electrocardiographic localization of coronary...

Electrocardiographic Localization of Coronary ArteryNarrowings: Studies During Myocardial Ischemiaand Infarction in Patients with One-vessel Disease

RICHARD M. FUCHS, M.D., STEPHEN C. ACHUFF, M.D., LouISE GRUNWALD, B.A.,FRANK C.P. YIN, M.D., PH.D., AND LAWRENCE S.C. GRIFFITH, M.D.

SUMMARY To investigate the accuracy of the 12-lead ECG in localizing the site of coronary arterynarrowings, we reviewed abnormal ECGs obtained during myocardial infarction, spontaneous angina orexercise stress testing in 134 patients with angiographically documented one-vessel disease. The presence ofQ waves, ST-segment elevation and T-wave inversion in leads I, aVL and V1-V4 were all highly correlatedwith the presence of left anterior descending coronary artery disease (p < 0.001), and the same ECGfindings in leads II, III and aVF were associated with right (RCA) or circumflex coronary artery (LCx)narrowings (p < 0.001). In contrast, ST depression alone was not useful in predicting the site of coronaryartery narrowing. Q waves correctly identified the location of the coronary disease in 98% of cases, STelevation in 91%, T-wave inversion in 84%, and ST depression in 60%. No electrocardiographic criteriadistinguished RCA from LCx disease, even in patients with a right-dominant circulation. These findingsshould lead to a better understanding of the value and limitations of the 12-lead ECG in localizing coronaryartery disease.

ABNORMALITIES in the 12-lead ECG are often usedto localize the anatomic site of myocardial infarctionand ischemia in patients with coronary artery dis-ease. 1-3This practice is based largely on autopsy seriescorrelating the site of myocardial infarction with thelocation of Q waves on antemortem ECGs: Q waves inthe precordial leads VI-V4 appear to reflect anteriorWai, infarction; Q waves in leads II, III and aVF inferi-or wall infarction; and Q waves in leads I, aVL, V5 andV6 lateral wall infarction. 9 These same ECG findingsare often assumed to correlate with coronary arteryanatomy as well. Anterior wall infarction is usuallyattributed to disease of the left anterior descendingcoronary artery (LAD), inferior wall infarction to dis-ease of the right coronary artery (RCA) except in pa-tients with left-dominant systems, and lateral wall in-farction to disease of the left circumflex (LCx)coronary artery.' Unfortunately, there is only limiteddocumentation for these correlations between the loca-tion of coronary artery narrowings or occlusions andthe findings of Q waves during myocardial infarc-tion. '01 I There is even less documentation of the accu-racy of electrocardiographic ST-segment or T-wavechanges in identifying the site of injury or ischemiaduring infarction, rest angina or stress testing. Studiesare often confounded by the inclusion of patients withmultivessel coronary artery disease, which makes itdifficult to determine in which vascular distribution

From the Cardiovascular Division, Department of Medicine, TheJohns Hopkins Medical Institutions, Baltimore, Maryland.

Presented in part at the 51 st Scientific Sessions of the American HeartAssociation, Dallas, Texas, November 1978.

Dr. Fuchs is the recipient of a fellowship grant from the AmericanHeart Association. His present address: Department of Medicine, TheNew York Hospital-Cornell Medical Center, 525 East 68th Street, NewYork, New York 10021.

Address for correspondence: Lawrence S. C. Griffith, M.D., Divi-sion of Cardiology Department of Medicine, The Johns Hopkins Hospi-tal, 600 North Wolfe Street, Baltimore, Maryland 21205.

Received January 19, 1982; revision accepted May 10, 1982.Circulation 66, No. 6, 1982.

ischemia occurred. Nonetheless, patients who developST depression in leads II, III and aVF during angina arecommonly referred to as having "inferior wall ische-mia" and are often presumed to have RCA disease;similar associations are often drawn between ST de-pression in anterior precordial leads and LAD disease,and between ST depression in so-called lateral leads Iand aVL and LCx disease. 'We have not found such associations to be uniform-

ly valid. Therefore, we undertook the present study toevaluate the value and limitations of the 12-lead ECGin localizing the site of coronary artery disease. Onehundred thirty-four patients with angiographicallydocumented one-vessel coronary disease and abnormalECGs recorded during myocardial infarction, sponta-neous rest angina or treadmill exercise testing wereevaluated, and electrocardiographic-angiographic cor-relations were obtained.

MethodsPatient SelectionThe records of all adult cardiac catheterization stud-

ies performed at the Johns Hopkins Hospital betweenJanuary 1971 and April 1981 were reviewed; patientswith a final diagnosis of one-vessel coronary arterydisease were selected for further evaluation. For eachcase, the coronary angiographic films were reviewedindependently by two observers without knowledge ofthe clinical or electrocardiographic findings. At leastfour views of the left coronary system and at least twoviews of the right coronary system were routinely ob-tained in each patient. Patients were considered to haveone-vessel disease only if both observers described a70% or greater diameter narrowing in one of the threemajor coronary arteries (LAD, RCA or LCx) withoutnarrowing > 40% in the other two coronary arteries ortheir branches. No patient with significant narrowingin the left main coronary artery was included. Hospitalrecords and stress test results were sought for all thesepatients.

