QUANTITATIVE ASSESSMENT OF LEFT VENTRICULAR ASYNERGY

Pedro R. Hernandez-Lattuf, M.D., Efrain Garcia, M.D.,Jose Suarez de Ljezo, M.D.,* William R. C. Murphy, M.D.,** and

Robert J. Hall, M.D.

ABSTRACT

Myocardial performance in the intact human heart can be assessed fromthe analysis of ejection phase indices. Accordingly, among 20 consecutivepatients who were studied by means of biplane left ventricular cineangio-cardiography, 18 were selected solely on the basis of high quality angio-grams. The characteristics of left ventricular contraction were expressedquantitatively by the systolic ejection fraction, the mean velocity of cir-cumferential fiber shortening at the left ventriculalr equator, and at sev-eral chords, the mean velocity of shortening of the hemichords and themean normalized systolic ejection rate. All 18 patients had abnormalitiesof contraction based on the velocity of the hemichords. Both ejectionfraction and mean normalized systolic ejection rate showed a low sensi-tivity in detecting depressed myocardial function in patients with seg-mental asynergy. Equatorial VCF provided additional information onlywhen the affected areas were adjacent to the left ventricular minor axis.The sensitivity of this index was markedly increased by construction ofseveral chords perpendicular to the left ventricular long axis (segmentalVCF). However, when only one wall was affected, measurement of thevelocity of shortening of the hemichords provided a better definition ofthe regional performance.

INTRODUCTION

During the last few years many indices have been developed for assessingcardiac function in man. Standard hemodynamic measurements such ascardiac output, stroke work and ejection fraction examine the left ventricleas a pump but provide limited information about the heart as a muscle.The application of the concepts of muscle mechanics to clinical cardiologydepends on several nonvalidated assumptions concerning the size and shapeof the heart, and the functional myocardial structure;1-4 regional disordersof wall motion make the assessment of contractile abnormalities even moredifficult. The search for a specific and sensitive index of myocardial con-tractility remains an important goal of cardiovascular research.

From the Clayton Foundation Cardiovascular Laboratory, St. Luke's Episcopal Hospital and theTexas Heart Institute, Houston, Texas.*Visiting Fellow from the Department of Thoracic Surgery, La Paz Hospital, Madrid, Spain.

* * Present address: Department of Surgery, University of Minnesota, Minneapolis, Minnesota.Presented in part before the Thirty-second Annual Regional Meeting of the American Federationfor Clinical Research, New Orleans, Louisiana; and the Sixth Annual Texas Heart InstituteSymposium, Houston, Texas.Address for reprints: Efrain Garcia, M.D., Clayton Foundation Research Laboratory, St. Luke'sEpiscopal Hospital, P.O. Box 20269, Houston, Texas 77025.

394 Cardiovascular Diseases, Bulletin of the Texas Heart Institute, Vol. 3, Number 4, 1976

Recent attempts to analyze ventricular function have emphasized theuse of left ventricular (LV) dimensional and volume changes duringejection.5'6 Although the mean velocity of circumferential fiber shorteningat the LV equatorial chord (eVcF) and the mean normalized systolic ejec-tion rate (MNSER) have been evaluated to detect depression of myocardialfunction,5-9 a study comparing these two indices and the ejection fraction(EF) to the more detailed measurements of mean segmental VCF (at severaldifferent chords, SVCF) and mean velocity of shortening of the hemichords(VHC) has not been conducted. The purpose of this study was to measureboth regional and non-segmental ejection phase indices of LV contractionand to test the sensitivity of these measurements in evaluating localizedand diffuse disorders of ventricular performance.

MATERIALS AND METHODS

The biplane left ventriculograms obtained from 18 patients during rightand left cardiac catheterization were analyzed. These patients were selectedfrom 20 consecutive cases and chosen solely on the basis of having highquality cineangiograms. The age, sex, diagnosis and the various hemo-dynamic and angiographic parameters for the group are shown in Table I.The studies were performed during the postabsorptive state and undermild sedation (Hydroxyzine hydrochloride, 100 mg and sodium pentobar-bital, 100 mg). Pressures were measured by means of external straingauges (Hewlett Packard Model 1280 C-02) and registered by a photo-graphic recording system (H-P 8890A). Ventriculograms were obtained byinjecting 50-60 cc of contrast material at a rate of 20 cc per second throughNo. 7 or 8F angiography catheters (Eppendorf), 100 cm long, with closeend-side holes positioned under the mitral valve. The angiocardiogramswere filmed, with simultaneous posteroanterior (PA) and left lateral(LAT) projections (planes), at 60 frames/sec. Selective coronary cinear-teriograms were performed with the use of open end or open end-side-hole arteriography catheters (Amplatz and Sones, respectively). Theventriculograms were studied frame by frame, and only early beats wereanalyzed to avoid possible secondary myocardial effects due to the contrastmaterial. All patients were in sinus rhythm and in no case was an ectopicor post extrasystolic beat used for calculations.

