Evaluation of Pulmonary Hypertension by M-mode Echocardiography in Children

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1 IN VSD/Silverman et al Acknowledgment We gratefully acknowledge the technical assistance of Olga Diner, the secretarial assistance of Barbara J. Voigt, and the assistance of Lance Laforteza in preparing the illustrations. We thank Jeanne Bloom for her editorial assistance. References 1. King DL, Jaffee CC, Schmidt DH, Ellis K: Left ventricular volume determination by cross-sectional cardiac ultrasonography. Radiology 14: 21, Gehrke J, Leeman S, Raphael M, Pridie RB: Noninvasive left ventricular volume determination by two-dimensional echocardiography. Br Heart J 37: 911, Schiller N, Drew D, Acquatella H, Boswell R, Botvinick E, Greenberg B, Carlsson E: Noninvasive biplane quantitation of left ventricular volume and ejection fraction with a real-time two-dimensional echocardiography system. (abstr) Circulation 54 (suppl Il): II-234, Schiller N, Botvinick E, Cogan J, Greenberg B, Acquatella H, Glantz S: Noninvasive methods are reliable predictors of contrast angiographic left ventricular volumes. (abstr) Circulation 56 (suppl III): , 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 left ventricle in dogs. Circulation 59: 114, 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, Kohn MS, Schapira JW, Beaver WL, Popp RL: In vitro estimation of canine left ventricular volumes by phased array sector scan. (abstr) Clin Res 26: 244A, Eaton LW, Maughan WL, Shoukas AA, Weiss JL: Accurate volume determination in the isolated ejecting canine left ventricle by two-dimensional echocardiography. Circulation 6: 32, Geiser EA, Bove KE: Calculation of left ventricular mass and relative wall thickness. Arch Pathol 97: 13, Gueret P, Lang TW, Wyatt HL, Heng MK, Meerbaum S, Corday E: Validation of cross-sectional echocardiography measurement of left ventricular volumes. Clin Res 27: 172A, 1979 Evaluation of Pulmonary Hypertension by M-mode Echocardiography in Children with Ventricular Septal Defect Downloaded from by on September 3, 218 NORMAN 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 ejection time () as a predictor of pulmonary hypertension in 16 children with ventricular septal defects (VSD) (group 1). The children ranged in age from 5 months to 18 years. The was measured at the time of cardiac catheterization by M-mode echocardiography from the pulmonary valve echogram and from a simultaneously displayed pulmonary arterial pressure signal obtained with a microtip, manometric catheter. The measured by both methods was comparable (r =.91). The was compared with the pulmonary artery diastolic pressure (PADP) (r =.54). The ratio correlated less well with the pulmonary arterial mean pressure and pulmonary vascular resistance. In a second group of 51 children with VSD, echocardiographic measurement of the right ventricular systolic time intervals was performed within 24 hours before cardiac catheterization. The same variables of pulmonary arterial pressure as for group 1 were compared with the ratio, and the results were similar. These data indicate that, although there is a relationship between the and pulmonary hypertension, the ratio alone is not accurate enough to avoid cardiac catheterization in patients considered at risk for pulmonary vascular disease. PERSISTENT ELEVATION of the pulmonary arterial pressure in children with ventricular septal defects may lead to irreversible pulmonary vascular disease.' Currently, the only reliable method for detecting alterations in the pulmonary arterial From the Department of Pediatrics and the Cardiovascular Research Unit, University of California, San Francisco, California. Supported by grant from the National Foundation, March of Dimes, White Plains, New York. Address for correspondence: Norman H. Silverman, M.D., 143- HSE, University of California, San Francisco, California Received October 15, 1979; revision accepted December 12, Circulation 61, No. 6, 198. pressure in the course of the disease is through repeated cardiac catheterization. Recently, M-mode echocardiographic measurement of the ratio of the right ventricular preejection period (RVPEP) to the right ventricular ejection time (RVET) has been used to detect pulmonary hypertension. The RVPEP/ RVET ratio has been reported to predict pulmonary arterial hypertension in children with left-to-right shunts2-4 and in infants with pulmonary hypertension complicating noncardiac neonatal problems.5-7 If the ratio of accurately predicted pulmonary arterial hypertension in children with ventricular septal defects, the need for repeated cardiac

