significance ofthe diagnostic wave of myocardial...

Significance of the Diagnostic Q Waveof Myocardial Infarction

By LEO G. HORAN, M.D., NANCY C. FLOWERS, M.D.,AND JENNIFER C. JOHNSON, M.D.

SUMMARYCorrelation between the QRS complex and postmortem ventricular anatomy was

made in 1184 instances of normal conduction:(1) Mechanical reliance on the sheer presence or absence of a Q wave greater than

0.03 sec in duration led to "correct" diagnosis of infarction or not in 79% of theseries.

(2) With normal conduction, abnormal Q waves isolated to either the anteroseptal(Vl-V4) or inferior (II, Ill, aVF) electrocardiographic zones were frequently false(46%). However, abnormal Q waves restricted to the lateral zone (V5-V6) or in acombination of more than one electrocardiographic zone, were rarely false predictorsof the presence of infarction (4%).

(3) Classical localization of infarction with normal conduction was statistically rela-tively reliable as compared with bundle-branch block. The increased frequency ofthe anatomic pattern of lateral basal infarction in association with normal QRScomplexes (but known infarction) suggests relative "electrical silence" of the latero-basal left ventricle in abnormal Q-wave genesis.

(4) Lesions confined to a given anatomic location in the left ventricle tended to placeparticular emphasis and limits on the spectrum of electrocardiographic expressionbut did not yield a uniform single pattern of Q-wave distribution.

Additional Indexing Words:Abnormal Q wave ClinicopathologElectrocardiogram

T-I HE ASSOCIATION between an ab-normally wide Q wave and myocardial

infarction has become so firmly entrenched inthe mind of the electrocardiographer as toapproach dogma. Monumental work of Feni-chel and Kugell,' Wilson and coworkers,2 andMyers and coworkers3-9 established the theo-retical and empirical basis for association

From the Section of Cardiology, Medical Service,FHD, Veterans Administration Hospital, and theDepartment of Medicine, Medical College of Georgia,Augusta, Georgia.

Supported by an award from the VeteransAdministration, U. S. Public Health Service Grant HE-11667, and Grant 69-783 from the American HeartAssociation.

Address for reprints: Dr. Horan, FHD, VeteransAdministration Hospital, Augusta, Georgia 30904.

Received November 6, 1970; accepted for publica-tion December 1, 1970.

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tic correlation Myocardial scar

between myocardial necrosis and Q-waveabnormality. All of these workers recognizedthat the association was high but not absolute.In a classic experiment, Bayley and LaDue'0demonstrated appearance of an abnormal Qwave within minutes after transient coronaryocclusion in the experimental animal-a find-ing later confirmed by many and shown to bereversible, thus providing evidence that thenew Q wave is not synonymous with myocar-dial necrosis. Simonson,"1 in examining thestatistical basis of clinical and electrocardio-graphic associations, reminded us that thearbitrary division between populations ofnormal and abnormal (with respect to myo-cardial infarction) by the width of the Q wavein lead III is at best a crude one.Our original interest in critical examination

of the relationship between the presence of anCirculation, Volume XLIII, March 1971

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DIAGNOSTIC Q WAVE OF MYOCARDIAL INFARCTION

NORMAL QRS38

Table 1

Number of Patients with Electrocardiograms inWhich Q Wave < 0.03 Seconds

Q < 0.03 sec wide With MI Without MI

Normal QRS 38 256Small septal Q (I, V5, V6) 40 242No septal Q (I, V5, V6) 85 184

Total 163 682

Abbreviation: MI = myocardial infarction.

abnormal Q wave and a demonstrable ana-tomic deficit in the myocardium was related tothe controversy surrounding the presence of Qwaves or Q equivalents with left bundle-branch block (LBBB). If a rigid and orthodoxpattern of depolarization in LBBB is assumed,the reliable diagnosis of infarction can bereasonably expected when this pattern isaltered by distinctive QRS abnormalities. Ifthis is not the case, diagnosis is uncertain. Wefound frequent examples of abnormal Qwaves or Q-equivalent patterns in the pres-ence of LBBB in electrocardiograms fromsubjects both with and without gross myocar-dial lesions.12We felt that the findings specifying the de-

gree of association between abnormal Q wavesand myocardial infarction in the presence ofconduction defects would have more meaningif viewed against a background of theirrelative association in the absence of conduc-tion defects. We, therefore, undertook acomparable examination of the hearts associ-ated with apparent normal conduction in thestandard clinical electrocardiogram.