End diastole was defined as having occurred with appearance of the firstframe showing maximal ventricular volume. The onset of LV ejection wasidentified by the opening of the aortic valve (AoV) or the fifth framefollowing end diastole (when the motion of the AoV leaflets could not beclearly distinguished). End systole was defined as the maximal inwardLV wall excursion. LV ejection time (LVET) was measured from the onsetof ejection to end systole. In patients with mitral regurgitation, mitral valveprolapse or ventricular septal defect, the preejection period was added tothe LVET. The LV endocardial surface was drawn (compensating forpapillary muscles and irregularities of the endocardium) at end diastoleand end systole. In each drawing a long axis was constructed from the LVapex to the angle formed by the LV outflow tract and either the AoVposterior cusp (PA view) or the AoV left cusp (LAT view). Five equi-distant chords, perpendicular to the long axis, were drawn for each view

395

at end diastole and end systole, and identified as A to E from the base tothe apex (Fig. 1). Chord E was not used for this study because of thefrequency of apical cavity obliteration. Chord A often coincided with themitral region and in these cases was not reported. Chord C correspondedto the equator of the ventriculogram.Mean Vcp (expressed in circumferences/sec) was calculated for each

chord as VCF= (Ded - Des) /Ded/LVET, where Ded and Des represent thechord at end diastole and end systole respectively. Analysis of each chordwas individual for each projection, with no averaging of correspondingchords. Mean VE[ also was calculated by substituting hemichord for D inthe above formula.* The degree of LV asynergy was expressed as diffuse,when 2/3 or more of the hemichordal velocities were abnormal, or local-ized, when less than 2/3 of the hemichords were affected. Ejection fractionwas derived as SV/EDV, where SV and EDV represent the LV stroke andend-diastolic biplane volumes respectively. The fractional change in vol-ume per second or mean normalized systolic ejection rate (in end-diastolicvolumes/sec) was determined as MNSER=SV/EDV/LVET. A grid with1 cm wire squares embedded in lucite was used for correction due to mag-nification and pincushion distortion during the angio volume calculations;the area-length method of Dodge10 was applied for simultaneous framesof the biplane angiograms. LV diastolic pressure (LVDP) (pre "a" wave)and LV end-diastolic pressure (LVEDP) (post "a" wave) were measuredbefore and after ventriculography, but only the preangiogram values arereported.

The values accepted as normal in our laboratory (using the fifth or

Fig. 1. Schematic drawing of left ventricular endocardium during end-diastole as seen on thePA projection. The long axis, chords and hemi-chords construction is depicted.

*The hemichords were identified with the same denomination as the chord of origin: a, a' for A;b, b' for B, etc. The apostrophes marked the inferior (PA view) and posterolateral (LAT view)wall, respectively.

396

95th percentile as cut-off) are as follows: LVDP and LVEDP<12 mm Hg,EF>54%, mean VCF>1.1 circumferences/sec (for any chord), meanVHC>1.1 hemichords/sec (for any hemichord) and MNSER>1.9 end-dias-tolic volumes/sec.

RESULTS

Data are shown in Tables I-II and Figures 1-6.

The ejection fraction was found to be normal in 12 of the 18 patients(67%o): Nos. 1, 3-8, 11, 14-16, and 18 (Table I).

MNSER (Table I) was normal in 11 cases (61%o): Nos. 1, 3, 5-8, 11, 12,15, 16, and 18. All these patients had a localized type of asynergy (exceptNo. 16) and a normal ejection fraction (except No. 12). Also, two of thepatients with diminished MNSER exhibited normal values for EF (Nos.4 and 14).

