RVPEP/RVET IN VSD/Silverman et al.

Acknowledgment

We gratefully acknowledge the technical assistance of OlgaDiner, the secretarial assistance of Barbara J. Voigt, and theassistance of Lance Laforteza in preparing the illustrations. Wethank Jeanne Bloom for her editorial assistance.

References

1. King DL, Jaffee CC, Schmidt DH, Ellis K: Left ventricularvolume determination by cross-sectional cardiac ultra-sonography. Radiology 104: 201, 1972

2. Gehrke J, Leeman S, Raphael M, Pridie RB: Noninvasive leftventricular volume determination by two-dimensional echocar-diography. Br Heart J 37: 911, 1975

3. Schiller N, Drew D, Acquatella H, Boswell R, Botvinick E,Greenberg B, Carlsson E: Noninvasive biplane quantitation ofleft ventricular volume and ejection fraction with a real-timetwo-dimensional echocardiography system. (abstr) Circulation54 (suppl Il): II-234, 1976

4. Schiller N, Botvinick E, Cogan J, Greenberg B, Acquatella H,Glantz S: Noninvasive methods are reliable predictors of con-

trast angiographic left ventricular volumes. (abstr) Circulation56 (suppl III): 111-221, 1977

5. Wyatt HL, Heng MK, Meerbaum S, Hestenes JD, Cobo JM,Davidson RM, Corday E: Cross-sectional echocardiography. I.Analysis of mathematic models for quantifying mass of the leftventricle in dogs. Circulation 59: 1104, 1979

6. Wyatt HL, Heng MK, Meerbaum S, Davidson R, Corday E:Evaluation of models for quantifying ventricular size by 2-dimensional echocardiography. (abstr) Am J Cardiol 41: 369,1978

7. Kohn MS, Schapira JW, Beaver WL, Popp RL: In vitro es-timation of canine left ventricular volumes by phased array sec-tor scan. (abstr) Clin Res 26: 244A, 1978

8. Eaton LW, Maughan WL, Shoukas AA, Weiss JL: Accuratevolume determination in the isolated ejecting canine left ventri-cle by two-dimensional echocardiography. Circulation 60: 320,1979

9. Geiser EA, Bove KE: Calculation of left ventricular mass andrelative wall thickness. Arch Pathol 97: 13, 1974

10. Gueret P, Lang TW, Wyatt HL, Heng MK, Meerbaum S, Cor-day E: Validation of cross-sectional echocardiographymeasurement of left ventricular volumes. Clin Res 27: 172A,1979

Evaluation of Pulmonary Hypertensionby M-mode Echocardiography in Children

with Ventricular Septal DefectNORMAN H. SILVERMAN, M.D., A. REBECCA SNIDER, M.D., AND ABRAHAM M. RUDOLPH, M.D.

SUMMARY We evaluated the ratio of the right ventricular preejection period to the right ventricular ejec-tion time (RVPEP/RVET) as a predictor of pulmonary hypertension in 16 children with ventricular septaldefects (VSD) (group 1). The children ranged in age from 5 months to 18 years. The RVPEP/RVET was

measured at the time of cardiac catheterization by M-mode echocardiography from the pulmonary valveechogram and from a simultaneously displayed pulmonary arterial pressure signal obtained with a microtip,manometric catheter. The RVPEP/RVET measured by both methods was comparable (r = 0.91). TheRVPEP/RVET was compared with the pulmonary artery diastolic pressure (PADP) (r = 0.54). TheRVPEP/RVET ratio correlated less well with the pulmonary arterial mean pressure and pulmonary vascularresistance.

In a second group of 51 children with VSD, echocardiographic measurement of the right ventricular systolictime intervals was performed within 24 hours before cardiac catheterization. The same variables of pulmonaryarterial pressure as for group 1 were compared with the RVPEP/RVET ratio, and the results were similar.

These data indicate that, although there is a relationship between the RVPEP/RVET and pulmonaryhypertension, the ratio alone is not accurate enough to avoid cardiac catheterization in patients considered atrisk for pulmonary vascular disease.

PERSISTENT ELEVATION of the pulmonaryarterial pressure in children with ventricular septaldefects may lead to irreversible pulmonary vasculardisease.' Currently, the only reliable method fordetecting alterations in the pulmonary arterial

From the Department of Pediatrics and the CardiovascularResearch Unit, University of California, San Francisco, California.