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ECG LOCALIZATION OF CORONARY NARROWING/Fuchs et al.

The study population consisted of all 134 patientswho met the following criteria: one-vessel coronarydisease as defined above; no significant valvular orcongenital heart disease; no bundle branch block or leftventricular hypertrophy on resting ECG; and an abnor-mal 12-lead ECG recorded during myocardial infarc-tion documented by cardiac enzyme elevations, spon-taneous angina at rest, with normal cardiac enzymesand reversible electrocardiographic changes or anginaduring exercise testing. Ten patients had positive stresstests after recovering from a myocardial infarction,and three patients had ECGs recorded during both restangina and stress testing; thus, 147 instances of abnor-mal ECGs form the basis for this report.

Exercise TestsAll tests were standard graded treadmill exercise

tests using a modified Bruce protocol. Electrodes wereplaced according to the method of Mason and Likar. 12The exercise protocol was a submaximal test; the pa-tient walked for 1 minute at 00 incline at 1 mph, then 2minutes at 100 and 2 mph, then 3 minutes each at 150and 3 mph, 200 and 3 mph and 22° and 4 mph. Twelve-lead ECGs were recorded at rest, during each minuteof exercise, upon termination of exercise and everyminute thereafter until the ECG returned to baseline.Tests were terminated when at least one of the follow-ing end points was reached: moderate or severe angina,severe dyspnea, claudication or fatigue; 2 mm of hori-zontal or downsloping ST-segment depression or 2mm of ST elevation; or 90% of the predicted maximalheart rate for age.

ElectrocardiogramAll ECGs were reviewed independently by two of

the investigators; only changes graded as abnormal byboth were included. Serial ECGs recorded during thecourse of myocardial infarction were analyzed, and 11leads (all except aVR) were evaluated individually ac-cording to a modification of the Minnesota code.'3 Qwaves were considered significant when their durationwas at least 0.04 second in any lead or at least 0.03second in association with a Q/R ratio greater than 1:3in leads I, II and V2-V6. ST-segment elevation wasconsidered significant if the J point was elevated morethan 1 mm and the ST segment remained elevatedmore than 1 mm 0.08 second beyond the J point.Similarly, ST-segment depression was considered sig-nificant if the J point was depressed by more than 1 mmand the ST segment was horizontal or downsloping andremained 1 mm below the baseline 0.08 second be-yond the J point. T-wave inversions were consideredsignificant in leads I, II and V2-V6 when the net ampli-tude was negative; in leads III, aV, and aV, when theQRS was isoelectric or mainly upright and the net T-wave amplitude was negative; and in lead VL when thenet amplitude was negative and represented a changefrom a previous tracing. The same criteria were usedfor ST-segment change and T-wave inversion duringangina at rest and for ST-segment change during stresstesting.

Statistical EvaluationData were tabulated comparing the prevalence of Q

waves, ST elevation, ST depression and T-wave inver-sion in each electrocardiographic lead in patients withone-vessel disease involving the LAD, RCA and LCx.To examine the importance of "reciprocal" STchanges, additional tables were prepared showing theprevalence of ST depression in tracings with and with-out concomitant ST elevation in any lead. The preva-lence of each ECG change was compared betweenpatients with LAD and non-LAD (RCA or LCx) dis-ease, lead by lead, with the chi-square test and, whereappropriate, by Fisher's exact test. To avoid type IIerrors when examining 11 leads in each of three clini-cal situations (i.e., myocardial infarction, unstable an-gina and exercise testing), differences were consideredsignificant if p < 0.01.

ResultsPatient PopulationThe study group consisted of 96 men and 38 wom-

en, ages 27-73 years (mean + SD 48 ± 9 years). Of 71patients with isolated LAD disease, 42 had had a myo-cardial infarction, seven had angina at rest and 30 hadpositive stress tests. Of 47 patients with one-vesselRCA disease, 29 had had a myocardial infarction, fourhad angina at rest and 19 had positive stress tests. Of16 patients with disease limited to the LCx, eight hadhad a myocardial infarction, one had angina at rest andseven had positive stress tests. Seven patients withLCx disease had a right-dominant circulation, six had abalanced circulation, and three had a left-dominantcirculation.

Myocardial InfarctionDuring the course of myocardial infarction, the lo-

cation ofQ waves was highly predictive of the locationof the obstructed coronary artery (table 1). Twenty-nine patients with LAD disease developed significantQ waves in one or more of leads I, aVL and V,-V4; withone exception, Q waves did not develop in these leadsin patients with RCA or LCx disease (p < 0.001 foreach lead). In contrast, Q waves in leads II, III and aVFreflected infarction in the RCA or LCx territory andoccurred in only one patient with LAD disease (p <0.001). Q waves were found in leads V5 and V6 inpatients with both LAD and non-LAD disease. Four ofthe six patients with LCx disease and Q waves duringinfarction had a right-dominant circulation; two had abalanced circulation. All six of these patients showedsignificant Q waves in at least two of the "inferior"leads (II, III and aVF), and none developed Q waves inlead I or aVL. ECG criteria did not distinguish betweenpatients with infarction due to RCA disease and thosewith infarction due to LCx disease.The associations between the location of ST-seg-

ment elevation during myocardial infarction and thelocation of the obstructed coronary artery were alsoquite strong, but exceptions were found more frequent-ly than with Q waves (table 2). ST-segment elevation