Normal values for eVCF (chord C only) were found for both planes inpatients No. 3, 5, 6, 8, 11, 12, 16, and 18 (44o) ; if only one plane was an-alyzed values likeWise were normal in patients No. 7 (PA) and No. 15(LAT).Segmental VCF was normal in one patient (No. 6)- (6%o) at both planes;

by a single plane analysis, sVCF also was normal in patients No. 11 (PA)and Nos. 3, 8, and 15 (LAT). Interestingly, nine patients (Nos. 1, 3, 5-8,12, 15, and 18) had a normal SVCF even in the presence of abnormal veloci-ties in a given wall. This was due to a "compensatory" increase in thevelocities of the unaffected opposing wall: patients No. 1 (chords B andD, PA plane), No. 3 (chord D, PA plane; chord B, LAT plane), No. 5(chord B, PA plane; chord C and D, bAT plane), No. 6 (chords B and C,PA plane; chords B, C, and D, LAT plane), No. 7 (chords B and C, PAplane), No. 8 (chords C and D, PA plane; chords B, C, and D, LAT plane),No. 12 (chord C, PA plane; chords C and D, LAT plane), No. 15 (chord D,LAT plane) and No. 18 (chord B, PA plane; chord C, LAT plane). (Table1 and Fig. 5).The wall motion on visual inspection of the ventriculogram was inter-

preted as normal in 8 patients (44%o) (Nos. 1, 3, 5, 7, 11, 12, 15, and 16).All of these patients (except #16) had localized asynergy (Table I).

Of additional interest were patients No. 7 and 16. Patient No. 7 (ventricu-lar septal defect and aortic insufficiency) displayed depressed septal andanterior wall motion, though MNSER, EF, and eVcF (PA) were normaland LVEDP was slightly elevated. In patient No. 16 (mitral valve prolapseand normal coronary arteries), a generalized hypokinetic pattern was ob-served;i MNSER and EF were normal, as were eVCF, LVDP and LVEDP.

DISCUSSION

With the knowledge currently available on the mechanics of isolatedmuscle, results of any comparative analysis of contractility indices in theintact heart must be arbitrary due to lack of a well validated index of the