Supported by grant 6-144 from the National Foundation, Marchof Dimes, White Plains, New York.

Address for correspondence: Norman H. Silverman, M.D., 1403-HSE, University of California, San Francisco, California 94143.

Received October 15, 1979; revision accepted December 12, 1979.Circulation 61, No. 6, 1980.

pressure in the course of the disease is throughrepeated cardiac catheterization. Recently, M-modeechocardiographic measurement of the ratio of theright ventricular preejection period (RVPEP) to theright ventricular ejection time (RVET) has been usedto detect pulmonary hypertension. The RVPEP/RVET ratio has been reported to predict pulmonaryarterial hypertension in children with left-to-rightshunts2-4 and in infants with pulmonary hypertensioncomplicating noncardiac neonatal problems.5-7 Ifthe ratio of RVPEP/RVET accurately predictedpulmonary arterial hypertension in children with ven-tricular septal defects, the need for repeated cardiac

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catheterization to measure pulmonary arterialpressure would be eliminated. In our early experience,we were unsuccessful in using this ratio to predict ac-curately the pulmonary arterial pressure in ourpatients with ventricular septal defects. We wereprompted, therefore, to reexamine the relationship ofRVPEP/RVET to pulmonary arterial pressure andpulmonary vascular resistance in children with ven-tricular septal defects.

Methods

Group 1 consisted of 16 children undergoing cardiaccatheterization for clinically suspected pulmonaryhypertension associated with a ventricular septaldefect. Before catheterization, we obtained informedconsent from the parents of these children to measurethe pulmonary arterial pressure with a Millarcatheter-tip micromanometer while recording thepulmonary valve echogram simultaneously. Thepatients ranged in age from 5 months to 18 years. Theventricular septal defects in these patients occurred asan isolated lesion, in combination with a patent ductusarteriosus or an atrial septal defect, or as part of anatrioventricular canal defect. The patients werepremedicated with diphenhydramine hydrochloride (1mg/kg) and droperidol (0.03 mg/kg). We determinedcardiac output by the Fick technique using measuredoxygen consumption8 and measured oxygen contents.We measured pulmonary arterial pressure with themicrotip, manometric catheter placed in the proximalpulmonary artery. The pulmonary vascular resistancewas calculated from the difference between thepulmonary arterial mean pressure and left atrial meanpressure divided by the pulmonary blood flow persquare meter of body surface area. The M-modeechograms of the pulmonary valve leaflets wererecorded with a Smith-Kline 20A ultrasonoscope in-terfaced with a strip-chart recorder. The transducerfrequency was appropriate for patient size. To studythe relationship of the echocardiographic measure-ments of the systolic time intervals to the pulmonaryartery pressure, we displayed the M-mode echo-cardiogram of the pulmonary valve leaflet simul-taneously with the pulmonary arterial pressure trac-ing. The tracings of the microtip manometer wererecorded on both the ultrasonic strip-chart recorder

and the Electronics-for-Medicine DR6 recorder usedin the cardiac catheterization laboratory. A standardlead II ECG was also displayed on the ultrasonicstrip-chart recorder. The accuracy of the paper speedof the ultrasonic recorder was checked by measuringRR intervals of the ECG on both strip-chart recordersrun at 100 mm/sec; the results were identical. Theechocardiographic recordings were made at paperspeeds of 100 mm/sec with time lines generated every500 msec. We measured RVPEP from the onset of theQRS complex to the pulmonary valve leaflet opening.The pulmonary valve leaflet opening was measured atthe point where the posterior velocity of thepulmonary valve leaflet increased markedly and theecho signal thinned.2 RVET was measured from thepoint of pulmonary valve leaflet opening, as describedabove, to the pulmonary valve leaflet closure.2 Fromthe pulmonary arterial pressure tracing, the preejec-tion period was measured from the onset of the QRScomplex to the onset of rapid rise of the pulmonaryarterial pressure, and the RVET was measured fromthe onset of the pulmonary pressure rise to the in-cisura of the pulmonary arterial trace (fig. 1). Theratio of RVPEP/RVET wag measured from at least10 complexes and then averaged. In this group ofpatients, there was one additional patient in whom thepulmonary valve echogram could not be recorded wellenough to make the systolic time interval measure-ment. We used an IBM 370-series computer and SASprogram to compare the RVPEP/RVET ratio withpulmonary arterial diastolic and mean pressure as wellas with pulmonary vascular resistance. To determinewhether there were any differences in theRVPEP/RVET ratio calculated by the microman-ometric and echocardiographic techniques, the twotechniques were compared by linear regression.Because it is important to examine whether the