MethodsBetween the years 1961 and 1967, we

examined over 1500 hearts by prospectiveprotocol for the distribution of coronary arteriallesions and ventricular myocardial lesions. Thehearts of those patients who died on the MedicalService of the Kennedy Veterans AdministrationHospital for whom electrocardiograms (ECGs)had been recorded during life were carefullydissected in the fresh state.As previously described,'2 we serially sectioned

the coronary arteries noting, on prepared forms,sites and degrees of luminal encroachment, and(after freeing the atria from the ventricles andremoving excess fat) we separated and weighedCirculation, Volume XLIII, March 1971

NO SEPTAL Q8S

Figure 1

Diagrammatic representation of frequency of localiza-tion of lesions in the left ventricular myocardiumrelative to the occurrence of "normal septal Q waves."The upper left circle illustrates the longitudinal divi-sion of the left ventricle (viewed from the apex) alongmajor arterial routes into septal, anterior, and postero-lateral inferior thirds and latitudinal division intobasal, central, and apical zone with further subdi-vision in the outer zones to give a total of 15myocardial sectors. Only those hearts with knownmyocardial scar or infarct somewhere were includedin these groups. In figures 1, 2, and 3 a sector en-tered by lesions in over one-half the subjects wasshaded with horizontal lines; in over three-quarters,with bold dots.

Abbreviations: normal QRS = normally conductedQRS complexes with neither small nor absent septalQ waves; small septal Q = Q waves of 0.5 mm or lessin depth and less than 0.03 sec in width in leads I,V5, and V6.

the right and left ventricles (including with theleft ventricular mass that of the interventricularseptum). We carefully laminated the left ven-tricle and septum and recorded the anatomic siteand distribution of scars, infarction, or, occasion-ally, metastatic lesions. This correlated file hasbeen examined carefully for instances of abnormalQ waves, defined as those greater than 0.03 secwide in the standard leads except for aVL. Thiscriterion was employed because we have observedthat while in discussion electrocardiographersfrequently attribute abnormality to the Q wave

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that is 0.04 sec wide, many of them in actualpractice "call" the Q wave that is slightly lessthan the 0.04-sec wide block, but not clearly as

short as 0.03 sec.We excluded the previously mentioned 192

instances of conduction defects and an additional47 instances of classical electrocardiographic rightventricular enlargement (extreme right axis andpeak of the early R' in V1 at 0.07 sec or soonerafter the QRS onset). Miscellaneous exclusionswere those where the manner of ventricularconduction in the available ECG was in doubt, aswith hyperkalemia, ventricular tachycardia, idio-ventricular rhythm, etc. We included with thegroup of normal conduction those who hadobvious left ventricular hypertrophy or enlarge-ment, but without abnormally prolonged QRScomplexes. Of the 1184 remaining examples, 845had ECGs in which no Q wave was wider than0.03 sec. As noted in table 1, the examples withECGs in which no Q wave exceeded 0.03 sec induration were divided into three groups: thosewith no septal Q wave-that is, no Q in I, V5,and V6; those with a small septal Q wave-thatis, a Q 0.5 mm or less in depth in one or more ofthe same leads; and finally, those with normalQRS complexes-that is, with the common septalQ present in these "lateral" leads.The question of localization of infarction was

approached in the following fashion. The leftventricular myocardium was divided into 15zones. As seen in figure 1 where the left ventricleis represented diagrammatically as a bull's eye

with the apex pointed toward and the base away

from the viewer, the paths of the major arteriesdivided the ventricular cone into three majorsubdivisions: one lying between the left anteriordescending and the right posterior descendingcoronary artery branches was the septal third, onebetween the left anterior descending and thecircumflex artery was the anterior third, and onebetween the circumflex and right posteriordescending artery was the posteroinferior andlateral free wall. These major subdivisions werefurther subdivided into apical, central, and basalportions, and, except for the apical sectors, afurther subdivision was necessary to producesectors of roughly equivalent area. Study of thepattern of localization was confined to the 416specimens that had either infarction or scar. Foreach electrocardiographic group, we tallied thenumber of entries in a given myocardial sector.Thus, when more than one-half of the subjectswith a given electrocardiographic pattern werefound to have lesions in a given sector, that sectorwas shaded with horizontal lines. When morethan three-quarters were involved, the sector wasmarked with bold dots. In none of our groups,was a sector involved in all instances.