397

TABLE 1. Sumnary of Clinical, Hemodynamic and Angiographic Data

Pt I LVDP LVEDP EFU. ^A ICv 1n U-n f-(t Un to I2

MNSER II F,nv,-/c,.,I

Ventricul ogram

Ant- Tnf at Cent AniC

VCF (circ/sec)AA B C D

1 53/M 0

2 66/F

3 57/M

4 54/M

5 52/F

6 61 /N

7 9/M

8 51/M

9 41 /M

1 0 60/N

11 24/F

12 54/F

1 3 53/M

1 4 42/M

15 54/M

16 48/F

1 7 55/M

1 8 36/M

14

2

18

0

5

7

7

11

10

25

10

12

8

13

6

9

8

11 67 2.17 N N

14 44 1.40

1 0 77 2.43

24 54 1.58

5 69 2.48

7 61 2.10

14 67 2.23

10 61 2.14

11 42 1.11

30 33 1.30

32 77 2.35

14 50 2.10

30 41 1 .29

10 54 1.68

22 87 2.10

9 62 1.98

12 50 1.69

8 75 2.83

H Dk

N N

Dk Dk

N N

Dk N

N N

N N

N H

H H

N N

N N

N H

N Ak

N N

N N

N N

N H

N N N PA - 1.27 0.90 1.3EL - 0.77 0.98 1.04

H H H PA 0.68 0.68 0.61 0.75L - 0.63 0.58 0.64

N N N PA 1.04 1.61 1.54 1.34L - 1 .79 1 .56 1 .56

N Dk N PA 0.35 0.70 0.43 0.46L - 0.53 0.21 0.38

N N N PA 0.85 1.15 1.76 2.25L - 0.68 1.10 1.10

N Ak H PA - 1.24 1.24 1.22L - 1.12 1.32 1.11

N N N PA - 1.20 1.22 1.06L - 1.03 1.01 0.96

N N H PA - 0.88 1.10 1.15L - 1.20 1.20 1.36

N N N PA - 0.43 0.53 0.50L - 0.52 0.45 0.38

H H H PA - 0.45 0.20 0.30L - 0.74 0.84 0.83

N N N PA - 1.38 1.54 1.36L - 1.02 1.35 1.31

N N N PA - 0.71 1.17 1.61L - 0.95 1.34 1.20

H Ak N PA 0.44 0.56 0.56 0.54L - 0.76 0.52 0.46

N N H PA 0.67 0.69 0.78 0.95L - 0.98 0.80 0.66

N N N PA - 1.13 1.05 1.33L - 1.47 1.41 1.14

N N N PA - 0.96 1.10 0.95L - 0.90 1.10 0.94

N H H PA - 0.95 0.85 0.82L - 0.85 0.71 0.69

N N N PA 0.83 1.18 1.49 1.83L - 0.85 1.57 1.91

*Both grafts patent; A = Chord A; a,a' = Hemichords for A; ACB = Aortocoronary bypass; Al = Aorticinsufficiency; Ak = Akinetic; Ant = Anterior wall; Apic = Apical wall; AS = Aortic stenosis; Asyn = Asynergy;B = Chord B; b,b' = Hemichords for B; C = Chord C; c,c' = Hemichords for C; CAD = Coronary artery disease;CCM = Congestive cardiomyopathy; Circ = Circumference; Cx = Circumflex; D = Chord D; d,d' = Hemichords for D;Df = Diffuse; Dk = Dyskinetic; EDVs = End-diastolic volumes; EF = Ejection fraction; F = Female;H = Hypokinetic; hc = Hemichord; Inf = Inferior wall; L = Left lateral projection; LAD = Left anteriordescending; Lat = Posterolateral wall; lc = Localized; LVDP = Left ventricular diastolic pressure;

398

MO. itge/ 3ex tiis" M4 i kilell- n4 j k/OJ__ t L. V v _'J z..' j _.. ... __ - - - " -

Velocity of Hemnichords (hc/sec)

a a' b b' c co d d' Asvn Diagnosis

- - 2.25 0.11 1.40 0.34 1.56 1.07 Lc CAD- - 0.96 0.28 1.70 0.86 1.34 0.67

0.35 1.22 0.48 0.98 0.43 0.90 0.86 0.69 Df Al, CCM- - (-) 1.64 (-) 1.57 (-) 1.56

0.61 2.0 1.22 2.06 1.50 1.60 1.04 1.64 Lc CAD, Post ACB(LAD,Cx)*- - 1.04 1.95 1.61 1.44 1.77 1.25

0.18 0.67 0.73 0.37 0.43 0.42 0.42 0.40 Df CAD- - 0.25 0.98 0.23 0.35 0.33 0.41

0.46 1.0 0.92 2.0 1.52 2.40 2.17 2.25 Lc CAD- - 0.63 0.83 1.29 0.80 1.42 0.70

- - 1.35 1.07 1.08 1.49 1.12 1.37 Lc CAD- - 1.44 0.75 2.25 0.36 1.86 0

- - 0.98 1.47 0.91 1.58 0.88 1.29 Lc VSD, AI- - 0.46 1.90 0.71 1.44 0.65 1.33

- - 0.76 1.08 0.97 1.31 1.04 1.33 Lc CAD- - 1.85 0.10 1.82 0.30 1.87 0.67

- - 1.0 0.40 1.0 0.40 0.20 0.90 Df CAD- - 0.43 0.68 0.30 0.68 0.46 0.38

- - 0.75 0 0.36 0 0.47 0.09 Df CAD, PMD + MR- - 1.03 0.29 1.05 0.52 0.96 0.64

- - 1.57 1.23 1.77 1.30 1.58 1.16 Lc MR(severe), PS(mild)- - 0.92 1.22 1.37 1.30 1.37 1.19

- - 1.43 (-) 1.53 0.62 1.76 1.38 Lc MS, AS + AI(both mild)- - 1.43 0.51 1.53 0.78 0.98 1.36

0.61 0.22 0.78 0.31 0.72 0.33 0.61 0.42 Df CAD, Mitral valve- - 0.49 1.18 0.21 0.89 0 0.87 prolapse + mild MR

0.51 1.19 0.66 0.73 0.72 0.89 1.0 0.84 Df CAD- - 0.87 1.16 0.75 0.86 0.40 0.93

- - 1.13 1.11 1.23 0.75 1.42 1.14 Lc CAD- - 1.45 1.49 1.29 1.56 0.90 1.27

- - 0.88 1.09 1.05 1.09 1.06 0.61 Df Mitral valve prolapse- - 0.67 1.25 0.85 1.22 0.83 1.09