2 1126 CIRCULATION VOL 61, No 6, JUNE 198 Downloaded from by on September 3, 218 catheterization to measure pulmonary arterial pressure would be eliminated. In our early experience, we were unsuccessful in using this ratio to predict accurately the pulmonary arterial pressure in our patients with ventricular septal defects. We were prompted, therefore, to reexamine the relationship of to pulmonary arterial pressure and pulmonary vascular resistance in children with ventricular septal defects. Methods Group 1 consisted of 16 children undergoing cardiac catheterization for clinically suspected pulmonary hypertension associated with a ventricular septal defect. Before catheterization, we obtained informed consent from the parents of these children to measure the pulmonary arterial pressure with a Millar catheter-tip micromanometer while recording the pulmonary valve echogram simultaneously. The patients ranged in age from 5 months to 18 years. The ventricular septal defects in these patients occurred as an isolated lesion, in combination with a patent ductus arteriosus or an atrial septal defect, or as part of an atrioventricular canal defect. The patients were premedicated with diphenhydramine hydrochloride (1 mg/kg) and droperidol (.3 mg/kg). We determined cardiac output by the Fick technique using measured oxygen consumption8 and measured oxygen contents. We measured pulmonary arterial pressure with the microtip, manometric catheter placed in the proximal pulmonary artery. The pulmonary vascular resistance was calculated from the difference between the pulmonary arterial mean pressure and left atrial mean pressure divided by the pulmonary blood flow per square meter of body surface area. The M-mode echograms of the pulmonary valve leaflets were recorded with a Smith-Kline 2A ultrasonoscope interfaced with a strip-chart recorder. The transducer frequency was appropriate for patient size. To study the relationship of the echocardiographic measurements of the systolic time intervals to the pulmonary artery pressure, we displayed the M-mode echocardiogram of the pulmonary valve leaflet simultaneously with the pulmonary arterial pressure tracing. The tracings of the microtip manometer were recorded on both the ultrasonic strip-chart recorder 1- ET and the Electronics-for-Medicine DR6 recorder used in the cardiac catheterization laboratory. A standard lead II ECG was also displayed on the ultrasonic strip-chart recorder. The accuracy of the paper speed of the ultrasonic recorder was checked by measuring RR intervals of the ECG on both strip-chart recorders run at 1 mm/sec; the results were identical. The echocardiographic recordings were made at paper speeds of 1 mm/sec with time lines generated every 5 msec. We measured RVPEP from the onset of the QRS complex to the pulmonary valve leaflet opening. The pulmonary valve leaflet opening was measured at the point where the posterior velocity of the pulmonary valve leaflet increased markedly and the echo signal thinned.2 RVET was measured from the point of pulmonary valve leaflet opening, as described above, to the pulmonary valve leaflet closure.2 From the pulmonary arterial pressure tracing, the preejection period was measured from the onset of the QRS complex to the onset of rapid rise of the pulmonary arterial pressure, and the RVET was measured from the onset of the pulmonary pressure rise to the incisura of the pulmonary arterial trace (fig. 1). The ratio of wag measured from at least 1 complexes and then averaged. In this group of patients, there was one additional patient in whom the pulmonary valve echogram could not be recorded well enough to make the systolic time interval measurement. We used an IBM 37-series computer and SAS program to compare the ratio with pulmonary arterial diastolic and mean pressure as well as with pulmonary vascular resistance. To determine whether there were any differences in the ratio calculated by the micromanometric and echocardiographic techniques, the two techniques were compared by linear regression. Because it is important to examine whether the ratio predicts pulmonary arterial variables as accurately in the echocardiography laboratory as it does in the cardiac catheterization laboratory, we examined 51 patients who underwent cardiac catheterization 24 hours after a routine echocardiographic study (group 2). The ventricular septal defect in these patients occurred alone, in combination with an atrial septal defect or patent ductus arteriosus, or as part of a more complex problem such as endocardial cushion defect or tricuspid atresia. All FIGURE 1. Technique for measuring sys- tolic time intervals by echocardiography and microtip manometer. The echocardiogram shows the pulmonary valve (PV) within the mm Hg pulmonary artery (PA). The techniques for measuring the right ventricular preejection period (R VPEP) and right ventricular ejection time (R VET) are shown. The pulmonary artery pressure (Pr) measured by microtip, manometric catheter is shown. 1 K