ResultsDetection of Myocardial Infarction orScar by Abnormal Q Waves

It can be seen that there is a relativelyhigher incidence of infarction (slightly lessthan 1 out of 3) when the septal Q wave isabsent than there is when it is present or small

Table 2

Major Groupings of Q-wave Distribution

Q > 0.03 sec V1_2 V1-4 I, Va-6. II, III, aVF -V1,2* With MI Without MI

I. Uncomplicated anteroseptal or inferior patternsAnterior + 4 2Septal + 18 21Anteroseptal + + 47 26Inferior + 25 31

Subtotal 94 80II. Lateral and combined patterns

Lateral + 8 0Anterolateral + + 48 3Inferolateral + + 24 1Inferoseptalt + + 61 1Anteroinferior plust + + 115 0Inferoposterior + + 3 1

Subtotal 159 6Total with abnormal Q 253 86

*-V1.2 indicates presence of widened R in V1V2.tInclude those with abnormal Q in II, III, a VF and either abnormal Q in V1V2 or absent septal Q in 1, VrVN.tThose with abnormal Q waves in V3V4 and II, III, a VF plus abnormal Q waves in either V.V2 or V5V6-or both.

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(slightly less than 1 out of 7) (table 1). Theoverall incidence of infarction in the presenceof a "normal QRS complex" was slightly under20%.

It became evident to us that there were twomajor groupings of Q-wave distribution basedon the occurrence of abnormal Q waves inspecific electrocardiographic zones. As notedin table 2, we called these two majorgroupings (I) uncomplicated anterior orinferior Q-wave patterns and (II) lateral andcombined Q-wave patterns. Uncomplicated Q-wave patterns were those in which anabnormally wide Q wave was found in onlyone of the electrocardiographic zones. Thelateral and combined Q waves were those inwhich abnormally wide Q waves were foundeither in V5 and V6 or in more than one of theclassical pair or trio of electrocardiographicleads making up a zone-e.g., (I, aVL), (II,III, aVF), (V1, V2), (V3, V4). One possibleexception to this rule for lumping besidesputting isolated Q waves in group II isapparent: Q waves in V1-V4 showed thecharacteristics of isolated Q waves; this is notunexpected, for in most of these, the Q-waveabnormality appeared in leads V2 and V3. Notinfrequently, however, a small Q wave alsopreceded the R wave in V, and V4.Q waves which could be classified as

uncomplicated anterior or inferior (group I)were not reliably associated with infarction orscar, but those classffied as lateral or com-bined (group II) were very reliable predictorsof myocardial deficit. The difference inpercentage of false positives was 46% ascompared to 4%. Another way of summarizingthis difference in reliability would be to saythat when abnormal Q waves were foundeither in V3-V6 or in II, III, and aVF incombination with some other leads, they wereten times more accurate in predicting infarc-tion than when isolated to V1-V4 or II, III,and aVF.

Anatomic Localization of Myocardial LesionsBased on Abnormal Q-wave Patterns

Of the 38 subjects with myocardial lesionsand with normally conducted QRS complexesand neither small nor absent septal Q wave,Circulation, Volume XLIII, Marcb 1971

over half had scars in the basolateral sector(fig. 1). This was true also for those withsmall septal Q waves and those with no septalQ waves at all, except that in each of the lattergroups, an inferior or lateral additional sectionwas involved over one-half of the time. Itwould be unrealistic to conclude that latero-basal infarctions produced normal QRS com-plexes; it would be more reasonable toconclude that the laterobasal sector is relative-ly silent and that infarctions in this zone maynot deform the QRS complex with characteris-tic Q-wave abnormalities. Figure 2 graphicallyillustrates the frequency of distinctive localiza-tion for the three patterns of abnormal Q in V,and V2, V3 and V4, and Vi-V4. Three of thesmall group of four patients with isolated Qwaves in V3 and V4 shared extensive damage

ANTEROSEPTAL MIP INFERIOR MIP25

Figure 2

Frequency of localization of lesions in the left ven-tricular myocardium of hearts associated with electro-cardiograms with abnormally wide Q waves in iso-lated anteroseptal or inferior leads. See figure 1 forconvention.

