-onset diabetes has not been entirely eliminated. Table VI shows a comparison of the incidence of infarction compared to the duration of the diabetes and no relationship was observed. Table VI also shows the relationship between size of lesions as diagnosed by the VCG and the duration of the diabetes in both the juvenile-onset and maturityonset groups. Again no relationship between size (severity of destructive disease) and duration was observed. However, when the juvenile and maturity sets of data were combined and compared with each other, there was a significantly different proportion of small lesions in the juvenile-

Table IV. Diagnosis by ECG and VCG in diabetics Juvenile

onset

ECG

Maturity

VCG

onset

ECG

VCG

/ Normal Borderline normal Infarct Possible infarct I.V.C.D. type undetermined L.B.B. block without infarct R.B.B. block without infarct Nonspecific ST-T changes Digitalis effect Pulmonary disease L.V.H. without infarct Totals

27 3

(84%) (10%) -

2 ( 6%) -

18

12 (38%) 2 ( 6%)

-

32 (100%)

(56%)

32

17 2

(27%) ( 3%)

:i

i:g;

-

1 4 4 7 5

( I.:%) ( 6%) (6%) (11%) (8%)

-

1 2

( 1.5%) ( 3%)

(1009;b)

64

(100%)

1

(1.5%)

55 (86%) 5 ( 8%) 1

( 1.570) -

2. 64

( 3%) (1000/o)

340

Sclvester

et 111.

onset as couipared to the maturity-onset group (p < 0.05). This is due to a predominance of small lesions within the juvenileonset group and a predominance of large lesions in the maturity-onset group. It should be noted that the abnormalities described occurred in the mid and terminal portions of the loop with about the same frequency as they did in the initial part of the loop. ECG kterpretation. The electrocardiographic interpretations of the cardiologists Table V. VCG evidence mndom populcrtion

of irqkrction

Myocardial .lge (!‘i.S.)

in

a

infarction

~-~ , ~ Definite

~ Possible

~

None

I

Total

1 7

1 0

-1-l 39

s2 46

Totals

11

1

86

98

Table \]I.

Severity

15 to 40 41+

disease as seen on the VCG comptrred

of destructive

VCG nz1KLti0n (Y.1

j

None

Possible

7 5 6

2 0 0

onset O-10 1 l-20 21+

chosen for this study revealed that in the juvenile-onset group there were no tracings diagnostic of myocardial infarction, although there were two tracings interpreted as possibly due to infarction. The tracings of the maturity-onset groups were diagnostic of infarction in 11 cases, while an additional 10 cases were suggestive of infarction. Therefore, the interpretations of the ECG’s revealed the suggestion of infarction in only 6 per cent of the juvenileonset group and 33 per cent of the maturity-onset group. The electrocardiographic interpretations are summarized in Table IV. Comparison qf ECG with VCG. A comparison of the electrocardiographic (concensus) readings with the vector readings is shown in Fig. 3 and Table IV. There Tvere 67 patients whose VCG’s revealed definite evidence of myocardial infarction in the total series; 11 of these patient’s KG’s were read as definite infarction and 56 failed to show definite evidence of infarction (Table VII). The diagnoses of possible infarct by either ECG or VCG was

diqrrosis:

definite

eoidence

to the duucrtion

of diabetes

oJ inJarction Totals

Juvenile

Subtotal ‘Totals Maturity onset O-10 1 l-20 21+ Subtotal Totals

0 0 0 0

18

2

12

2 2 0

1 3 1

9 5 1

4

S

*Criteria for size: (0) no infarct, (?) diffuse fibrosis, (1) single small, (2) multiple and multiple small or multiple medium, (5) large and one IX more medium

15

-

0 0 0 0

11 6 0 17 -

0 0 0 -

0

6 5 5 16

55

small, (3) medium or large

12 s 12 -

64

_+ single small,

(4) large or medirlrn

New quuntitutive

Analysis of ECG misses. AREA. Using the activation

sequence of Scher and Youngz2 and the theoretical model of the VCG proposed by US,~~it was possible to divide the septum and left

32

Fig.

ECG 64

VCG 32

VCG 64 Peapie

3.

