Echocardiographic Estimation of Pulmonary Artery Pressurein Transposition of the Great Arteries

HOWARD P. GUTGESELL, M.D.

SUMMARY To determine their usefulness in estimatingpulmonary artery pressure, left ventricular systolic time intervals(STI) were determined by echocardiography in 65 patients withdextro-transposition of the great arteries (TGA). The STI weremeasured from recordings of pulmonary valve motion at 100 mm/secpaper speed.The pre-ejection period (PEP) and the ratio of PEP to left ventric-

ular ejection time (PEP/LVET) were directly related to pulmonaryartery pressure. The strongest correlations were that betweenPEP/LVET and pulmonary artery diastolic pressure (r = 0.70) and

PATIENTS WITH dextro-transposition of the greatarteries (TGA) frequently develop pulmonary hypertensionat an earlier age than children with other forms of congenitalheart disease.'15 Since the history, physical examination,electrocardiogram and chest roentgenogram are frequentlyunreliable indicators of pulmonary artery pressure in TGA,serial cardiac catheterizations are often necessary to planmedical and surgical therapy.

Hirschfeld et al.6 have demonstrated that echocar-diography can be used to determine the systolic time inter-vals (STI) of the systemic and pulmonary ventricle and thatthe STI of the latter can be used to estimate pulmonaryartery pressure and reisistance.7 In the present study, thismethodology has been applied to a group of patients withvarious forms of TGA to determine its utility in estimatingpulmonary artery pressure, both before and after intra-cardiac surgery.

Methods and Materials

Echocardiograms were obtained on 65 patients with TGAwithin 48 hours of cardiac catheterization. The patientsranged in age from one day to 25 years; 12 had un-complicated TGA, 19 had an associated ventricular septaldefect (VSD), six had pulmonic stenosis (PS), nine had VSDand PS, and 18 patients had undergone an intra-atrial bafflerepair (Mustard procedure). Fifty-five patients were receiv-ing maintenance digoxin therapy at the time of the study.

Echocardiograms were performed with a Hoffrel Model101 ultrasonoscope, coupled to a Honeywell Model 1856strip chart recorder. Transducers of 2.25, 3.5 or 5.0 MHzwere used, depending on the patient's size. Recordings weremade from the second, third or fourth interspace at the leftsternal edge, with the patient supine or in a shallow leftlateral decubitus position.

Since the pulmonary artery arises from the left ventriclein TGA, left ventricular STI were compared to pulmonarypressure. Recordings of posterior semilunar valve

From the Section of Cardiology, Department of Pediatrics, Baylor Collegeof Medicine, and The Texas Children's Hospital, Houston, Texas.

Supported in part by Grant HL-5756 from the NIH and by USPH GrantRR-00188 from General Clinical Research Branch, NIH.Address for reprints: Howard P. Gutgesell, M.D., Pediatric Cardiology,

Texas Children's Hospital, 6621 Fannin, Houston, Texas 77030.Recceived December 23, 1977; revision accepted January 23, 1978.

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that between PEP/LVET and the ratio of mean pulmonary pressureto mean systemic pressure (r = 0.71).A value of PEP/LVET of less than 0.26 was consistently

associated with pulmonary artery diastolic pressures of less than 20mm Hg and, in 28 of 31 patients, pulmonary artery pressure less thanone-third of mean systemic arterial pressure. Pulmonary hyper-tension was present in 18 of 22 patients with PEP/LVET of 0.30 orgreater; elevated PEP/LVET was also present in four patients withabnormalities of cardiac rhythm or conduction, two of whom also hadangiographic evidence of myocardial dysfunction.

(pulmonary valve) motion were made at 100 mm/sec paperspeed. The pre-ejection period (PEP) was considered to bethe time from the onset of the QRS complex of the electro-cardiogram to pulmonary valve opening, and left ventric-ular ejection time (LVET) was measured from thepulmonary valve opening to closing (fig. 1). In the case offluttering or mid-systolic closure of the pulmonary valveleaflets, the point at which the fluttering ceased and theleaflets assumed their typical linear diastolic appearance wasconsidered the end of left ventricular ejection. The ratioPEP/LVET was then calculated. If there was respiratoryvariation, the cycles with the shortest LVET were used in theestimation of pulmonary artery pressure. Measurementswere rounded off to the nearest 5 msec. In the initial half ofthe study, 0.5 sec time lines generated by the echograph wereused. During the remainder of the study, 0.02 sec time linesgenerated from a quartz crystal oscillator were available.Use of these time lines revealed that the timing strobe of theechograph consistently underestimated correct time by2-3%. This error was felt to be insignificant and the datafrom the two parts of the study were combined.Pulmonary artery pressure was measured with fluid filled

catheters at the time of cardiac catheterization. Patientswere sedated with a mixture of meperidine, chlorpromazineand promethazine; none received general anesthesia.