Abbreviations: MIP = myocardial infarction pat-tern; anterior MIP = abnormal Q waves in VY4;septal MIP = abnormal Q waves in V1V2; antero-septal MIP = abnormal Q waves in V1-V4; inferiorMIP = abnormal Q waves in II, III, aVF.

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INFEROLATERAL MIP

AbR PAL-"INFmRIOR MAP

~1over 2 .....

Figure 3Frequency of localization of lesions in the left ventricular myocardium of hearts associated withelectrocardiograms with abnormal Q waves in lateral leads or in two or more lead groups.See figure 1 for convention.

Abbreviations: MIP = myocardial infarction pattern; lateral MIP = abnormal Q waves inV5V6; anterolateral MIP = abnormal Q waves in V3-V6; inferolateral MIP = abnormal Qwaves in II, III, aVF, V5V6; inferoseptal MIP = abnormal Q waves in II, III, aVF, V1V2 or

absent Q in I, V5V6; anteroseptal-inferior MIP = abnormal Q waves in II, III, aVF, V1-V4;inferoposterior MIP = abnormal Q waves in II, III, aVF plus a wide R or R' in V1 V2 (withoutother evidence of RBBB).

in the septum and posteroinferior walls, butnot in the anterior wall. In 18 patients with"septal infarct" Q waves in V1 and V2, thedistribution of the pattern of scar was widelyvariable except that slightly over half didenter the inferior central septum, whereas, in47 patients with Q waves in V1-V4 andmyocardial infarction, over one-half of theinfarctions entered the apical septal sector. Bycontrast (fig. 3), in the 48 patients with Qwaves in V1-V6, over 75% had scar or

infarction in the apical one-third of the leftventricle extending into the septum andinferior wall, and over one-half showed lesions

in the surrounding septal, anterior, lateral, andinferior walls as noted in the diagram. Notethe "lateralization" in pattern when just I, V5,and V0 held abnormally wide Q waves.

In figure 3 also are shown the patterns ofmyocardial localization in the groups withabnormally wide Q waves both in the"footward lead group" (II, III, aVp) and inanother lead pair or group. Notice thatinferolateral myocardial infarction was wellpredicted by Q waves in V5 and V6, plus thefootward leads. Similar good prediction ofinfarction sites with II, III, and aVF alone(fig. 2) was found, but the proviso must be

Circulation, Volume XLIII, March 1971

ANTEROLATERAL MI P48

FIFEROSEPTAL MIP61

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recalled that in the particular group ofpatients under discussion the actual presenceof infarction was not in question. Inferoseptalinfarction was consistent in localization by itsclassical pattern or patterns as noted in thediagram (fig. 3).

Frequency with Which Specific AnatomicLesions Lead to Certain ElectrocardiographicPatterns

When we received the data from the"forward" point of view (i.e., heart current-to-skin voltage) instead of from the "inverse"approach (i.e., ECG finding-to-heart ana-tomy), we noted the following points. Whenthe posterolateral third of the left ventriclewas the sole site of a lesion, the most commonelectrocardiographic result was the absentseptal-Q pattern and a wide variety ofpatterns was found. By contrast, when theanterior one-third was the sole site (asoccurred less commonly), electrocardiograph-ic patterns were normal, or anteroseptalinfarction patterns were found. When bothseptum and posterolateral wall were dam-

Posterior

r

Septal

1-4l

aged, the most frequent electrocardiographicpattern to result was that of wide Q in II, III,and aVF accompanied by loss of normal septalQ in I, V5, or V6. When all three sectors ofmyocardium were entered, the combinedinferior and "anterolateral" pattern was themost frequent result. Figure 4 illustrates theserelative distributions of the electrocardio-graphic sequellae of specific patterns ofmyocardial damage.