3 IN VSD/Silverman et al of these patients had satisfactory echocardiographic and hemodynamic measurements to allow comparison of the same variables of pulmonary pressure and resistance as in group 1. The pressure recordings in group 2 were made using fluid-filled, rather than microtip, manometric catheters. With regard to the echocardiographic data, at least five complexes from each patient were available for comparison of the echocardiographic with the hemodynamic variables. Results The relevant clinical, hemodynamic and echocardiographic data are shown in table 1. There was no significant difference between the systolic time intervals measured by microtip manometer and echocardiography (r =.91, SEE ±.3, fig. 2). Because of the extremely close agreement between echocardiographic and manometrically derived RVPEP/ RVET ratio, the statistical comparisons with variables of pressure and pulmonary vascular resistance were made with the echocardiographic ratio alone. The ratio was determined by averaging the measurement of 1 complexes. Maximum variability of the ratio was 1% during these 1 complexes. The regression equations relating the variables of Echo.. y=/.3x-./ r=.9/ s.e.e.±.3 N=/6 Millor FIGURE 2. Comparison between right ventricular preejection period/ejection time ratio (R VPEP/R VET) by echocardiography (Echo) and Millar catheter-tip micromanometer. The regression equation, correlation coefficient and the standard error of the estimate are shown. Downloaded from by on September 3, 218 TABLE 1. (Group 1) Clinical, Cardiac Catheterization and Simutltaneous Echocardiographic Data Recorded in 16 Patients PA pressures Pt Diagnosis Age (years) BSA (m2) Digitalis Qp/Qs S (mm Hg) D M PVR 1 VSD, trisomy : VSD, small PDA, trisomy : Complete AV canal, trisomy : VSD : VSI), trisomy : VSD, PDA : VSD, MR : VSD : VSD : VSD, trisomy : VSD, trisomy : VSD, PDA, trisomy : VSD, PDA : AV canal : VSD, PDA, trisomy ,: AV Canal, trisomy : Abbreviations: BSA - body surface area; Qp/Qs - pulmonary-to-systemic flow ratio; PA pulmonary artery; S = systolic; D = diastolic; M = mean; PVR = pulmonary vascular resistance; = ratio of right ventricular preejection period; RVET = right ventricular ejection time; VSD = ventricular septal defect; PDA = patent ductus arteriosus; MR = mitral regurgitation; AV = atrioventricular.

4 1128 CIRCULATION VOL 61, No 6, JUNE 198 TABLE 2. Regression Equations for vs Pulmonary Arterial Mean Pressure and Pulmonary Vascular Resistance Arterial Diastolic Pressure, Pulmonary Slope Intercept r SEE p Echocardiogramrs performed at cardiac catheterization (n = 16, group 1) PADP <.5 PAP >.5 PVR i.93 >.1 Echocardiograms performed 24 hours before cardiac catheterization (n = 51, group 2) PADP >.1 PAP >.1 PVR >.5 Group 1 + group 2 (n = 67) PADP *.19 <.1 Y =, X = catheterization variable (PADP, PAP or PVR). Abbreviations: = ratio of right ventricular preejection period to right ventricular ejection time; PADP = pulmonary arterial diastolic pressure; PAP- pulmonary arterial mean pressure; PVP pulmonary vascular resistance. Downloaded from by on September 3, 218 pulmonary arterial diastolic and mean pressures and pulmonary vascular resistance are shown in table 2. For group 1, correlated best with the pulmonary arterial diastolic pressure (r =.54, p <.5, fig. 3). Examination of residual plots indicated that the correlation would not be improved by further curve-fitting manipulations. Whereas the appeared to increase with increasing mean pulmonary arterial pressure, the relationship was not statistically significant (p >.5) (table 2)..6r.4f,2k y-.3 x Pa4OP /9 r=.54 p.5 s.e.e =,8 There was no significant correlation between and pulmonary vascular resistance (table 2). The data for 51 patients who had ratios calculated in the 24 hours before cardiac catheterization (group 2) are shown in table 3, and the statistical comparisons are shown in table 2. Despite the time delay between the catheterization and echocardiographic studies and the absence of sedation in group 2 patients, the results were similar to those in y=,16x PAOP 62/ r=2 p> O. / * * c * :* * *S _D *m@. CL FIGURE PADP Comparison between right ventricular preejection period/ejection time ratio (R VPEP/R VET) and pulmonary arterial diastolic pressure (PA DP) (mm Hg) for the 16 patients in group 1. The regression equation, correlation coefficients, p value for the slope of the line and the standard error of the estimate are shown. 6 u- n PADP FIGURE 4. Comparison between right ventricular preejection period/ejection time ratio (R VPEP/R VET) and pulmonary arterial diastolic pressure (PA DP) (mm Hg) for the 51 patients in group 2. The regression equation, correlation coefficients, p value for the slope of the line and the standard error of the estimate are shown.