Linear regression analysis was used to determine therelationship of PEP, LVET, and PEP/LVET to pulmonaryartery systolic, diastolic and mean pressure, and to the ratioof mean pulmonary artery pressure to mean systemic arterypressure.

Results

The left ventricular PEP and the ratio PEP/LVET weredirectly related to pulmonary artery pressure. The strongestcorrelations were that between PEP/LVET and pulmonarydiastolic pressure (r = 0.70) and that between PEP/LVETand the ratio of mean pulmonary to mean systemic pressure(r = 0.71). The correlation coefficients relating PEP topulmonary diastolic pressure and the ratio of meanpulmonary to mean systemic pressure were 0.62 and 0.66,respectively.The STI were more accurate in predicting low pulmonary

pressure than in predicting pulmonary hypertension. In 31patients, PEP/LVET was less than 0.26; in each of these

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CIRCULATION VOL 57, No 6, JUNE 1978

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tricular intervals are measured from pulmonary valve motion intransposition of the great arteries. PEP = pre-ejection period;L VET - left ventricular ejection time; PA = pulmonary artery;LA left atrium.

patients, pulmonary diastolic pressure was 20 mm Hg or lessand in 28 of the 31, mean pulmonary pressure was less thanone-third of mean systemic pressure (fig. 2).

In patients with PEP/LVET of 0.26-0.30, pulmonaryartery diastolic pressures ranged from 4 to 70 mm Hg andfrom 12 to 100 percent of systemic. A PEP/LVET of 0.30 or

greater was generally associated with pulmonary hyper-tension. However, in four patients, PEP/LVET was 0.30 or

greater despite normal pulmonary artery pressure (fig. 2).Each of these patients had previous intra-atrial baffle repairand two required reoperation for pulmonary vein obstruc-tion. All four had electrocardiographic abnormalities at thetime of study (one case each of right bundle branch block,left bundle branch block, atrial flutter, and atrioventriculardissociation). In two of these patients, including the one withright bundle branch block, cardiac catheterization andangiography demonstrated biventricular dysfunction as

manifest by elevated enddiastolic pressure and reduced ejec-tion fraction.The relationship between PEP/LVET and pulmonary

artery pressure was also present when the different types ofTGA were analyzed individually. For patients with TGAand VSD, TGA and PS, and TGA post-Mustard procedure,the correlation coefficients between PEP/LVET and theratio of mean pulmonary to mean systemic artery pressure

were 0.62, 0.65, and 0.74 respectively. Low ratios ofPEP/LVET also correctly predicted the low pulmonaryartery pressure in patients with simple TGA and TGA,VSD, and PS. However, the correlation coefficients were notstrong for these two groups because all of the data pointswere clustered together in the lower left corner of figure 2.

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FIGURE 2. Plots of PEP/L VET versus (top) pulmonary artery(PA) diastolic pressure and (bottom) the ratio of mean pulmonaryartery pressure (PAP) to mean systemic artery pressure (SAP). Asindicated by the crossmarks, PEP/LVET of less than 0.26 wasassociated with pulmonary diastolic pressure of 20 mm Hg or lessand, with three exceptions, mean pulmonary pressure less than one-third of mean systemic pressure. In four patients (triangles)PEP/L VET was 0.30 or greater despite low pulmonary arterypressure; each of these patients had cardiac arrhythmia or conduc-tion delay and two had biventricular dysfunction. PA diastolicpressure =-25.4211 + 189.0584 (PEP/LVET), r = 0. 70, SEEt 17mm Hg. PAP/SAP 0.2638 + 2.6579 (PEP/L VET), r = 0. 71,SEE = 0.24.