RVPEP/RVET ratio predicts pulmonary arterialvariables as accurately in the echocardiographylaboratory as it does in the cardiac catheterizationlaboratory, we examined 51 patients who underwentcardiac catheterization 24 hours after a routineechocardiographic study (group 2). The ventricularseptal defect in these patients occurred alone, in com-bination with an atrial septal defect or patent ductusarteriosus, or as part of a more complex problem suchas endocardial cushion defect or tricuspid atresia. All

1 KFIGURE 1. Technique for measuring sys-

°° tolic time intervals by echocardiography andmicrotip manometer. The echocardiogramshows the pulmonary valve (PV) within the

mm Hg pulmonary artery (PA). The techniques formeasuring the right ventricular preejectionperiod (R VPEP) and right ventricular ejec-tion time (R VET) are shown. Thepulmonary artery pressure (Pr) measured bymicrotip, manometric catheter is shown.

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of these patients had satisfactory echocardiographicand hemodynamic measurements to allow comparisonof the same variables of pulmonary pressure andresistance as in group 1. The pressure recordings ingroup 2 were made using fluid-filled, rather thanmicrotip, manometric catheters. With regard to theechocardiographic data, at least five complexes fromeach patient were available for comparison of theechocardiographic with the hemodynamic variables.

ResultsThe relevant clinical, hemodynamic and echocar-

diographic data are shown in table 1. There was nosignificant difference between the systolic time inter-vals measured by microtip manometer and echocar-diography (r = 0.91, SEE ± 0.03, fig. 2). Because ofthe extremely close agreement between echocar-diographic and manometrically derived RVPEP/RVET ratio, the statistical comparisons with variablesof pressure and pulmonary vascular resistance weremade with the echocardiographic ratio alone. TheRVPEP/RVET ratio was determined by averagingthe measurement of 10 complexes. Maximumvariability of the RVPEP/RVET ratio was 10% dur-ing these 10 complexes.The regression equations relating the variables of

EchoRVPEP/RVET

0. 0

.

y=/.03X-0.0/r= 0.9/s.e.e.± 0.03 N=/6

Millor RVPEP/RVETFIGURE 2. Comparison between right ventricular preejec-tion period/ejection time ratio (R VPEP/R VET) by echo-cardiography (Echo) and Millar catheter-tip microman-ometer. The regression equation, correlation coefficientand the standard error of the estimate are shown.

TABLE 1. Clinical, Cardiac Catheterization and Simutltaneous Echocardiographic Data Recorded in 16 Patients(Group 1)

PA pressuresAge BSA (mm Hg)

Pt Diagnosis (years) (m2) Digitalis Qp/Qs S D M PVR RVPEP/RVET1 VSD, trisomy 21 9.0 1.02 - 1.4:1 100 50 70 9.7 0.402 VSD, small PDA,

trisomy 21 6.0 0.44 - 1.1:1 90 52 80 31.0 0.173 Complete AV

canal, trisomy 21 3.5 0.50 - 2.9:1 70 15 40 2.1 0.304 VSD 5.0 0.83 - 1.0:1 80 30 50 8.9 0.235 VSI), trisomy 21 4.0 0.60 + 2.3:1 80 30 55 6.0 0.346 VSD, PDA 12.0 1.02 - 2.5:1 93 27 60 5.8 0.357 VSD, MR 0.8 0.29 + 6.0:1 80 25 45 1.2 0.198 VSD 18.0 2.02 - 1.0:1 120 60 82 35.0 0.459 VSD 1.1 0.36 + 4.4:1 60 16 34 1.4 0.2010 VSD, trisomy 21 9.5 0.76 - 2.2:1 90 50 70 13.0 0.3211 VSD, trisomy 21 2.0 0.42 + 1.5:1 100 48 70 12.0 0.2912 VSD, PDA,

trisomy 21 1.5 0.36 - 8.0:1 70 40 54 2.5 0.3913 VSD, PDA 8.5 0.83 - 1.5:1 32 16 20 2.0 0.2014 AV canal 1.25 0.35 + 1.9:1 100 48 80 12.0 0.3515 VSD, PDA,

trisomy 21 0.40 0.24 + 2,0:1 100 50 70 11.6 0.2916 AV Canal,

trisomy 21 6.0 0.68 + 1.3:1 90 45 65 11.8 0.46

Abbreviations: BSA - body surface area; Qp/Qs - pulmonary-to-systemic flow ratio; PA pulmonaryartery; S = systolic; D = diastolic; M = mean; PVR = pulmonary vascular resistance; RVPEP/RVET= ratio of right ventricular preejection period; RVET = right ventricular ejection time; VSD = ventricularseptal defect; PDA = patent ductus arteriosus; MR = mitral regurgitation; AV = atrioventricular.