DiscussionDiagnostic Efficiency of the AbnormalQ Wave Alone

The data in tables 1 and 2 may be reducedto estimates of sensitivity and specificity.'3Thus, the abnormal Q wave was present 339times out of 1184 in the total population. Itwas truly positive 253 times out of 416 in theabnormal population, and truly negative 682times out of 768 in the noninfarct population.There was thus a sensitivity of 61%, aspecificity of 89% averaging to a performanceof 75%. Another estimate may be expressed in

Anterior

-6- Allc: 40-

30--20.21

1 2345678910111213LR

NormalIQRS c septa I Q2SmallseptalQ in l,V5,V63No septalQ in I,V5,V64 Q in V3,V45Q in Vi,V26Q in Vi-V47Q in ,I,Il,aVf8 Q in V5,V6

9 Q in II,l1l,aVf,V6-V610Q in l1,lI,aVf,V5,V6,RinVlV2I I Q in III,111aVf,V,V2 abQin12 Q in I1,111,aVf,Vi-V413 Q in I 1, 11, aVf,R`inVi,V2L LBBBR RBBB

Incomplete LBBBFigure 4

The relative frequency of electrocardiographic QJRS patterns in the presence of myocardiallesions according to site.

Abbreviations: P =posterior = lesions in posterolateral inferior one-third of the left ven-tricular wall (see fig. 1); A = anterior =lesions in anterior one-third of left ventricular wall;S = septal = lesions in septal one-third of left ventricular wall.


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this way: the number of "correct" positive and"correct" negative diagnoses divided by thetotal number of opportunities. When reducedto percentage, this reflects an absolute diag-nostic reliability of the criterion-in thisinstance, 79%. Comparative estimates forabnormal Q waves in the presence ofconduction defects suggested from previouswork are 74% for RBBB, 67% for LBBB, and57% for incomplete LBBB.12Study of the effect of separating ECGs with

diminished septal Q waves from those withotherwise normal QRS complexes can be seen

in table 1. No assurance is forthcoming as tothe usefulness of predicting infarction fromthe diminution or absence of the normal septalQ in I, V5, and V6 from these figures.However, it is interesting to note that therelative incidence of hidden infarction was 13%with normal septal Q waves, 14% with smallseptal Q waves, but 32% when septal Q waves

were absent. Thus the clinician's uneasinessupon discovering the septal Q wave absentfinds some justification here,'4 but we were

unable to extract individual diagnostic power

from the observation.These findings in the presence of normal

conduction may be compared with the find-ings with conduction defects.'2 In 72 subjectswith LBBB, 28 were without infarction. It isof interest that there were eight instances of Qwaves in II, III, and aVF with LBBB andproven myocardial infarction, and no in-stances of this Q-wave abnormality in thegroup without infarction. By way of contrast,76 patients with RBBB were found in theseries, and of the 40 of these withoutinfarction at autopsy, there were five eachwith either abnormal Q waves in V1-V4 or

abnormal Q waves in II, III, and aVF. In eachof these instances of false Q wave with RBBB,there was strong clinical evidence of eitherpulmonary embolism or chronic or acuteobstructive lung disease, so that clinicianswere provided with a good basis for suspect-ing the alternative explanation of Q waves ofcor pulmonale in these anterior and footwardelectrocardiographic leads. Finally, there were44 cases of incomplete LBBB in the study(QRS complexes of greater than 0.10 but notgreater than 0.12 sec in the limb leads).Although the incidence of true positiveabnormal Q waves associated with infarctionwas slightly higher than false negative Qwaves, diagnostic performance of the Q wave

was even poorer than with complete LBBB.The so-called septal Q waves in leads I, aVL,V5, and V6 were either small or absent, as

would be expected in any complete LBBBin the remainder without abnormally wideQ waves.

Because false abnormal Q waves in thepresence of RBBB had been found consistent-ly associated with hearts with large rightventricles,12 we searched for similar evidencein the absence of a conduction defect. Asshown in table 3, the relative mass of rightand left ventricular walls was compared forthe three major groupings with and withoutmyocardial infarction. The right ventricularweight was not found to be increased in thegroup with falsely abnormal Q waves in theisolated right precordial or foot leads, as

might have been expected by analogy with theacute cor pulmonale patterns showing RBBB.(Obviously these data cannot exclude physio-logic right loading insufficient in degree or

duration to produce right ventricular hyper-

Table 3

Mass of Right and Left Ventricular Walls

With MI LV (g) RV (g) Without MI LV (g) RV (g)

"Normal" QRS patterns* 163 220 - 83 60 17 682 194 - 73 56 - 19Uncomplicated anteroseptal or

inferior Q-patterns 94 229 - 73 62 19 80 221 - 80 62 - 24Lateral and combined Q-patterns 159 246 - 80 67 23 6 220 1 83 67 - 17

*Including ECGs with voltage and ST-T criteria for left ventricular hypertrophy, but not otherwise abnormal asto QRS morphology or duration.