Table VII. Infarcts diagnosis of infarction

dejinitely

diagnosed

341

criteriu

ventricle into seven large areas (Fig. 2). There was no relationship between the area of infarction as interpreted by the VCG and the accuracy of the ECG (Table VIII). This agrees with the findings of Rubin and Weiss3 SIZE. Out of 67 patients from the total series whose VCG’s were diagnostic of infarction, 34 had small or medium infarcts and 32 (94 per cent) were missed by the ECG (Table VII). There were 33 cases in which the VCG demonstrated single or multiple large lesions and 24 (72 per cent) of these failed to show definite evidence of infarction by the ECG. The ECG was more accurate with large lesions than with medium-sized and small lesions, and this difference was significant (p < 0.05). This indicates that our current ECG criteria are, in general, less sensitive to the smaller lesions. CONDUCTION DEFECTS. In four of the 24 cases, the VCG depicted large infarcts and a conduction defect (Table VII), and the ECG showed only the conduction defect without evidence of infarction. As previously pointed out by Zinn and Cosbyz4 and Rubin and Weiss,3 conduction defects may mask the ECG diagnosis of infarcts in diabetic patients. However, in this study when the ECG diagnosis of infarction in the presence or absence of a conduction defect was compared to the over-all ac-

called negative for the purpose of the following analysis.

ECG

vectorcurdiogvuph~ic

by proposrd

VCG

criteria

and

tabulation

of ECG

Large ECG

diagnosis Medium (size

LIefinite Possible

infarct or no infarct

und small 1, 2, 3y

2 32 -

Srtbtotals Totals

Single (size J)

Multiple (size 5)

:

8 --34

I 1

_______

Condzictim defect and lnrge

8 13

(2H 4

21

1

33

Table VII is compressedfor the definite infarcts diagnosed by the proposed VCG criteria in Table VI. “See Table VI for size classification. tone casgwith VCG showing small, and one casf with KG showing single large, in addition to a conduction defect.

T&l

11 56

67

342

Selvester

Table VIII.

Am Heaut 1. March, 1968

et al.

Accuracy of ECG related to area of &$arction Area

E CG diagnosis

No. of , patients

1’

I

)

as seen on the VCG*

of infarct by

VCG

Total

zl,,q-q-,rJ-i

inj’aycts

a2E:

I Juvenile-onset diabetes No infarct Possible infarct Definite infarct Maturity onset diabetes No infarct Possible infarct Definite infarct

10 2 0

3 0 0

0 0 0

4 1 0

2 0 0

1 0 0

0 0 0

1 1 0

11 2 0

34 10 11

4 0 6

0 0 0

11 0 7

10 4 3

6 3 1

4 0 2

16

51 15 26

;

*Patientsin thistablehavedefiniteinfarctionby theVCGcriteriaproposed in thispaper.Thenumberof infarctsdiagnosed is greater thanthe numberof patientsin manycategories because multiplelesions werediagnosed frequentlyby theproposed VCGcriteria.

curacy of the ECG, no relationship was observed. In this series the ECG was as accurate in diagnosing infarction in the presence of a conduction defect as in its absence. The sample size of conduction defects was small, however, and may have obscured a real difference had it been present. MULTIPLE LESIONS. A total of 13 of the 24 had multiple lesions on the VCG’s (Table VII), and in such cases it has been suggested by several authors15,25+26that a second lesion may produce changes neutralizing the first lesion and hence obscuring either or both lesions by conventional electrocardiographic criteria. However, in our series the statistical analysis of ECG accuracy in the diagnosis of single and multiple lesions failed to show a significant difference between the diagnostic accuracies in the two classes. We also have no explanation for the additional seven cases in which the VCG showed a single large infarct and the ECG failed to show infarction (Table VII). The fact that the vast majority of the precordial leads of the ECG’s used in this study were recorded at 0.5 cm. per millivolts rather than 1.0 cm. per millivolts may have contributed to the failure of the ECG in some instances. Discussion

In evaluating VCG’s of diabetic patients it was felt that more specific criteria for the diagnosis of myocardial infarc-

tion should be formulated. Other authors have described criteria involving dramatic changes in the vectorcardiographic loop, and in the cases that have come to autopsy a rather large area of myocardial involvement was usually n0ted.l’ Burch described the small changes so often seen in the VCG as ‘
New quantitative vectorcardiographic