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TABLE 2. Regression Equations for RVPEP/RVET vs PulmonaryArterial Mean Pressure and Pulmonary Vascular Resistance

VOL 61, No 6, JUNE 1980

Arterial Diastolic Pressure, Pulmonary

Slope Intercept r SEE p

Echocardiogramrs performed at cardiaccatheterization (n = 16, group 1)PADP 0.0003 0.19 0.54 + 0.080 < 0.05PAP 0.002 0.17 0.49 0.083 > 0.05PVR 0.002 0.29 0.22 i 0.093 > 0.10

Echocardiograms performed 24 hoursbefore cardiac catheterization(n = 51, group 2)PADP 0.0016 0.21 0.20 00.117 > 0.10PAP 0.001 0.21 0.20 0.117 > 0.10PVR 0.005 0.22 0.24 0.116 > 0.05

Group 1 + group 2 (n = 67)PADP 0.002 0.20 0.33 * 0.109 < 0.01

Y = RVPEP/RVET, X = catheterization variable (PADP, PAP or PVR).Abbreviations: RVPEP/RVET = ratio of right ventricular preejection period to right ventricular ejection

time; PADP = pulmonary arterial diastolic pressure; PAP- pulmonary arterial mean pressure; PVPpulmonary vascular resistance.

pulmonary arterial diastolic and mean pressures andpulmonary vascular resistance are shown in table 2.For group 1, RVPEP/RVET correlated best with thepulmonary arterial diastolic pressure (r = 0.54,p < 0.05, fig. 3). Examination of residual plots in-dicated that the correlation would not be improved byfurther curve-fitting manipulations. Whereas theRVPEP/RVET appeared to increase with increasingmean pulmonary arterial pressure, the relationshipwas not statistically significant (p > 0.05) (table 2).

There was no significant correlation betweenRVPEP/RVET and pulmonary vascular resistance(table 2).The data for 51 patients who had RVPEP/RVET

ratios calculated in the 24 hours before cardiaccatheterization (group 2) are shown in table 3, and thestatistical comparisons are shown in table 2. Despitethe time delay between the catheterization andechocardiographic studies and the absence of sedationin group 2 patients, the results were similar to those in

RVPEP/RVETy-0.003 x Pa4OP 0 /9r=0.54p 0.05s.e.e = 0,080

0

0

20 40

0.64

0.48

0.32

0.16

u-60

0

y=0,0016x PAOP 62/

r=020p> O. /0

0 0

0

.0

.

* *c

0*

:*0

* *S

_D *m@

20 40 60

PADP

FIGURE 3. Comparison between right ventricular preejec-tion period/ejection time ratio (R VPEP/R VET) andpulmonary arterial diastolic pressure (PA DP) (mm Hg) forthe 16 patients in group 1. The regression equation, correla-tion coefficients, p value for the slope of the line and thestandard error of the estimate are shown.

PADPFIGURE 4. Comparison between right ventricular preejec-tion period/ejection time ratio (R VPEP/R VET) andpulmonary arterial diastolic pressure (PADP) (mm Hg) forthe 51 patients in group 2. The regression equation, correla-tion coefficients, p value for the slope of the line and thestandard error of the estimate are shown.

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RVPEP/RVET0.6r

0.4f

0,2k

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y=0002 x PADPf 0.20

a r=0.33

p -0.0/'s e e. =±Q/Q19

0.64k

0481

0.32

0.16

0~~~~~~0

0~~~~~~~~~~

0

0*

00

,~~~~0

0) 0 @00 0

c*

0 0 40

*0 00 0 00 0

0 0 0

0

40 0 0

0

I~~~~~

20 40 60

PA DPFIGURE 5. Comparison between right ventricular preejec-

tion period/ejection time ratio (R VPEP/R VET) andpulmonary arterial diastolic pressure (PADP) (mm Hg) inthe pooled group 1 and group 2 patients (n = 67). Theregression equation, correlation coefficients, p value for theslope of the line and the standard error of the estimate are

shown.