5 IN VSD/Silverman et al Downloaded from by on September 3, k a y=2 x PADPf.2 r=.33 p./ - 's e e. =±Q/Q19 ~~~~~~ ~~~~~~~~~~ c* *,~~~~ 4 * 4 I~~~~~ PA DP FIGURE 5. Comparison between right ventricular preejection period/ejection time ratio (R VPEP/R VET) and pulmonary arterial diastolic pressure (PADP) (mm Hg) in the pooled group 1 and group 2 patients (n = 67). The regression equation, correlation coefficients, p value for the slope of the line and the standard error of the estimate are shown. group 1. The closest correlation was between and pulmonary artery diastolic pressure (r =.2, p >.1, fig. 4). As in group 1, comparisons between and pulmonary arterial mean pressure or between and pulmonary vascular resistance were not significant (table 2). Because the slopes, intercepts and standard errors of the estimate for the relationship between pulmonary artery diastolic pressure and were not significantly different between groups 1 and 2 by analysis of covariance, the data were pooled; this caused no increase in statistical significance (table 2, fig. 5) (r =.33, p <.1). Discussion Several investigators have used the M-mode echocardiogram to predict the pulmonary arterial pressure. Initial studies by Nanda et al.9 and Weyman et al."' suggested that a diminutive or absent "aa" wave and a diminished BC slope on the pulmonary valve echogram were predictors of pulmonary hypertension in adults. These findings were later contested by Pocoski and Shah" and Aquatella et al.12 Goldberg et al.13 reported that notching of the pulmonary valve echogram indicated pulmonary hypertension in congenital heart disease, especially in ventricular septal defects. Heger and Weyman,'4 however, demonstrated that pulmonary root dilatation in the absence of pulmonary hypertension may produce the same M- mode echocardiographic findings. Serwer and colleagues15 correlated right ventricular hypertension with the detection of right-to-left shunting by contrast M-mode echocardiography. Because right-to-left shunting occurred in ventricular septal defects with moderately elevated pulmonary arterial pressure, contrast echocardiography proved too sensitive as a technique for quantitating the pulmonary arterial pressure. Nonetheless, the absence of a right-to-left shunt on M-mode echocardiography in a patient with a ventricular septal defect was strong evidence for the absence of pulmonary hypertension. Hirschfeld and colleagues first used right ventricular systolic time intervals measured from the M-mode echocardiogram to estimate the pulmonary arterial pressure.2 Reports indicated that the ratio was useful in predicting pulmonary hypertension in patients with left-to-right shunts2-4 and in infants with pulmonary hypertension from noncardiac causes.5 7 In adults, studies in which micromanometric recordings of right ventricular and pulmonary arterial pressure were used supported these observations. Curtissl6 reported significant prolongation of the isovolumic contraction time and shortening of the right ventricular ejection time in adults with pulmonary hypertension. However, no linear relationship was found between isovolumic contraction time and pulmonary artery diastolic pressure. Using the data from this study, we calculated the correlation between the ratio and pulmonary arterial mean pressure and pulmonary artery diastolic pressure. The results were similar to those reported in this paper. For pulmonary artery diastolic pressure (PADP), y =.3 PADP (r =.313, SEE i.13). For pulmonary arterial mean pressure (PAP), =.1 PAP (r =.1, SEE ±.144). Spooner and colleagues4 reported a correlation between the pulmonary vascular resistance and the ratio similar to that obtained by Hirschfeld. Considering that a stronger correlation was necessary, however, these authors showed that the ratio of the to the similar ratio of left ventricular preejection period/ejection time (LVPEP/ LVET) was related to the logarithm of the pulmonaryto-systemic vascular resistance ratio. Unfortunately, because the systemic vascular resistance is variable, this ratio is less useful for predicting the degree of pulmonary hypertension. Using the criteria reviewed above, we have not been able to predict the pulmonary arterial pressure in children with ventricular septal defects. Therefore, the current study was undertaken to reexamine the accuracy with which the ratio predicts the pulmonary arterial pressure in patients with ventricular septal defects who are at risk for developing pulmonary vascular disease. We do not know what effect digitalis and diuretic therapy might have on pulmonary systolic time intervals and pulmonary hypertension due to left-to-right shunts. It is possible that the right-sided hemodynamics and ratio may be altered by left-sided events. It is also possible that a direct in-