Johnson, Achor, Burchell, and Edwards4 reviewed 1,267 autopsies at the Mayo Clinic with adequate medical records, and found an incidence of definite infarction of 11 per cent. Half of these were unsuspected clinically. In view of the previously demonstrated inaccuracy of electrocardiographic diagnosis of autopsy-proved myocardial infarction in diabetic patients, it is not surprising to find this diagnosis made infrequently in the diabetic population of this study in which many have no history of heart disease. The high percentage (94 percent) of persons with maturity-onset diabetes that showed vectorcardiographic abnormalities consistent with infarction, on the other hand, is consistent with the pathological observation that extensive coronary artery disease is almost universally present in those with maturity-onset diabetes who come to autopsy.2s12z27 The frequent lack of classical electrocardiographic evidence of infarction in diabetes may be explained in one of three ways, and likely all mechanisms are operative. First, recent studies28-30 have shown that there is extensive microarteriolar disease in this group. Blumenthal, Alex, and Goldenberg”l have shown that these lesions involve the coronary arteries as well as the kidneys, central nervous system, retinae, and conjunctivae. In such cases, one might expect multifocal fibrosis of the myocardium without large unifocal infarcts. Multifocal fibrosis has been demonstrated in patients with disease in the small intramuscular coronary arteries in the absence of main coronary disease by Domomae, Matsumoto, and Ueda.32 Ischemic multifocal fibrosis has also been observed in about one half of patients with the usual variety of main coronary artery narrowing and/or occlusion when careful pathological studies are done such as those reported by Woods, Laurie, and Smith* and by Ehrlich and Shinohara.33 Such multifocal disease may well fail to produce the electrocardiographic changes of the classical localized unifocal infarction. Second, when size, as diagnosed by the proposed vectorcardiographic criteria, is compared to the ECG diagnosis (Table VIII), it is clear that small abnormal “bite out” lesions on the VCG consistently failed

criteria

343

to produce ECG changes diagnostic of infarction, and these were rarely classified as possible infarction. When small and single medium-sized lesions (sizes 1, 2, and 3 of Table VI) were lumped together for the entire series, again the inability of the ECG to diagnose such lesions (6 per cent accuracy) is readily apparent (Table VII). The diagnostic accuracy of the ECG, on the other hand, increased to nearly 40 per cent when multiple large lesions (indicated by the proposed vectorcardiographic criteria) were present. It has been suggested that when multiple infarcts occur, a second, third, or fourth infarct may produce counterbalancing vectors that obscure earlier clear-cut evidence of infarction, and leave behind only nonspecific ST and T changes. Our data, however, do not support this hypothesis; when single large lesions were compared to multiple large lesions, no difference in the diagnostic accuracy of the ECG was found. In summary, it appears that the larger the infarct as seen by the VCG and the more evidence for myocardial destruction that there is, the greater the accuracy of the ECG. Third, these data indicate that the notion that the diagnosis of infarction is made only from changes in the initial portions (initial 0.04 vector) of the QRS is untenable. With infarction of the basal portions of the septum and left ventricle one would expect changes limited to the terminal QRS. Such changes are generated by our modeP and have also been reported by Burch and associates,r8-20 Massey and Walsh,15 and others34,35 (Fig. 4 & 5). Infarction of the outer one half of the apex or free left ventricular wall near the apex will produce changes limited to the mid portion of the QRS (Fig. 6 & 7). Criteria for infarction such as those proposed in conventional ECG texts which are limited to changes in the initial 0.04 second of the QRS could not be expected to diagnose such infarcts. The VCG, because of its increased gain, high-frequency oscilloscopic records, and its depiction of phase changes between two leads, is much more likely to pick up small high-frequency “bite outs” or irregularities in the depolarization of the ventricular myocardium such as would occur in single small scars and in multifocal infarction.

344

Selvestev et d.

SPATIAL VCG

PAPER SPEED JQ mmhec

TIMED VCG

I HDRlZDNTAL

SAGITTAL

Fig. 3. The spatial and timed VCG the QRS that lasts for 10 msec. and as multiple small infarcts mainly in a medium-sized one in over-all loss normal.

!

j

I

PLANE

PLANE

in this patient reveals notching and slurring in the terminal portion of deviates from a smooth loop by 0.1 mv. This lesion was classified, therefore, the posterobasal region (area 6) of the left ventricle. This lesion approaches of posterior basal x-ectors. The initial 0.04 sec. of the QRS loop is relatively

OVR aVL aVF

Fig. 5. This I3-lead ECG, from the same patient whose vector is shown in Fig. 4, demonstrates symmetrical wave inversion in Leads I, AVL, and VJ to V,+ The r-wave progression in anterior precordial leads is normal no diagnostic Q waves are seen. There is slight terminal slurring of the QRS in Leads I, 11, III, AVL, and through VB. Tracing was interpreted as left ventricular &hernia and probable enlargement.

T and VIR

New qunntitcdive vectomudiographic

SFWIAL

VCG

TIMED VCG

Fig, 6. Spatial and timed vectorcardiograms (area 4) by the proposed criteria. This patient approximately six months prior to this record. The first 0.04 sec. is relatively normal.

PAPER SPEED JQ. -...__

critek

345

mm/!&.

showing a large infarct in the true posterior wall near the apex is an 8%year-old man who had a clinically documented infarct Note that the abnormalities are mainly from 0.036 to 0.054 sec.