group 1. The closest correlation was betweenRVPEP/RVET and pulmonary artery diastolicpressure (r = 0.20, p > 0.10, fig. 4). As in group 1,comparisons between RVPEP/RVET and pulmonaryarterial mean pressure or between RVPEP/RVETand pulmonary vascular resistance were not signifi-cant (table 2). Because the slopes, intercepts and stan-dard errors of the estimate for the relationshipbetween pulmonary artery diastolic pressure andRVPEP/RVET were not significantly differentbetween groups 1 and 2 by analysis of covariance, thedata were pooled; this caused no increase in statisticalsignificance (table 2, fig. 5) (r = 0.33, p < 0.01).

DiscussionSeveral investigators have used the M-mode echo-

cardiogram to predict the pulmonary arterialpressure. Initial studies by Nanda et al.9 and Weymanet al."' suggested that a diminutive or absent "aa" waveand a diminished BC slope on the pulmonary valveechogram were predictors of pulmonary hypertensionin adults. These findings were later contested byPocoski and Shah" and Aquatella et al.12 Goldberg etal.13 reported that notching of the pulmonary valveechogram indicated pulmonary hypertension in con-genital heart disease, especially in ventricular septaldefects. Heger and Weyman,'4 however, demonstratedthat pulmonary root dilatation in the absence ofpulmonary hypertension may produce the same M-mode echocardiographic findings. Serwer and

colleagues15 correlated right ventricular hypertensionwith the detection of right-to-left shunting by contrastM-mode echocardiography. Because right-to-leftshunting occurred in ventricular septal defects withmoderately elevated pulmonary arterial pressure, con-trast echocardiography proved too sensitive as atechnique for quantitating the pulmonary arterialpressure. Nonetheless, the absence of a right-to-leftshunt on M-mode echocardiography in a patient witha ventricular septal defect was strong evidence for theabsence of pulmonary hypertension.

Hirschfeld and colleagues first used right ven-tricular systolic time intervals measured from theM-mode echocardiogram to estimate the pulmo-nary arterial pressure.2 Reports indicated that theRVPEP/RVET ratio was useful in predicting pul-monary hypertension in patients with left-to-rightshunts2-4 and in infants with pulmonary hypertensionfrom noncardiac causes.5 7 In adults, studies in whichmicromanometric recordings of right ventricular andpulmonary arterial pressure were used supported theseobservations. Curtissl6 reported significant prolonga-tion of the isovolumic contraction time and shorten-ing of the right ventricular ejection time in adults withpulmonary hypertension. However, no linear rela-tionship was found between isovolumic contractiontime and pulmonary artery diastolic pressure. Usingthe data from this study, we calculated the correlationbetween the RVPEP/RVET ratio and pulmonaryarterial mean pressure and pulmonary artery diastolicpressure. The results were similar to those reported inthis paper. For pulmonary artery diastolic pressure(PADP), y = 0.003 PADP + 0.295 (r = 0.313,SEE i 0.13). For pulmonary arterial mean pressure(PAP), RVPEP/RVET = 0.001 PAP + 0.368(r = 0.10, SEE ± 0.144).

Spooner and colleagues4 reported a correlationbetween the pulmonary vascular resistance and theRVPEP/RVET ratio similar to that obtained byHirschfeld. Considering that a stronger correlationwas necessary, however, these authors showed that theratio of the RVPEP/RVET to the similar ratio of leftventricular preejection period/ejection time (LVPEP/LVET) was related to the logarithm of the pulmonary-to-systemic vascular resistance ratio. Unfortunately,because the systemic vascular resistance is variable,this ratio is less useful for predicting the degree ofpulmonary hypertension.