- - 0.61 1.44 0.62 1.22 0.57 1.23 Df CAD, Mitral valve- - 0.75 1.06 0.53 0.96 0.52 0.92 prolapse

0.35 1.67 1.10 1.30 1.50 1.49 1.58 2.21 Lc CAD- - 0.90 0.71 0.91 2.70 1.38 2.84

CONTINUATION OF CODE:LVEDP = Left ventricular end-diastolic pressure; M = Male; MNSER = Mean normalizedsystolic ejection rate; MR = Mitral regurgitation; MS = Mitral stenosis; N = Normal;No. = Number; P. = Angiographic projection; PA = Posteroanterior projection;PS = Pulmonic stenosis; Pt = Patient; PMD = Papillary muscle dysfunction;Sec = Second; Sept = Septal wall; VCF = Velocity of circumferential fiber shortening;Ventriculogram = Left ventriculogram on visual inspection; VSD = Ventricular septaldefect; - = Not measured; (-) = Systolic expansion.

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contractile state. Nevertheless, ejection parameters have been creditedwith the advantage of their simple theoretic bases and pragmatic measure-ment.8 This study, therefore, was undertaken to evaluate five ejectionvariables (EF, eVOF, SVCF, VHC and MNSER) in the detection of diffuse andlocalized disorders of the LV myocardial contraction.

Ejection fraction is reliable as an index of pump function when a biplaneangiocardiographic analysis is used." As EF relates the extent of systolicfiber shortening (stroke volume) to initial fiber length (end-diastolic vol-ume) it can be considered as a numerical expression describing the posi-tion of one point on a ventricular function curve. Therefore, it may (atnormal afterload) provide indirect knowledge concerning contractility.'2However, it has been demonstrated by others," and found by us, that EFsometimes remains normal despite evidence of decreased myocardialfunction (Fig. 2).

Concepts of normalized velocity were employed in this report to providea uniform approach to the assessment of cardiac function and to allowcomparisons among patients." Previous analyses of the circumferentialfiber shortening rate in several chords of the normal left ventricle revealedsimilar mean and instantaneous values in all chords.9 Within a given normalventricle, any intracavitary pressure will be associated with uniform levels

80

:600*0

0

U_0

° 40 _ 0

LU

LLI

o DIFFUSE DISEASE* LOCALIZED ASYNERGY

20

1.0 1.5 2.0 2.5 3.0

MNSER (EDVS/sec)Fig. 2. Relation between ejection fraction and mean normalized systolic ejection rate for the 18

patients, adopting a value of 54% for the lower limit of ejection fraction and 1.9 end-diastolic volumes/sec for the MNSER as discussed in the text. EDVS=end-diastolicvolumes, MNSER=mean normalized systolic ejection rate, sec=second.

401

2. 0

- S1.5 _ 0

0

0(-) -00 0_ *o o~Q 1.0_*

0.5 _ oo 0

o 0

.0I I_

PA LATFig. 3. Comparison of the posteroanterior and left lateral plane determination of mean equatorial

VoF (chord C). Open circles identify patients with diffuse asynergy; solid dots, patientswith localized asynergy. Circ=circumference; eVcF=mean equatorial velocity of circum-ferential fiber shortening; LAT=left lateral; PA=posteroanterior; sec=second.

402

2. 0

a,' 1.5

1.0_

0

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-E 0CDVLU

L 0

o 0

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Fig. 4. Lowest values obtained at any chord by the use of segmental VCF in the posteroanteriorand left lateral projections. Open circles and solid dots identify patients with diffuse andlocalized asynergy respectively; circ=circumference; LAT= left lateral; PA=posteroan-terior; sec=second; segmental VcF=mean segmental velocity of circumferential filbershortening.