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trophy, as a cause of false but transient Qwaves.) Indeed, the only item of interestnoted in the comparison of ventricular weightsis the finding of greater left ventricular massin the groups with infarction than in thecorresponding groups without infarction, butnot to a statistically impressive degree. (Theelevated mean right and left ventricularweights for the "normal" QRS patterns with-out anatomic infarction reflect the inclusion inthis group of ECG voltage patterns of leftventricular enlargement but with no otherQRS deformity, such as conduction delay. Abetter inclusive label for "normal" activationin hearts with and without left ventricularenlargement is obviously desirable.)

Accuracy of Localization of Lesion According toOrientation of Abnormal Q WaveWhen considering localization as contrasted

with absolute detection of infarction, theclassical association between abnormal Qwaves and regions of myocardium may besummarized as follows. The lateral free wallof the left ventricle is associated with leads I,V5, and V6. Infarction of the inferior ordiaphragmatic aspect of the left ventricle isexpected to be expressed by abnormal Qwaves in leads II, III, and aVF. Lesions of theanterior or apical free wall of the left ventricleare reflected by Q waves in V3 and V4, and ofthe interventricular septum by Q waves in V,and V2. Combinations of lesions in more thanone myocardial region would be expected toproduce Q waves in more than one corre-sponding electrocardiographic zone. Ordinari-ly, in the presence of normal conduction,infarction of the septum might also beexpected to produce loss of Q wave in the"lateral leads" I, V5, and V6. The addition oftrue or strict posterior wall infarction to aninferior wall infarction might be expected toproduce widening of the R wave in V1 and V2,or increase in the R/S ratio of V, and V2.As previously discussed, inspection of fig-

ures 1, 2, and 3 provides a portrait of thetrends of actual anatomic localization withvarious combinations of abnormal Q waves inthe standard electrocardiogram. Focusing onfigure 3, we note that, in general, the wordsCirculation, Volume XLIII, March 1971

classifying the Q orientation describe therelative left ventricular concentration of le-sions. However, we also notice that there areno 100% correlations and that frequent associa-tions are omitted from the prediction: theinferior and anterior overlap is not predictedfrom the lateral myocardial infarction pattern(MIP) (wide Q in V5V6); the commoninferior and septal involvement is not predictedfrom the anterolateral MIP (Q in V3-V6); theseptal extent is not predicted from theinferolateral MIP (Q in V5V6 plus Q in II, III,and aVF). It is not clear why the difference ofadding Q in V3V4 to the "inferoseptal"combination (Q in II, III, and aVF plus Q inV1 and V2) should shift the basal aspect oflocalization from septum to lateral free wallbut not increase the commonness of lesions inthe anatomic anterior free wall.

It is worthwhile to comment on thevariation in localization seen in conductiondefects as compared with these findings.12Classical uncomplicated LBBB patterns withautopsy-proven myocardial infarctions showedconsistent involvement by scar or infarction inthe inferior basal sector near the point wherethe bundle of His sends over the left bundleand its ramifications. Similarly, in six out of 10patients with classical patterns of RBBB andno abnormal Q waves, the same sector wasinvolved consistently. Q waves in V1-V4, Qwaves in I, V5, and V6, and Q waves in II, III,and aVF consistently predicted appropriatemyocardial lesions in over one-half of thepatients with known infarction and RBBB, butsome paradoxes appeared in LBBB. Forexample, the only consistent lesion in thosepatients with Q waves in V1-V4 and LBBBwas a scar or infarction in the posterolateralbasal sectors. Q wave or Q-equivalent in I, V5,and V6 was associated with extensive lesionsin the septum and apex in all seven patientswith this pattern, with extension beyond thiszone into the central anteroseptal region infive, and into all zones in four. Thus, thisparticular electrocardiographic pattern couldbe said to be predictive of septal, lateral, orwrap-around scar or infarction. All eightpatients with abnormal Q waves in II, III, and

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aVF and LBBB had scars or infarction in theinferior central zone with frequent extensioninto the surrounding zones to a lesser degree.