Using the criteria reviewed above, we have not beenable to predict the pulmonary arterial pressure inchildren with ventricular septal defects. Therefore, thecurrent study was undertaken to reexamine the ac-

curacy with which the RVPEP/RVET ratio predictsthe pulmonary arterial pressure in patients with ven-tricular septal defects who are at risk for developingpulmonary vascular disease.We do not know what effect digitalis and diuretic

therapy might have on pulmonary systolic time inter-vals and pulmonary hypertension due to left-to-rightshunts. It is possible that the right-sided hemo-dynamics and RVPEP/RVET ratio may be altered byleft-sided events. It is also possible that a direct in-

RVPEP/RVET

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TABLE 3. Clinical, Cardiac Catheterization and Nonsimultaneous Echocardiographic Data Recorded in 51Patients (Group 2)

PA pressuresBSA (mm Hg)

Pt Diagnosis Age* (m2) Digitalis Qp/Qs S D M PVR RVPEP/RVET

1 TAPVR (SVC),Interruptedaortic arch, MS/atresia, VSD

2 DORV,subpulmonic VSD,S/P resection,interruptedaortic arch

3 VSD, ASD,trisomy 21

4 VSD5 VSD6 VSD7 VSD, S/P PA

band, subvalvarAS, recoarctation

8 VSD, PS9 VSD, PS10 VSD,

subvalvar AS11 VSD, trisomy 2112 VSD13 VSD14 VSD, PDA,

trisomy 2115 VSD, primum ASD,

valvar PS16 VSD17 VSD18 VSD, ASD19 VSD20 VSD21 VSD, ASD22 VSD23 VSD, trisomy 2124 VSD, tric atres25 AV canal26 VSD27 VSI), ASD, PDA28 VSD, coarctation,

ASD, PDA29 D-TGTA, VSD

2 days 0.19 - - 71 42 50 10.0

0.3 0.25 - 1.0:1 1 50 60 14.0

0.72.0

2.0

0.5

0.260.520.520.28

+

4.0 0.67 +

11.0 1.09 -

1.0 0.36 -

6.04.01.21.0

0.850.600.440.41

1.5 0.36

2.03.05.01.2

11.0

0.480.570.720.381.19

14 days 0.2310.5 0.841.5 0.442.0 0.421.3 0.41

1 day 0.191.0 0.430.25 0.22

2 days 0.20

+

+

2.7:1 100 40

2.7:1 60 20

2.5:1 60 20

3.3:1 124 70

0.5:1 8 5

1.3:1 24 10

1.8:1 24 9

1.5:1 20 8

2.3:1 80 30

1.7:1 51 20

1.8:1 45 15

- 8.0:1 70 40

- 0.7:1 13 8

+ 2.9:1 44 10- 1.3:1 26 8

- 3.6:1 27 12- 1.3:1 26 12

- 2.3:1 40 20- 2.1:1 28 8- 5.5:1 90 40

+ 1.5:1 100 48

+ 2.3:1 17 2

+ 1.6:1 55 26- 1.9:1 50 20- 1.5:1 107 48

+ 5.0:1 86 24

65 5.9

38 3.038 3.092 11.0

5 0.417 1.214 0.7

12 0.7

55 6.0

36 3.328 2.8

54 2.5

11 2.0

24 1.2

18 1.818 1.8

16 1.3

25 2.6

16 1.6

65 4.2

70 12.0

10 1.0

35 6.835 3.5

70 18.8

056 5.0

0.20

0.40

0.550.130.21

0.19

0.120.270.25

0.260.210.340.39

0.37

0.430.160.14

0.200.200.220.160.390.300.520.670.240.43

0.18

PDA 11 days 0.19 - 1.4:1 70 55 60 12.2 0.15

30 VSD 0.5 0.29 + 4.3:1 71 24 48 2.3 0.21

*Age given in vears except as indicated.Abbreviations: TAPVR = total anomalous pulmonary venous return; VSD = ventricular septal defect;

DORV = double outlet right ventricle; PA band = pulmonary arterial banding; AS = aortic stenosis; PS- pulmonic stenosis; PDA = patent ductus arteriosus; ASD = atrial septal defect; AV canal = atrioven-tricular canal; D-TGA = D-transposition of the great arteries; double-chamber RV- double-chamber rightventricle; S = systolic; D = diastolic; M = mean; PVR = pulmonary vascular resistance; 6p/ s-pu1-monary/systemic flow ratio; S/P = status post.