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VOL 66, No 6, DECEMBER 1982

TABLE 1. Q Waves During Myocardial InfarctionI L V1 V2 V3 V4 V5 V6 II III F

LAD (n=29) 10* 15* 24* 27* 26* 23* 11 7 1* 1* 1*RCA (n=25) 0 0 0 0 0 0 1 4 18 25 24LCx (n=6) 0 0 0 0 0 1 3 4 3 5 5

*Significant difference in prevalence of Q waves in that lead between LAD and non-LAD patients, p < 0.001.Abbreviations: LAD = left anterior descending coronary artery; RCA = right coronary artery; LCx = left circumflex

coronary artery.

in leads I, aVL and V -V5 during myocardial infarctioncorrelated with the presence of LAD disease(p < 0.005 for each lead); ST-segment elevation inleads LI, III and aVF was associated with RCA or LCxdisease (p < 0.005). All patients with LCx diseaseand ST elevation during myocardial infarction had ele-vation in at least two of the inferior leads (II, III andaVF). Three of the LCx patients had a right-dominantcirculation; two had a balanced circulation.T-wave inversion in leads I, aVL and V2-V6 during

myocardial infarction was strongly associated withLAD disease (p < 0.005 in each case) (table 3), andT-wave inversion in leads II, III and aVF occurredpredominantly in patients with RCA or LCx disease(p < 0.005). All five patients with LCx disease and T-wave inversions during infarction had inversion in atleast two of the inferior leads. One of these patientshad a right-dominant circulation, one left-dominant,and three balanced. The exceptions to the electrocar-diographic-angiographic associations were more fre-quent with T-wave inversion than with Q waves or ST-segment elevation, but the association was still strong.

ST-segment depression during myocardial infarc-tion followed a different pattern. Depression in leads I

and aVL was associated with RCA or LCx disease, anddepression in leads III and aVF was associated withLAD disease (all p < 0.001) (table 4). These STdepressions probably represent "reciprocal" changes.Of the 42 patients with ST depression during myocar-dial infarction, 37 also had simultaneous ST elevationin other leads. Patients with ST elevation in leads I,

aVL and V1-V5 tended to have ST depression in leadsIL, III and aVF, whereas patients with ST elevation inleads II, III and aVF tended to have ST depression inleads I and aVL.

Rest AnginaPatients in whom ECGs were recorded during rest

angina tended to have ST elevation and T-wave inver-sion in the same leads as during myocardial infarction(tables 2 and 3). The number of ECGs recorded duringrest angina was small, however, and significant associ-ations were present only between T-wave inversion inlead V4and LAD disease (p < 0.005) and between T-wave inversion in lead aVF and RCA or LCx disease(p < 0.005). Only five patients had ST depressionduring rest angina; no significant associations werepresent (table 4).

TABLE 2. ST-segment ElevationI L VI V2 V3 V4 V5 V6 II III F

OverallLAD (n= 54) 16t 24t 31t 45t 40t 34t 26t 16 6t 2t 3tRCA (n=23) 0 1 4 3 3 2 2 2 16 22 21LCx (n=6) 1 0 1 0 0 1 2 2 4 4 5

During myocardial infarctionLAD (n=36) 15t 17t 24t 34t 31t 29t 25t 15 6t 2t 3tRCA (n=16) 0 0 3 3 3 2 2 2 12 16 16LCx (n=5) 1 0 0 0 0 1 2 2 4 4 5

During rest anginaLAD (n=4) 1 1 1 4 4 3 1 1 0 0 0RCA (n=2) 0 0 1 0 0 0 0 0 2 2 2LCx (n = 0)

During stress testingLAD(n=14) 0 6 6 7 5 2 0 0 0 0* 0RCA (n=5) 0 1 0 0 0 0 0 0 2 4 3LCx (nl1) 0 0 1 0 0 0 0 0 0 0 0Symbols indicate a significant difference in prevalence of ST-segment elevation in that lead between LAD and non-

LAD patients:*p < 0.01.tp < 0.005.4p < 0.001.

Abbreviations: See table 1.

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TABLE 3. T-wave Inversion

I L V1 V2 V3 V4 V5 V6 H III F

OverallLAD (n=45) 33t 39t 12* 34t 35t 40t 39t 33* 7t 9t 2t

RCA (n=30) 7 8 1 4 6 9 11 12 20 28 28

LCx (n=6) 1 0 0 0 0 1 2 3 5 6 6

During myocardial infarctionLAD (n=38) 29* 34* 9 28* 29* 33* 32* 29* 7* 7* 2*

RCA (n=27) 7 8 1 4 6 9 11 12 20 25 25

LCx (n=5) 1 0 0 0 0 1 1 2 4 5 5

During rest anginaLAD (n=7) 4 5 3 6 6 7* 7 4 0 2 0*

RCA (n=3) 0 0 0 0 0 0 0 0 0 3 3

LCx (n= 1) 0 0 0 0 0 0 1 1 1 1 1

Symbols indicate a significant difference in prevalence of T-wave inversion in that lead between LAD and non-LADpatients:

*p < 0.005.tp < 0.001.