6 113 CIRCULATION VOL 61, No 6, JUNE 198 Downloaded from by on September 3, 218 TABLE 3. Clinical, Patients (Group 2) Cardiac Catheterization and Nonsimultaneous Echocardiographic Data Recorded in 51 PA pressures Pt Diagnosis Age* BSA (m2) Digitalis Qp/Qs S (mm Hg) D M PVR 1 TAPVR (SVC), Interrupted aortic arch, MS/ atresia, VSD 2 DORV, subpulmonic VSD, S/P resection, interrupted aortic arch 3 VSD, ASD, trisomy 21 4 VSD 5 VSD 6 VSD 7 VSD, S/P PA band, subvalvar AS, recoarctation 8 VSD, PS 9 VSD, PS 1 VSD, subvalvar AS 11 VSD, trisomy VSD 13 VSD 14 VSD, PDA, trisomy VSD, primum ASD, valvar PS 16 VSD 17 VSD 18 VSD, ASD 19 VSD 2 VSD 21 VSD, ASD 22 VSD 23 VSD, trisomy VSD, tric atres 25 AV canal 26 VSD 27 VSI), ASD, PDA 28 VSD, coarctation, ASD, PDA 29 D-TGTA, VSD 2 days : days day days : : : : : : : : : : : : : : : : : : : : : : : : : : PDA 11 days : VSD : *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 = atrioventricular canal; D-TGA = D-transposition of the great arteries; double-chamber RV- double-chamber right ventricle; S = systolic; D = diastolic; M = mean; PVR = pulmonary vascular resistance; 6p/ s-pu1- monary/systemic flow ratio; S/P = status post..18

7 IN VSD/Silverman et al Downloaded from by on September 3, 218 TABLE 3. (Continued) PA pressures Pt Diagnosis Age* BSA (mm Hg) (m2) Digitalis Qp/Qs S D M PVR 31 VSD : VSD, PS : VSD : VSD, S/P resection interrupted aortic arch 21 days : VSD, ASD : VSD, trisomy : DORV, VSD, S/P PA band VSD : VSD : VSD, coarctation : VSD, ASD, PDA : Supracristal VSD, infundibular PS : VSD, doublechamber RV : VSD 14 days : VSD, ASD, PDA, trisomy : DORV, VSD infundubilar and valvar PS : VSD : VSD, PDA : VSD, trisomy : VSD, infundibular PS : VSD, PDA 2 days : otropic effect might change right-sided time intervals. Most of the patients in group 1 were on digitalis and diuretic therapy, and there was no clear separation of systolic time intervals based on whether patients were receiving this therapy. We considered that this therapy did not influence our results. In this study, pulmonary artery diastolic pressure and the ratio correlated satisfactorily, but this relationship was not strong in either group. In contrast to previous reports, pulmonary artery mean pressure and pulmonary vascular resistance appeared to have weaker correlations with the ratio. We can explain some of the differences between our data and previous studies on the wide scatter in the correlation we obtained from the different comparisons. The patients in group 1 were highly selected, and admission to group 1 was permitted only if there was a strong suspicion of pulmonary hypertension. The selection of patients, therefore, was entirely prospective. The results in group 1 are noteworthy because noninvasive determination of pulmonary arterial hypertension would be of most benefit to this type of patient. Previous studies have correlated an ratio of.3 or greater with a pulmonary artery diastolic pressure of 2 mm Hg or greater.3 However, patients 2, 1, 11 and 15 in group 1 had normal ratios and significantly elevated pulmonary artery diastolic pressures. In patient 3 (group 1), the pulmonary artery diastolic pressure was less than 2 mm Hg, but the ratio was.3. Group 2 patients were more heterogeneous because they had a ventricular septal defect not necessarily associated with pulmonary hypertension. Again, the echocardiographic and cardiac catheterization data demonstrated a weak correlation between RVPEP/ RVET ratios and the hemodynamic variables. Our data show similar trends to previous studies,2 4 but ratios correlated more poorly with pulmonary arterial pressures. It is unfortunate that the pulmonary artery diastolic pressure appears to correlate best with the echocardiographic data,