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TABLE 3. (Continued)PA pressures

BSA (mm Hg)Pt Diagnosis Age* (m2) Digitalis Qp/Qs S D M PVR RVPEP/RVET31 VSD 0.8 0.37 + 3.8:1 72 30 45 2.0 0.1732 VSD, PS 0.13 0.22 - 2.7:1 32 10 20 1.7 0.12

33 VSD 3.0 0.58 - 2.2:1 24 12 16 0.6 0.22

34 VSD, S/Presectioninterrupted aorticarch 21 days 0.19 + 2.0:1 55 15 34 2.9 0.27

35 VSD, ASD 1.0 0.39 - 3.4:1 65 25 45 5.5 0.2236 VSD, trisomy 21 2.0 0.56 - 3.0:1 80 20 43 2.9 0.1137 DORV, VSD, S/P

PA band 5.5 0.68 + 0.75 17 10 12 2.0 0.1338 VSD 0.8 0.37 - 2.5:1 26 14 20 1.0 0.29

39 VSD 4.0 0.58 + 2.0:1 38 16 23 2.2 0.18

40 VSD, coarctation 13.0 1.41 + 2.0:1 32 14 22 1.3 0.1941 VSD, ASD, PDA 0.13 0.22 + 8.5:1 55 21 35 1.7 0.2842 Supracristal VSD,

infundibular PS 5.0 0.60 - 2.2:1 22 6 10 0.4 0.1743 VSD, double-

chamber RV 1.0 0.36 - 1.8:1 36 8 24 2.0 0.2144 VSD 14 days 0.21 + 2.8:1 54 15 30 2.4 0.2845 VSD, ASD, PDA,

trisomy 21 5.0 0.60 - 1.1:1 90 52 80 31.0 0.30

46 DORV, VSDinfundubilar andvalvar PS 0.8 0.38 + 1.9:1 42 12 20 0.8 0.12

47 VSD 16.0 1.6 + 1.4:1 24 14 17 0.6 0.21

48 VSD, PDA 0.5 0.27 + 2.0:1 100 50 66 11.1 0.24

49 VSD, trisomy 21 0.6 0.28 + 3.6:1 75 30 55 5.4 0.22

50 VSD, infundibularPS 1.0 0.44 - 3.5:1 37 12 24 1.1 0.21

51 VSD, PDA 2 days 0.21 + 5.0:1 90 32 56 4.5 0.13

otropic effect might change right-sided time intervals.Most of the patients in group 1 were on digitalis anddiuretic therapy, and there was no clear separation ofsystolic time intervals based on whether patients werereceiving this therapy. We considered that this therapydid not influence our results.

In this study, pulmonary artery diastolic pressureand the RVPEP/RVET ratio correlated satisfac-torily, but this relationship was not strong in eithergroup. In contrast to previous reports, pulmonaryartery mean pressure and pulmonary vascularresistance appeared to have weaker correlations withthe RVPEP/RVET ratio. We can explain some of thedifferences between our data and previous studies onthe wide scatter in the correlation we obtained fromthe different comparisons. The patients in group 1were highly selected, and admission to group 1 waspermitted only if there was a strong suspicion ofpulmonary hypertension. The selection of patients,therefore, was entirely prospective. The results ingroup 1 are noteworthy because noninvasive deter-

mination of pulmonary arterial hypertension would beof most benefit to this type of patient. Previous studieshave correlated an RVPEP/RVET ratio of 0.30 orgreater with a pulmonary artery diastolic pressure of20 mm Hg or greater.3 However, patients 2, 10, 11 and15 in group 1 had normal RVPEP/RVET ratios andsignificantly elevated pulmonary artery diastolicpressures. In patient 3 (group 1), the pulmonary arterydiastolic pressure was less than 20 mm Hg, but theRVPEP/RVET ratio was 0.30.Group 2 patients were more heterogeneous because

they had a ventricular septal defect not necessarilyassociated with pulmonary hypertension. Again, theechocardiographic and cardiac catheterization datademonstrated a weak correlation between RVPEP/RVET ratios and the hemodynamic variables.Our data show similar trends to previous studies,2 4

but RVPEP/RVET ratios correlated more poorlywith pulmonary arterial pressures. It is unfortunatethat the pulmonary artery diastolic pressure appearsto correlate best with the echocardiographic data,

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because it does not take into account pulmonary bloodflow. A closer relationship with the pulmonaryvascular resistance that took into account pulmonaryblood flow would have been more desirable. For ex-ample, if the mean and diastolic pressures are elevatedand the flow is elevated also, pulmonary vascularresistance may still be within an acceptable limit forsurgical intervention. The 95% confidence limits of thedata shown in figures 3, 4 and 5 show that theRVPEP/RVET ratio does not predict pulmonaryartery diastolic pressure with sufficient accuracy toavoid cardiac catheterization.