Exercise TestingAll 56 patients with positive stress tests had typical

angina pectoris during exercise; ST-segment elevationdeveloped in 20 of these patients. Angiographic corre-

lations with the leads in which ST elevation occurredduring exercise testing revealed a pattern similar to thecorrelations with ST elevation during myocardial in-farction (table 2), but a significant association was

found only between ST elevation in lead III and RCAdisease (p < 0.01).

ST-segment depression developed in 54 of the 56patients with positive stress tests. There was no corre-

lation between the diseased coronary artery and theleads in which ST depression occurred (table 4). This

lack of correlation was unaffected by excluding pa-

tients who also had ST-segment elevation during stresstesting, in whom ST depression might be assumed tobe reciprocal.

ST-segment ElevationThe data on ST-segment elevation can also be exam-

ined primarily with respect to electrocardiographicchanges, regardless of the clinical event associatedwith those electrocardiographic changes. When ECGsrecorded during myocardial infarction, rest angina andstress testing were combined, ST-segment elevation inleads I, aVL and V-V5 appeared to be associated withLAD disease (p < 0.005) (table 2), and ST elevation

TABLE 4. ST-segment DepressionI L VI V2 V3 V4 V5 V6 II III F

OverallLAD (n=49) 2* 0* 0 7 12 22 29 22 31 32* 33*

RCA (n=37) 19 19 1 6 10 16 22 16 13 10 11

LCx (n=ll) 2 3 2 4 5 6 7 7 5 4 5

During myocardial infarctionLAD (n=1i7) 0* 0* 0 1 2 4 3 0 7 14* 10*

RCA (n=17) 15 16 1 5 4 6 6 3 1 0 0

LCx (n=4) 2 3 2 4 4 4 2 2 0 0 0

During rest anginaLAD (n=3) 0 0 0 1 2 2 2 1 0 1 1

RCA (n=2) 1 1 0 0 1 1 1 1 0 0 0

LCx (n = 0) - - -

During stress testingLAD (n=29) 2 0 0 5 8 16 24 21 24 17 22

RCA (n=18) 3 2 0 1 5 9 15 12 12 10 11

LCx (n=7) 0 0 0 0 1 2 5 5 5 4 5

*Significant difference in prevalence of ST-segment depression in that lead between LAD and non-LAD patients, p <0.001.


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in leads II, III or aVF with RCA or LCx disease(p < 0.001).

T-wave InversionWhen ECGs recorded during infarction and rest an-

gina were combined, T-wave inversion in leads I, aVL,V1 V6 was associated with LAD disease (p < 0.005,table 3), and T-wave inversion in leads II, III or aVFwas associated with RCA or LCx disease (p < 0.001).

ST Depression and Reciprocal ChangesWhen ECGs recorded during infarction, rest angina

and stress testing were combined, ST depression inleads I and aVL was associated with RCA or LCxdisease (p < 0.001) (table 4), and ST depression inleads III and aVF with LAD disease (p < 0.001).These findings are opposite to those found with Qwaves, ST elevation and T-wave inversion and areprobably due to a high prevalence of "reciprocal" ST-segment depression. If tracings with ST depressionalone are examined (excluding tracings with ST eleva-tion in some leads and depression in others), thesesignificant associations disappear (table 5).Of the 57 patients in whom ST elevation was record-

ed during the course of myocardial infarction, 31(54%) had ST depressions in other leads on the sametracing. These "reciprocal" changes were seen lessoften in patients with infarctions due to LAD occlusion(39%) than in patients with LCx (80%) or RCA (88%)disease. In patients with reciprocal changes, ST de-pression was noted in lead II, III or aVF in every case ofLAD disease, and in lead I or aVL in every case of RCAdisease. ST depression in the precordial leads was seenin eight of 15 patients with RCA disease. In the fourcases of reciprocal change due to LCx infarction, STdepression was found in at least three precordial leadsin all four patients and in lead I or aVL in three of thefour (table 6).

Eighteen of the 20 patients with ST-segment eleva-tion during stress testing had significant ST depressionin other leads on the same record. The distribution ofthese ST-segment depressions was similar to that of the

reciprocal changes found during myocardial infarc-tion: ST depression in lead II, III or aVF was generallyassociated with ST elevation in lead aVL or V1-V4 andLAD disease. ST depression in lead I, aVL or V2-V4was generally associated with ST elevation in lead II,

III or aVF and RCA or LCx disease. In this group, STdepression in leads V and V6 was found frequentlywith one-vessel disease of the LAD, RCA and LCx.