8 1132 CIRCULATION VOL 61, No 6, JUNE 198 Downloaded from by on September 3, 218 because it does not take into account pulmonary blood flow. A closer relationship with the pulmonary vascular resistance that took into account pulmonary blood flow would have been more desirable. For example, if the mean and diastolic pressures are elevated and the flow is elevated also, pulmonary vascular resistance may still be within an acceptable limit for surgical intervention. The 95% confidence limits of the data shown in figures 3, 4 and 5 show that the ratio does not predict pulmonary artery diastolic pressure with sufficient accuracy to avoid cardiac catheterization. Because of the wide variability in the predicted pulmonary artery pressure and pulmonary vascular resistance for a given ratio, sequential comparisons of the ratio in a given patient may not indicate progressive pulmonary hypertension. Kerber and colleagues'7 recently demonstrated that the ratio varies with heart rate, cardiac output and the pharmacologic state of the patient. Therefore, sequential changes in the ratio can be due to several factors other than changes in pulmonary artery pressure. We conclude that the current echocardiographic techniques, although useful in providing some assessment of pulmonary hypertension in association with ventricular septal defects, are not accurate enough to predict pulmonary arterial pressure in the individual patient and do not eliminate the need for repeated cardiac catheterization. This is especially important because an inappropriate decision may have disastrous consequences for the patient. References 1. Hoffman JIE, Rudolph AM: The natural history of ventricular septal defects in infancy. Am J Cardiol 16: 634, Hirschfeld S, Meyer R, Schwartz DC, Korfhagen J, Kaplan S: Echocardiographic assessment of pulmonary artery pressure and pulmonary vascular resistance. Circulation 52: 642, Riggs T, Hirschfeld S, Borkat G, Knoke J, Liebman J: Assessment of the pulmonary vascular bed by echocardiographic right ventricular systolic time intervals. Circulation 57: 939, Spooner EW, Perry BL, Stern AM, Sigmann J: Estimation of pulmonary/systemic resistance ratios from echocardiographic systolic time intervals in young patients with congenital or acquired heart disease. Am J Cardiol 42: 81, Riggs T, Hirschfeld S, Bormuth C, Fanaroff A, Liebman J: Neonatal circulatory changes: on echocardiography. Pediatrics 59: 338, Riggs T, Hirschfeld S, Fanaroff A, Liebman J, Fletcher B, Meyer R, Bormuth C: Persistence of fetal circulation syndrome: an echocardiographic study. J Pediatr 91: 626, Halliday H, Hirschfeld S, Riggs T, Liebman J, Fanaroff A, Bormuth C: Respiratory distress syndrome: echocardiographic assessment of cardiovascular function and pulmonary vascular resistance. Pediatrics 6: 444, Lister G, Hoffman JIE, Rudolph AM: Oxygen uptake in infants and children: a simple method for measurement. Pediatrics 53: 656, Nanda NC, Gramiak R, Robinson TI, Shah PM: Echocardiographic evaluation of pulmonary hypertension. Circulation 5: 575, Weyman AE, Dillon JC, Feigenbaum H, Chang S: Echocardiographic patterns of pulmonary valve motion with pulmonary hypertension. Circulation 5: 95, Pocoski DJ, Shah PM: Physiologic correlates of echocardiographic pulmonary valve motion in diastole. Circulation 58: 164, Acquatella H, Schiller NB, Sharpe N, Chatterjee K: Lack of correlation between echocardiographic pulmonary valve morphology and simultaneous pulmonary arterial pressure. Am J Cardiol 43: 946, Goldberg SJ, Allen HD, Sahn D: Pediatric and adolescent echocardiography. Chicago, Year Book Medical Publishers, 1975, pp Heger JJ, Weyman AE: A review of M-mode and cross sectional echocardiographic findings of the pulmonary valve. J Clin Ultrasound 7: 98, Serwer GA, Armstrong BE, Anderson PAW, Sherman D, Benson W, Edwards SB: Use of contrast echocardiography for evaluation of right ventricular hemodynamics in the presence of ventricular septal defects. Circulation 58: 327, Curtiss El, Reddy PS, O'Toole JD, Shaver JA: Alterations of right ventricular systolic time intervals by chronic pressure and volume overloading. Circulation 53: 997, Kerber RE, Martins JB, Barnes R, Manuel WJ, Maximov M: Effects of acute hemodynamic alterations on pulmonic valve motion. Experimental and clinical echocardiographic studies. Circulation 6: 174, 1979