Discussion

A knowledge of pulmonary artery pressure is necessaryfor the management of patients with TGA. If pulmonarypressure is low and the patient is clinically stable, we havedeferred intra-atrial baffle repair until the second year oflife.8 However, rising pulmonary pressure and resistancemay necessitate either palliative or corrective surgery atan earlier age. After the Mustard procedure, elevated pul-monary artery pressure may reflect obstruction of thepulmonary veins,' or progression of pulmonary vascular ob-structive disease.'0 Obviously a noninvasive method of esti-mating pulmonary pressure would be valuable in the man-

agement of patients with TGA.In subjects with normally related great arteries, left ven-

tricular STI have most commonly been used to assess leftventricular function,'1 rather than to estimate systemicarterial pressure. This emphasizes the fact that manyvariables affect the STI, only one of which is the pressure or

resistance of the distal vascular bed. The hypothesis tested inthis study is that pulmonary artery pressure is the most im-

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ECHO IN TGA/Gutgesell

portant determinant of left ventricular STI in children withTGA, irrespective of age, heart rate, associated cardiaclesions, digoxin therapy or previous surgery. Increasedpulmonary artery pressure should prolong the PEP (in par-ticular, the isovolumetric contraction time) and shortenLVET, thus producing a higher ratio of PEP/LVET.12The results of the study demonstrate a direct relationship

between pulmonary artery pressure, either in absolute termsor in comparison to systemic arterial pressure, and the leftventricular PEP and the ratio PEP/LVET. The latter had astronger correlation with pulmonary pressure, probablybecause it is less influenced by heart rate than PEP itself.7The wide range of pressures among patients with values ofPEP/LVET of 0.26 or greater would seem to preclude aprecise estimate of pulmonary artery pressure from the STI.However, a ratio of PEP/LVET of less than 0.26 was almostinvariably associated with low pulmonary pressure.

If left ventricular STI are used as a screening test forpulmonary hypertension in children with TGA, there will besome false positives. As demonstrated in four patients in thisstudy, cardiac arrhythmia, conduction delay, or reducedmyocardial contractility may prolong PEP and increase thePEP/LVET ratio, causing overestimation of pulmonarypressure. Digoxin therapy, which tends to lowerPEP/LVET,'3 might be expected to produce an un-derestimate of pulmonary pressure, although this was notapparent in the present study. Our patients with pulmonaryhypertension had elevated ratios despite digoxin therapy.

Previous echocardiographic studies of pulmonary hyper-tension",'"5 have demonstrated a lack of posterior movementof the pulmonary valve in early and mid-diastole, diminishedvalve motion ("A" dip) following atrial contraction andrapid rates of valve opening. Although these features wereoften present in patients with pulmonary hypertension in thepresent study, the wide range of patient size and heart ratemade it difficult to quantitate these findings. The results arein agreement with those of Hirshfeld et al.,7 who found adirect relationship between PEP/LVET and pulmonaryartery pressure. Because of the difficulty in accuratelymeasuring pulmonary blood flow in patients with TGA, noattempt was made to compare the STI with pulmonaryresistance in the present study.The technique described is particularly useful for

longitudinal studies of individual patients, since serialechocardiograms can be performed safely and rapidly on anoutpatient basis. In the clinical setting, it does not seempossible to completely neutralize the effects of myocardialcontractility, cardiac medications, heart rate, and intra-

cardiac conduction on left ventricular STI. Nonetheless, thepresence of an elevated ratio of PEP/LVET (0.30 or higher)in a patient with TGA 'suggests that one of the complica-tions of this condition may be present. In this study;pulmonary hypertension was the most common complica-tion. Conversely, the presence of a low PEP/LVET (under0.26) seems to offer reasonable assurance that a significantelevation of pulmonary artery pressure is not present.

Acknowledgment

The cardiac catheterization data were obtained by the staff of the Car-diology Section, Department of Pediatrics, Baylor College of Medicine andthe Texas Children's Hospital. Echocardiograms were performed by Mrs.Linda Kaufman and Miss Paula Kligman. Miss Lauren Pate assisted in thestatistical analysis, and the manuscript was prepared by Miss Sue Lambert.

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H P Gutgesellarteries.

Echocardiographic estimation of pulmonary artery pressure in transposition of the great

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1978 American Heart Association, Inc. All rights reserved.

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