Variations in Coronary Anatomy, Collateral Vesselsand Severity of Coronary Stenosis

Inferior ST-segment depression during stress testingof patients with one-vessel LAD disease might havebeen due to the presence of an unusually large LADthat extended around the cardiac apex to supply thedistal inferior wall. Our data showed that this was notthe case: 15 of the 18 patients with one-vessel LADdisease in which the LAD wrapped around the cardiacapex had ST depression in at least one inferior leadduring stress testing, while nine of 11 patients withLAD obstruction and short LADs (stopping at or be-fore the apex) developed ST depression in lead II, IIIor aVF during stress testing.

Similarly, the presence or absence of angiographi-cally visible collateral vessels arising from the RCA orLCx and supplying the diseased LAD coronary arteryterritory did not correlate with the presence of inferiorST depression during myocardial infarction or stresstesting. Of 29 patients with LAD disease and ST de-pression during stess testing, eight had angiographical-ly visible collaterals. Six of these eight (75%) had STdepression in leads II, III or aVF, while 18 (86%) of the21 patients without collaterals had ST depression in atleast one inferior lead.

Finally, some coronary nafrowings in "nondis-eased" arteries that appeared to involve no more than40% of the lumen diameter might have been hemody-namically significant. If so, some of our patients mighthave had two- or three-vessel disease. However, ex-cluding all patients with any detectable narrowing inthe nondiseased vessels did not alter the conclusions:The location of Q waves, ST elevation and T-wave

TABLE 5. ST-segment Depression Excluding Tracings with Simultaneous ST-segment Elevation

I L V1 V2 V3 V4 V5 V6 II III F

Overall

LAD (n=22) 1 0 0 7 12 18 19 9 13 7 10RCA (n= 15) 3 1 0 1 4 8 13 10 10 7 8LCx (n=6) 0 0 0 0 1 1 4 4 4 3 4

Differences between LAD and non-LAD patients were not significant.Abbreviations: See table 1.

TABLE 6. "Reciprocal" Changes: Prevalence ofST-segment Depression in Tracings with Simultaneous ST Elevationin Other Leads During Myocardial Infarction

I L VI V2 V3 V4 V5 V6 II HI FLAD (n=14) 0 0 0 0 0 1 1 0 7 14 10RCA(n=15) 13 15 1 5 4 5 5 2 0 0 0LCx (n=4) 2 3 2 4 4 4 2 2 0 0 0


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inversion remained predictive of the location of coro-nary disease, but ST depression alone was notpredictive.

Predictive ValueTable 7 illustrates the usefulness of electrocardio-

graphic location of Q waves and ST-T changes in lo-calizing coronary artery disease in this selected patientpopulation. The presence of a Q wave in two or moreof leads I, aVL and V,-V4 during myocardial infarctionwas 100% predictive of LAD disease; ST elevation intwo or more of these leads during infarction, rest angi-na or stress testing was 94% predictive; and T-waveinversion in two or more of these leads during infarc-tion or rest angina was 83% predictive. Similarly, thefinding of Q waves in two or more of leads II, III andaVF during infarction was 97% predictive of RCA orLCx disease; ST elevation in two or more of theseleads during infarction, rest angina or stress testingwas 90% predictive; and T-wave inversion in two ormore of these leads during infarction or rest angina was89% predictive. Excluding patients who had simulta-neous ST elevation and depression, ST depression intwo or more of leads I, aVL and V,-V4 during infarc-tion, rest angina or stress testing was 60% predictive ofLAD disease; ST depression in two or more of leads II,III and aVF was 56% predictive of RCA or LCx dis-ease. By these criteria, the ECG location of Q waves,ST elevation and T-wave inversion were highly predic-tive of the anatomic location of coronary disease(p < 0.001 in each case), but ST depression was notpredictive (p > 0.25).

DiscussionThe present study shows that (1) the development of

Q waves, ST elevation or T-wave inversion in lead I,aVL or V,-V4 is highly predictive of LAD disease; (2)the development of Q waves, ST elevation or T-waveinversion in lead II, III or aVF is highly predictive ofthe presence of RCA or LCx disease, regardless ofwhether a right, left or balanced distribution is present;(3) RCA disease cannot be distinguished from LCxdisease by ECG criteria; (4) "reciprocal" ST depres-sion frequently develops during infarction and stresstesting; and (5) the ECG location of ST depression isnot very useful in predicting the location of coronaryartery disease.

These conclusions are based on a study of patientswith one-vessel coronary disease in which many trac-ings were recorded during myocardial infarction andduring stress testing and smaller numbers during restangina. Although this study did not include a largenumber of patients with angina at rest, the patterns ofST-segment and T-wave changes in this group general-ly paralleled those recorded during infarction andstress testing; hence, the above conclusions probablyapply to all three clinical circumstances. Investigationof patients with one-vessel coronary disease is impor-tant, because only in such patients can one be reason-ably certain in which vascular distribution ischemia orinfarction is occurring.