Fig. 7. This 13-lead ECG, on the patient whose vector is ities in many leads and a relative!y normal initial QRS standard, are the only chest leads available and show a initial r-waves in right-sided leads. Increasing the gain slurring and notching in t.his patient, even with a direct-writer

shown in Fig. 5, throughout. The slurred S in V,R and the paper recorder.

demonstrates chest leads, and VI and speed would

terminal QRS irregularwhich are recorded at >$ normal progression of the undoubtedly show more

346

Selvester

et al.

Over-all, the major reason for failure to diagnose infarction by the ECG in this series was attributable to the inability (at any gain) of the conventional directwriter ECG to record high-frequency components, This, coupled with the fact that current accepted ECG criteria for infarction do not include slurs or notches in the QRS, or changes in the terminal QRS as diagnostic of infarction, accounted for the vast majority of failures of the ECG to diagnose infarctions in this group. In a small percentage the diagnosis of infarction may have been missed because the precordial leads were taken at ,I$$standard (0.5 cm. = 1 mv.). However, a review of these ECG’s suggests that this was a possible factor in less than 5 per cent of records over-all. It would appear from the work of Langer and co-workers36 which has been confirmed by Durrer,37 by Corday38 and by us that the amount of high frequency energy in the ECG is much greater in patients with coronary artery disease. The present study is highly consistent with this hypothesis, and suggests that current ECG recording techniques and instrumentation are badly in need of overhaul. As a first step, using options available on most directwriter ECG machines, we propose that all tracings be recorded at 2 cm. per millivolt and at a 50 mm. per second paper speed to make maximum use of the limited frequency response that is present in such instruments. It is also clear from this study that both ECG and VCG criteria need to be refined to include these small changes, and changes in mid and terminal QRS as well. It must be emphasized again that these patients do not all have proved infarction by conventional clinical criteria. Myocardial fibrosis and/or infarction is assumed on the basis of the known almost universal association of advanced coronary artery disease and maturity-onset diabetes. What is now needed is a careful correlation of these vectorcardiographic changes with complete pathological maps of the myocardium at autopsy such as those done by Ehrlich and Shinollara,33 and Woods, Laurie, and Smith.* It is hoped that this report will stimulate such investigation in a number of centers. The entire field of

cardiac electrophysiology benefit by such a study. Summary

and

would

clearly

conclusions

1. Sew quantitative VCG criteria are proposed for the diagnosis of small and medium-sized myocardial infarcts to supplement criteria for large infarcts previously established by other workers. These changes occurred in the initial and terminal portions of the QRS with about the same frequency. 2. These criteria were tested on a random population and defined the expected number of infarctions. 3. Of the cases of maturity-onset diabetes in the present series, 86 per cent were read as defmite infarction by these proposed criteria, and 8 per cent were read as possible infarct. Therefore, 94 per cent were at least suggestive of infarction. 4. Of the cases of juvenile-onset diabetes, 38 per cent were read as definite infarction by these criteria and 6 per cent were read as possible. Only small lesions were observed in juvenile-onset cases. 5. Single and multiple large lesions were common in maturity-onset diabetes. 6. The severity of the VCG changes was unrelated to the severity or duration of diabetes in this series. 7. The ECG’s were interpreted as possible infarction in only 6 per cent of the cases of juvenile-onset diabetes and as definite or possible infarction in 33 per cent of the cases of maturity-onset diabetes. 8. The ECG’s missed 94 per cent of small or medium-sized lesions diagnosed by the VCG in this series, but missed only 62 per cent of those with multiple large lesions. 9. The fourfold increase in accuracy of the VCG in this series is presumed to be due to the greater gain, frequency response, and two-dimensional vectorcardiographic display, and to the use of the proposed criteria which include changes in the entire QRS as diagnostic. 10. It is apparent from these data that current ECG recording instruments are inadequate to record a great deal of potentially useful information at the body surface, and attention is called to the urgent need of improving such instrumentation. 11. The ECG’s recorded with most direct writers can be significantly improved by

Volume

75

Numbw

3

New quantitative vectorcardiographic

routinely recording tracings at a gain of 2 cm. per millivolt and a paper speed of 50 mm. per second. 12. Routine pathological studies are inadequate to find and classify small destructive lesions of myocardium, and attention is called to the urgent need of more, carefully detailed studies of these lesions to correlate with the type of VCG changes reported in this paper. Special acknowledgment is given to William Paul Thompson, M.D., Eugene J. Ellis, M.D., and Erwin I,. Hoffman, M.D., for their assistance in reading the ECG’s in this series.

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