Because of the wide variability in the predictedpulmonary artery pressure and pulmonary vascularresistance for a given RVPEP/RVET ratio, sequentialcomparisons of the RVPEP/RVET ratio in a givenpatient may not indicate progressive pulmonaryhypertension. Kerber and colleagues'7 recentlydemonstrated that the RVPEP/RVET ratio varieswith heart rate, cardiac output and the pharmacologicstate of the patient. Therefore, sequential changes inthe RVPEP/RVET ratio can be due to several factorsother than changes in pulmonary artery pressure.We conclude that the current echocardiographic

techniques, although useful in providing some assess-ment of pulmonary hypertension in association withventricular septal defects, are not accurate enough topredict pulmonary arterial pressure in the individualpatient and do not eliminate the need for repeated car-diac catheterization. This is especially importantbecause an inappropriate decision may have dis-astrous consequences for the patient.

References

1. Hoffman JIE, Rudolph AM: The natural history of ventricularseptal defects in infancy. Am J Cardiol 16: 634, 1965

2. Hirschfeld S, Meyer R, Schwartz DC, Korfhagen J, Kaplan S:Echocardiographic assessment of pulmonary artery pressureand pulmonary vascular resistance. Circulation 52: 642, 1975

3. Riggs T, Hirschfeld S, Borkat G, Knoke J, Liebman J: Assess-

ment of the pulmonary vascular bed by echocardiographic rightventricular systolic time intervals. Circulation 57: 939, 1978

4. Spooner EW, Perry BL, Stern AM, Sigmann J: Estimation ofpulmonary/systemic resistance ratios from echocardiographicsystolic time intervals in young patients with congenital or ac-quired heart disease. Am J Cardiol 42: 810, 1978

5. Riggs T, Hirschfeld S, Bormuth C, Fanaroff A, Liebman J:Neonatal circulatory changes: on echocardiography. Pediatrics59: 338, 1977

6. Riggs T, Hirschfeld S, Fanaroff A, Liebman J, Fletcher B,Meyer R, Bormuth C: Persistence of fetal circulation syn-drome: an echocardiographic study. J Pediatr 91: 626, 1977

7. Halliday H, Hirschfeld S, Riggs T, Liebman J, Fanaroff A,Bormuth C: Respiratory distress syndrome: echocardiographicassessment of cardiovascular function and pulmonary vascularresistance. Pediatrics 60: 444, 1977

8. Lister G, Hoffman JIE, Rudolph AM: Oxygen uptake in in-fants and children: a simple method for measurement.Pediatrics 53: 656, 1974

9. Nanda NC, Gramiak R, Robinson TI, Shah PM: Echocar-diographic evaluation of pulmonary hypertension. Circulation50: 575, 1974

10. Weyman AE, Dillon JC, Feigenbaum H, Chang S: Echocar-diographic patterns of pulmonary valve motion with pulmonaryhypertension. Circulation 50: 905, 1974

11. Pocoski DJ, Shah PM: Physiologic correlates of echocar-diographic pulmonary valve motion in diastole. Circulation 58:1064, 1978

12. Acquatella H, Schiller NB, Sharpe N, Chatterjee K: Lack ofcorrelation between echocardiographic pulmonary valvemorphology and simultaneous pulmonary arterial pressure. AmJ Cardiol 43: 946, 1979

13. Goldberg SJ, Allen HD, Sahn D: Pediatric and adolescentechocardiography. Chicago, Year Book Medical Publishers,1975, pp 238-240

14. Heger JJ, Weyman AE: A review of M-mode and cross sec-tional echocardiographic findings of the pulmonary valve. JClin Ultrasound 7: 98, 1989

15. Serwer GA, Armstrong BE, Anderson PAW, Sherman D, Ben-son W, Edwards SB: Use of contrast echocardiography forevaluation of right ventricular hemodynamics in the presence ofventricular septal defects. Circulation 58: 327, 1978

16. Curtiss El, Reddy PS, O'Toole JD, Shaver JA: Alterations ofright ventricular systolic time intervals by chronic pressure andvolume overloading. Circulation 53: 997, 1976

17. Kerber RE, Martins JB, Barnes R, Manuel WJ, Maximov M:Effects of acute hemodynamic alterations on pulmonic valvemotion. Experimental and clinical echocardiographic studies.Circulation 60: 1074, 1979

1132 CIRCULATION

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N H Silverman, A R Snider and A M Rudolphventricular septal defect.

Evaluation of pulmonary hypertension by M-mode echocardiography in children with

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