TABLE 7. One-vessel Disease: Electrocardiographic-Angio-graphic Correlations

Present Presentin 2 or in 2 ormore of more ofleads I, leadsaVL, II, III,V1-V4 aVF p

Q waves (n = 57)LAD 28 1 <.0RCAILCx 0 29 <0.001

ST elevation (n = 70)LAD 44 3 <.0RCA/LCx 3 26 <0.001

T-wave inversion (n = 78)LAD 43 4 <.0RCA/LCx 9 34 <0.001

ST depression (n = 82)LAD 14 33 <.0RCAfLCx 34 15 <0.001

ST depression excludingtracings with ST elevation(n= 35)LAD 12 1 1 >02RCA/LCx 8 14 >0.25


The correlation between the leads in which patho-logic Q waves occur and the anatomic location of theinfarction was noted as long ago as 19354 and has beenrepeatedly confirmed.5-9 With the advent of coronaryangiography, these correlations were extended to in-clude coronary artery anatomy. 10'" Early studies werelimited, however, by the frequent occurrence of mul-tivessel disease; furthermore, ECGs were not exam-ined lead by lead, and leads I and aVL were not evaluat-ed in many cases. Our data from a more homogeneouspatient population show that infarctions termed ante-rior, anteroseptal, anterolateral and lateral are allcaused by LAD occlusion, whereas inferior or dia-phragmatic infarctions are due to RCA or LCx disease.Contrary to some suggestions,' "lateral" infarctionswith changes in leads I and aVL did not occur in pa-tients with LCx occlusions. Q waves in these leadsmay reflect infarction of the LAD diagonal territory.We are aware of no systematic study relating the

ECG location of ST-segment elevation during myocar-dial infarction to the pathologic site of injury or theangiographic site of coronary disease in patients. Ex-perimental studies have shown that ST-segment eleva-tion on the surface ECG develops during epicardial ortransmural myocardial injury.2' 3, 1-17 ST-segmentmapping studies during myocardial infarction'8 andanalyses of electrocardiographic-angiographic correla-tions during coronary spasm'9-2' or exercise-inducedST-segment elevation22-26 have generally supported thebelief that ST elevation in precordial leads indicatestransmural ischemia or injury in the LAD distribution,and ST elevation in the "inferior" leads (II, III andaVF) indicates transmural ischemia or injury in theRCA or LCx distribution. In the present study, we

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confirmed these findings and further analyzed the cor-relations lead by lead.Most studies have indicated that ST-segment eleva-

tion during stress testing is uncommon, although manyof these studies did not record 12 leads during thetest.27-29 The finding that more than one-third of thepatients who underwent stress testing in the currentstudy had ST elevation may be related to the monitor-ing of all 12 leads and use of patients with one-vesseldisease only. This finding was not related exclusivelyto the presence of prior infarction; only five of 20patients with ST elevation during stress testing hadevidence of prior infarction. Dunn et al.25' 26 examineda similar population of patients with one-vessel diseaseand found a similar incidence of ST-segment elevationduring stress testing.

Although T-wave changes have long been recog-nized as a marker for myocardial ischemia and infarc-tion,'- few data are available as to their usefulness inlocating the anatomic site of the perfusion deficit. Thepresent study shows that the location of new T-waveinversions on the resting ECG during myocardial in-farction is useful in predicting the site of coronaryartery disease; in some patients, this appears to be trueduring episodes of rest angina as well.The present study has shown that ST-segment de-

pression alone does not accurately reflect the site ofischemia, probably because ST-segment depressionoccurs frequently both as a primary change due tosubendocardial ischemia or infarction and as a secon-dary "reciprocal" change. ST elevation during myo-cardial infarction is sometimes accompanied by recip-rocal ST depression in "opposite" leads.30 The presentstudy defined the frequency of this reciprocal changein patients with one-vessel disease and indicated thatreciprocal changes are seen more often with RCA andLCx (88% and 80%) than with LAD disease (39%)during myocardial infarction.Our finding of the nonspecificity of the site of ST

depression during stress testing for localizing the likelyregion of myocardial ischemia (i.e., the region per-fused by the vessel with significant stenosis) is in ac-cord with some studies25' 36 but at variance with oth-ers.37-3 Ours, however, is the largest series of positivestress tests in patients with one-vessel disease, wherelocalization of ischemia is more certain.Much has been written about which ECG leads are

most "sensitive" for detecting ischemia during stresstesting.40'41 Our findings, like others, show that leadsVP,V6 and II are the leads with the highest prevalenceof positivity (table 4). However, approximately one-eighth of all positive stress tests were negative in thesethree leads. Monitoring all 12 leads significantly in-creases the yield of positive exercise stress testing andpermits the localization of coronary disease in patientswith ST-segment elevation during exercise.We believe that the nonspecificity of ST-segment

depression in localizing the site of ischemia or infarc-tion is due to the multiple ways in which ST depressioncan be produced. Animal experiments have shown thatsubendocardial ischemia or injury can produce ST de-

pression in leads overlying the area of damage, andtransmural ischemia or injury can produce ST depres-sion in distant "reciprocal" leads.''6' 30, 42 Thus, STdepression in lead II, III or aVF might be due to suben-docardial ischemia in the distribution of the LCx orRCA or to transmural ischemia in the distribution ofthe LAD. There is no clear means of differentiating thetwo possibilities based on the ECG alone. Studies in-volving ST-segment mapping'8 43 and vectorcardiog-raphy33 34 in patients confirm these findings and em-phasize the variability in translation of epicardial leadsinto body surface precordial and limb leads.44 The de-velopment of ST elevation in significant numbers ofpatients during exercise in our study suggest that trans-mural ischemia may develop in some patients undergo-ing stress testing, and ST depression in these casesmay be reciprocal.22 23,30 In some instances, smallareas of transmural ischemia not manifest in the 12-lead ECG by at least 1 mm of ST-segment elevationmay produce reciprocal ST depression in "opposite"leads on the surface ECG. A more sensitive lead sys-tem or a more sensitive criterion for ST elevation (e.g.,¢ 0.5 mm in some leads) might reveal the "primary"ST elevation in some of these cases. An alternativeexplanation, while unlikely, is that ischemia may actu-ally develop in a region supplied through a nonstenoticcoronary artery (e.g., due to coronary spasm or abnor-mal wall stress).