Clinical Significance of the Abnormal Q Wave

The clinical implications of these datashould be approached with the customarycaution to be exercised in translating informa-tion from a population sample selected byautopsy to the wider population faced byclinicians. Such provisos are to be consideredas: (1) a physiologic event of importance(e.g., sudden right ventricular load, transientischemic electrical shut-down of a segment ofventricular wall, or transient alteration ofconduction in the distal fascicles of theconduction system) may leave no anatomictrace; (2) death may select a relatively higherpercentage of these "physiologic abnormali-ties" than would be encountered among theunselected living. However, if our sampling offalse positives and negatives is not drasticallyinappropriate, then table 2 tells the clinicalelectrocardiographer that the "cold reading"of abnormal Q waves in leads II, III, and aVFof an isolated uncompared electrocardiogramrequires a variable response: if present inthose leads alone, a causative myocardialinfarction or scar is quite possible, but ifanother lead set also contained abnormal Qwaves, it is highly probable. Any furtherrefinement of interpretation requires individ-ual clinical context for which electrocardio-graphic rules of thumb cannot substitute.

References

1. FENICHEL NM, KUGELL VH: The large Q-waveof the electrocardiogram. A correlation withpathological observations. Amer Heart J 7:235, 1931

2. WILSON FN, MAcLEoD AG, BARKER PS, ET AL:The electrocardiogram in myocardial infarctionwith particular reference to the initial deflec-tions of the ventricular couple. Heart 16: 155,1933

3. MYERS GB, KLEIN HA, STOFER BE: I. Correla-tion of electrocardiographic and pathologicfindings in anteroseptal infarction. Amer HeartJ 36: 535, 1948

4. MYERS GB, KLEIN HA, HIRATZKA T: II.Correlation of electrocardiographic and patho-logic findings in large anterolateral infarcts.Amer Heart J 36: 838, 1948

5. MYERS GB, KLEIN HA, HIRATZKA T: III.Correlation of electrocardiographic and patho-logic findings in anteroposterior infarction.Amer Heart J 37: 205, 1949

6. MYERS GB, KLEIN HA, HIRATZKA T: IV.Correlation of electrocardiographic and patho-logic findings in infarction of the interventricu-lar septum and right ventricle. Amer Heart J37: 720, 1949

7. MYERS GB, KLEIN HA, HIRATZKA T: V.Correlation of electrocardiographic and patho-logic findings in posterior infarction. AmerHeart J 38: 547, 1949

8. MYERS GB, KLIUN HA, HiRA1rzKA T: VI.Correlation of electrocardiographic and patho-logic findings in posterolateral infarction. AmerHeart J 38: 837, 1949

9. MYERS GB, KLEIN HA, STOFER BE: VII.Correlation of electrocardiographic and patho-logic findings in lateral infarction. Amer HeartJ 37: 374, 1949

10. BAYLEY RH, LADUE JS: Differentiation of theelectrocardiographic changes produced in thedog by prolonged temporary occlusion of acoronary artery from those produced bypostoperative pericarditis. Amer Heart J 28:233, 1944

11. SIMONSON E: Differentiation Between Normaland Abnormal in Electrocardiography. St.Louis, C.V. Mosby Co, 1961, chap 2

12. HORAN LG, FLOWERS NC, TOLLESON WJ, ET AL:The significance of diagnostic Q waves in thepresence of bundle branch block. Chest 58:214, 1970

13. HOLT JH JR, BARNARD ACL, LYNN MS: A studyof the human heart as a multiple dipoleelectrical source. II. Diagnosis and quantitationof left ventricular hypertrophy. Circulation40: 697, 1969

14. BURCH GE, DEPASQUALE N: A study at autopsyof the relation of absence of the Q wave inleads I, aVL, V5 and V, to septal fibrosis.Amer Heart J 60: 336, 1960


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LEO G. HORAN, NANCY C. FLOWERS and JENNIFER C. JOHNSONSignificance of the Diagnostic Q Wave of Myocardial Infarction

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1971 American Heart Association, Inc. All rights reserved.

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