403

of wall stress throughout the ventricle, so long as the ratio of radius towall thickness remains constant.13 If all areas of the left ventricle are sub-jected to similar inotropic influences and to similar loading conditions,uniform shortening velocities can be expected. Mean equatorial VCF, re-flecting the average speed of shortening only at the minor axis of the leftventricle, can be misleading in the presence of nondiffuse LV disease (Fig.3). Moreover, the sensitivity of this method is not significantly differentin single or biplane calculations (Figs. 3 and 6). Conversely, analysis ofseveral chords'4'15 and their velocity (segmental VCF)9 has proved to beuseful by providing a better definition of regional performance (Fig. 4).The existence of areas of increased motion in diseased ventricles is a

relatively common phenomenon.9" 4" 6 Although its mechanism is not clear,several possibilities have been postulated, including hypertrophy of theuninvolved myocardium,17 rise in circulating catecholamines18 or localmetabolic readjustments.'9 In addition, it has been suggested that the twodeterminants of end-diastolic myocardial fiber stretch are end-diastolicstress and end-diastolic compliance.20 An increase in the LV end-diastolicvolume and pressure, as a consequence of reduced stroke volume, will re-sult in increased LV end-diastolic stress; and if regional compliance isnormal, the Starling mechanism will lead to an increased extent of short-

2.5 r-. *,Postero Lateral Hemichords v Anterior Hemichords

--, "v -Septal Hemichords A Inferior Hemichords2.0 - , ".. *Chords Lat. Plane 0 Chords PA Plane

1.50,,"o, -.F,. F_________i-J> 1.0

zE~~~~~~~~~~~~~~~~~

0.5

0

B C D B C D

Fig. 5. Mean segmental Vcr for chords B through D and mean velocity of the respective hemi-chords in two patients. Case 6 (left) shows normal velocities for all the measured chords(lateral plane only) despite the presence of asynergy in the posterolateral wall, asdemonstrated by the decreased velocities of the lateral hemichords. All chords and hemi-chords (both planes) are shown in case 8 (right), that similarly depicts "compensation"by an unaffected septal wall resulting in normal velocities for the chords of the lateralplane. LAT=left lateral; PA=posteroanterior; sec=second.

404

ening in the areas of preserved myocardium. In some of our patients themagnitude of this compensatory "hypercontractility" was great enoughto mask the presence of regional disease in opposing walls. Measurementsof the shortening velocity of hemichords made the affected areas becomeevident (Fig. 5).

The mean rate of ventricular volume reduction during ejection orMNSER has been introduced as a simplified ejection parameter.8'24 Thisindex is proposed to reflect the average of all dimensional changes of theventricle and, as such, to be useful in the presence of segmental wall mo-tion abnormalities without the limitations of mean equatorial VcF.8 Inthis study MNSER did not differ from EF in detecting depressed cardiacfunction (Fig. 2 and Table II). MNSER was found to be sensitive (seven

2.0

1.5

a)

L-

LU

1.0

0.5

0

00

0

0

Of_

I

0

000

8

eVCF

WII00

00

8

W

SVCF

.

OD0

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found in any of the two planes (posteroanterior and left lateral); open circles and soliddots identify patients with diffuse and localized asynergy respectively. eVc,z=meanequatorial velocity of circumferential fiber shortening; sec=second, sVcr=mean segmentalvelocity of circumferential fiber shortening; VHC=mean velocity of shor-tening of thehemichords.

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of eight cases) when diffuse LV asynergy was present, but not in the pres-ence of localized segmental abnormalities of wall motion (Fig. 2).Angiographic descriptions of the prolapsing mitral valve syndrome have

been focused primarily on the abnormalities of the mitral valve apparatus,but additional information has indicated that the disorder is not limited tothe mitral itself. Recent reports have described abnormalities of left ven-tricular contraction,9'21'22 including a generalized diffuse hypokinetictype22 as in our patient No. 16.To the best of our knowledge no quantitative analysis of wall motion in

patients with the association of high ventricular septal defect and aorticinsufficiency has been reported. Hyperdynamic and dyskinetic septal mo-tion have been described echocardiographically in cases of aortic insuf-ficiency, but the mechanism of the phenomenon is poorly understood.23

Finally, it should be emphasized that the visual inspection of the ven-triculogram failed to detect disorders of wall motion in over 40% of cases.The fact points toward the necessity of the measurements of the left ven-tricular wall's displacement for an accurate assessment of areas of asyn-ergy, particularly during comparative studies.

ACKNOWLEDGMENTS

We gratefully acknowledge the assistance of Kenneth Rothman, M.D., School of Public Health,Harvard University, in the statistical analysis and Virendra Mathur, M.D., Baylor College ofMedicine, for his critical comments; Joyce Staton, B.S., for editorial assistance; and EleanorMonkouski and Christine Abrams for secretarial aid in the preparation of the manuscript.

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