In patients with acute transmural myocardial infarc-tion, several authors have attempted to predict thepresence of a second jeopardized vascular territory bythe presence of ST depression in "opposite" electro-cardiographic leads, often with disparate results. Forexample, anterior precordial ST-segment depression inthe setting of acute inferior myocardial infarction hasbeen variously attributed to concomitant anterior(LAD) disease45'I or to extensive posterolateral (RCAor LCx) infarction.47 48 However, the high prevalenceof "reciprocal" ST depression in patients with one-vessel disease suggests that localization of additionalregions at risk for ischemia or infarction may not bepossible by examining ST-segment depression alone.This is particularly important in populations with ahigh prevalence of multivessel disease, such as pa-tients with myocardial infarction. Our data suggest thatthe presence of ischemia or infarction in more than onevascular territory may only be reliably identified whenQ waves, ST elevation or T-wave inversion are presentin both anterior and inferior leads.We examined the correlation between ECG changes

and coronary anatomy, but did not directly examinewhich myocardial region was ischemic or injured.Given the moderate degree of interpatient variability inthe myocardial area supplied by a given coronary ar-tery,49 it is not surprising that abnormalities in certainleads- notably V5 and V6 -were not very useful inlocalizing the site of myocardial infarction, even whenQ waves occurred in these leads. Changes in the otherleads correlated strongly with narrowings in specificcoronary arteries.

In conclusion, we emphasize the specificity of elec-

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trocardiographic-anatomic correlations in patientswith Q waves, ST-segment elevation and T-wave in-version during myocardial infarction and ischemia.We suggest closer scrutiny of ST segments for eleva-tion during stress testing (particularly in little-usedleads, such as aVL. V1 and V2) and greater caution inthe use of such terms as "anterior" and "inferior"ischemia based solely on ST-segment depression.

AcknowledgmentThe authors gratefully acknowledge the statistical advice of Clayton

Kallman and the assistance of Janet Lewis in preparation of themanuscript.

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3. Chung EK: Electrocardiography: Practical Applications with Vec-torial Principles. New York, Harper & Row, 1980, pp 89-133

4. Wolferth CC, Wood FC: Acute cardiac infarction involving ante-rior and posterior surfaces of the left ventricle. Arch Intern Med 56:77, 1935

5. Myers GB, Klein HA, Stofer BE: Correlation of electrocardio-graphic and pathologic findings in large anterolateral infarcts. AmHeart J 36: 535, 1948

6. Myers GB, Klein HA, Hiratzka T: Correlation of electrocardio-graphic and pathologic findings in large anterolateral infarcts. AmHeart J 36: 838, 1948

7. Myers GB, Klein HA, Stofer BE: VII. Correlation of electrocar-diographic and pathologic findings in lateral infarction. Am Heart J37: 374, 1949

8. Myers GB, Klein HA, Hiratzka T: V. Correlation of electrocardio-graphic and pathologic findings in posterior infarction. Am Heart J38: 547, 1949

9. Savage RM, Wagner GS, Ideker RE, Podolsky SA, Hackel DB:Correlation of postmortem anatomic findings with electrocardio-graphic changes in patients with myocardial infarction. Circulation55: 279, 1977

10. Williams RA, Cohn PF, Vokonas PS, Young E, Herman MV,Gorlin R: Electrocardiographic, arteriographic and ventriculo-graphic correlations in transmural myocardial infarction. Am JCardiol 31: 595, 1973

11. Hamby RI, Hoffman I, Hilsenrath J, Amtablian A, Shanies S,Padmanabhorn VS: Clinical, hemodynamic and angiographic as-

pects of inferior and anterior myocardial infarctions in patients withangina pectoris. Am J Cardiol 34: 513, 1974

12. Mason RE, Likar I: A new system of multiple lead exercise electro-cardiography. Am Heart J 71: 196, 1966

13. Rose GA, Blackburn H: Electrocardiographic reading codes (Ap-pendix D). In The Coronary Drug Project: Design, Methods andBaseline Results. Circulation 47 (suppl 1): 1-39, 1973

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15. Ekmekci A, Toyoshima H, Kwoczynski JK, Nagaya T, PrinzmetalM: Angina pectoris. IV. Clinical and experimental difference be-tween ischemia with ST elevation and ischemia with ST depres-sion. Am J Cardiol 7: 412, 1961

16. Guyton RA, McClenathan JH, Newman GE, Michaelis LL: Sig-nificance of subendocardial ST segment elevation caused by coro-

nary stenosis in the dog. Epicardial ST segment depression, localischemia and subsequent necrosis. Am J Cardiol 40: 373, 1977

17. Vincent GM, Abildskov JA, Burgess MJ: Mechanisms of ischemicST segment displacement. Circulation 56: 559, 1977

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19. MacAlpin R: Relation of coronary arterial spasm to sites or organicstenosis. Am J Cardiol 46: 143, 1980

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iani GP, Salerno J, Bobba P: Coronary arterial spasm in angina atrest associated with transient ST segment changes. Clin Cardiol 3:54, 1980

21. Yasue H, Omote S, Takizawa A, Masao N, Hyon H, Nishida S,Horie M: Comparison of coronary arteriographic findings duringangina pectoris associated with ST elevation or depression. Am JCardiol 47: 539, 1981

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High-density Lipoprotein Cholesterol andPrognosis After Myocardial Infarction

Prepared for the Coronary Drug Project Research Group by

KENNETH G. BERGE, M.D., PAUL L. CANNER, PH.D. , AND ADRIAN HAINLINE, JR., PH.D.

SUMMARY The Coronary Drug Project was a randomized, placebo-controlled trial of lipid-influencingdrugs in men who had recovered from one or more documented myocardial infarctions. Determinations ofhigh-density lipoprotein (HDL) cholesterol were made at baseline in a group of 354 men randomized to theplacebo group. Five-year mortality was highest (33.0%) in men with baseline serum HDL cholesterol levelsof less than 35 mg/dl; it was 15.9%, 17.7%, and 21.8% in men with levels of 35-39, 40-44, and 45 mg/dl,respectively (for the linear inverse relationship between HDL cholesterol and 5-year mortality, p = 0.029).Adjustment for 40 baseline variables had a minimal effect on this relationship (p = 0.042).

IN RECENT YEARS, several epidemiologic studieshave indicated that low levels of high-density lipopro-tein (HDL) cholesterol in the blood are associated withan increase in incidence and severity of coronary heartdisease and with ischemic cerebrovascular disease.1-9To our knowledge, no prospective data have been re-ported regarding possible prognostic significance ofHDL cholesterol levels determined after recovery fromacute myocardial infarction (MI). Limited data avail-able from the baseline period of the Coronary DrugProject allow an assessment ofHDL cholesterol in thiscircumstance.

MethodsThe Coronary Drug Project10 was a randomized,

double-blind, placebo-controlled trial of lipid-influ-encing drugs in the secondary prevention of coronaryheart disease. Men ages 30-64 years (mean 52.4 years)who had recovered from one or more documented MIswere recruited by 53 project clinical centers. Men with

The Coronary Drug Project was carried out as a collaborative studysupported by research grants and other funds from the National Heart,Lung, and Blood Institute.From the Department of Internal Medicine, Mayo Clinic, Rochester,

Minnesota; the Department of Epidemiology and Preventive Medicine,University ofMaryland, Baltimore, Maryland; and the Clinical Chemis-try Division, Center for Environmental Health, Center for Disease Con-trol, Atlanta, Georgia.

Address for correspondence: Paul L. Canner, Ph.D., Division ofClinical Investigation, Department of Epidemiology and PreventiveMedicine, University of Maryland, 600 Wyndhurst Avenue, Baltimore,Maryland 21210.

Received February 2, 1982; revision accepted May 5, 1982.Circulation 66, No. 6, 1982.

chronic conditions other than coronary heart diseasewere excluded from the study; thus, 88% of the deathswere from cardiovascular causes. As part of their base-line clinical assessment, three sets of lipid determina-tions were carried out under fasting conditions in themorning, after a low-fat meal the previous evening.During the early phases of the enrollment period, base-line lipid analyses included determination of the HDLcholesterol to be used in later assessment of adherenceto the estrogenic treatment groups. This procedure wasdiscontinued after such sets of data were obtained on1038 men, including 354 men randomized to the place-bo group. The latter group forms the basis of thisreport.

Laboratory MethodsTotal cholesterol was determined by the AutoAna-

lyzer N-24a method modified to give results compara-ble to the method of Abell et al. 1012 Serum HDL cho-lesterol was determined by the method of Walton andScott,'3 which was modified to permit measurement ofcholesterol by the AutoAnalyzer on the supernatantobtained by precipitation of low-density lipoproteinsby a reagent composed of dextran sulfate, barbital andcalcium chloride. Serum triglyceride was determinedon the AutoAnalyzer using the chromotropic acid reac-tion with a silicic acid chloroform extract of se-rum 10 14-16

Univariate and multivariate linear regression analy-ses were used to determine the relationship of baselineHDL cholesterol levels to 5-year mortality in the pla-cebo group, both unadjusted and adjusted for 40 base-

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R M Fuchs, S C Achuff, L Grunwald, F C Yin and L S Griffithmyocardial ischemia and infarction in patients with one-vessel disease.

Electrocardiographic localization of coronary artery narrowings: studies during

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1982 American Heart Association, Inc. All rights reserved.

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