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Ann Thorac Surg 1999;68:549-555
© 1999 The Society of Thoracic Surgeons

Original Articles

Left ventricular growth in selected hypoplastic left ventricles: outcome after repair of coarctation of aorta

Ernerio T. Alboliras, MDa,b,c,d, Constantine Mavroudis, MDa,b,c,d, Elfriede Pahl, MDa,b,c,d, Samuel S. Gidding, MDa,b,c,d, Carl L. Backer, MDa,b,c,d, Albert P. Rocchini, MDa,b,c,d

a Divisions of Division of Cardiology, Children’s Memorial Hospital, Chicago, Illinois, USA
b Division of Cardiothoracic Surgery, Children’s Memorial Hospital, Chicago, Illinois, USA
c Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois, USA
d Department of Cardiothoracic Surgery, Northwestern University Medical School, Chicago, Illinois, USA

Address reprint requests to Dr Mavroudis, Division of Cardiothoracic Surgery, Children’s Memorial Hospital, 2300 Children’s Plaza, Box 22, Chicago, IL 60614
e-mail: c-mavroudis{at}nwu.edu


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. Models that predict survival in neonates with left ventricular hypoplasia and critical aortic stenosis may not be applicable to neonates with left ventricular hypoplasia and coarctation.

Methods and Results. We report 8 infants with severe aortic coarctation and left ventricular hypoplasia. Mean age was 18 days (range 1–48 days), and mean weight was 3.5 kg (range 2.7–4.3 kg). Associated diagnoses included mild aortic stenosis (4), ventricular septal defect (2), and venous anomalies (2). All had coarctation repair as a primary procedure (3 of these had concomitant intracardiac procedures); 7 had subsequent operations. All are alive and well 1.1–6.7 years (mean 3.1 years) after the first surgery. Progressive increases were observed in aortic and mitral diameters, and in left ventricular dimensions, areas, and volumes when the preoperative, earliest postoperative, and most recent echocardiograms were compared.

Conclusions. Despite severe left ventricular hypoplasia, a two-ventricle repair is possible in selected cases. The prognostic criteria for left ventricular hypoplasia in critical aortic stenosis may not be applicable to infant coarctation. Relief of coarctation may result in the growth of the very small left ventricle, especially when the aortic root and mitral diameters are satisfactory.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
Hypoplasia of the left ventricle (LV) may be seen in certain congenital obstructive lesions of the left heart such as mitral stenosis, aortic stenosis (AS), and coarctation of the aorta (CoA) [1]. A staged single-ventricle repair (the Norwood operation) or cardiac transplantation may be recommended as alternatives to a two-ventricle repair when the LV is deemed too small to function as a systemic pumping chamber [2].

Rhodes and associates [3] developed two methods to predict survival when a two-ventricle repair is considered in critical AS. One method uses a formula for a discriminating score based on body size, aortic root, ratio of LV-to-cardiac length, and mitral valve (MV) area; whereby a score of <= -0.35 was predictive of death. The second method for prediction of nonsurvival is the presence of two or more risk factors that include LV-to-heart length ratio, indexed aortic root diameter, indexed MV area, and indexed LV mass.

The purposes of this study were: 1) to review the left ventricular echocardiographic characteristics in severe CoA associated with LV hypoplasia; 2) to test whether the prognostic criteria for critical AS are applicable to this set of patients; and 3) to determine if there are other parameters that can be used to predict biventricular repair.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
We reviewed the medical records and echocardiographic studies of all infants treated at the Children’s Memorial Hospital in Chicago during the period 1989–1995, with an echocardiographic diagnosis of severe CoA and LV hypoplasia, who required surgical intervention by the age of 6 months. Exclusion criteria were significant aortic valve stenosis (peak Doppler gradient >= 36 mm Hg), aortic atresia, mitral atresia, transposition of great arteries, and common atrioventricular canal.

Echocardiographic analysis
Echocardiographic parameters from three time periods were evaluated: the preoperative, earliest postoperative, and most recent follow-up study. Measurements and calculations from three cardiac cycles from videotaped images were performed using the analysis software package of an ultrasound machine (Sonos 2500; Hewlett-Packard, Andover, MA).

Parasternal views
Parasternal short axis was used to measure MV area, LV dimension, and LV area. The MV area was the planimetered area of the mitral annulus (Fig 1A). The diastolic LV dimension and planimetered LV short-axis area were taken at the midcavitary level (Fig 1B). From the parasternal long-axis view, the aortic annulus and aortic root were measured during systole (Fig 1C). The aortic annular diameter was the dimension from anterior to posterior hinge-point of the aortic valve cusps. The aortic root diameter was the maximal diameter at the level of the sinus of Valsalva.



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  		Fig 1. Short-axis two-dimensional echocardiogram at the mitral annulus level (A) demonstrating the planimetry site for calculation of mitral valve area, and at the mid-ventricular level (B) where the left ventricular area and dimension were measured. In this infant with severe coarctation of the aorta, the left ventricular cavity had a flattened shape, not spheroidal. The aortic annulus and root were measured at the parasternal long-axis view (C). Measurements of left ventricular length, area, volume, and heart-left ventricle length ratio were taken from the apical four-chamber view (D). This figure shows a very small left ventricle and the cardiac apex formed by the right ventricle. Ann = aortic annulus; LA = left atrium; LV = left ventricle; MV = mitral valve; Root = aortic root; RV = right ventricle.

 
Four-chamber view
The MV annulus diameter, LV length, area, and volume, and cardiac long axis were measured at end-diastole (Fig 1D). MV annulus diameter was the distance from the medial to the lateral aspect the annulus. LV length was the distance between the MV annulus level and the LV apex. LV area was determined by tracing the endocardial surface, drawing a straight line through the MV annulus plane, and excluding the papillary muscles. The cardiac long axis was the distance from the crux of the heart to the endocardial surface of the apex of either the right or LV, whichever forms the apex of the heart [3].

LV volume was calculated using two methods: 1) method of discs from single-plane, four-chamber view [4], and 2) a modified Bullet method [5] that was used by Rhodes and associates [3]. The formula for LV volume was similarly applied, using the epicardial surface of the free wall and the right ventricular septal surface as the borders. LV mass was obtained as the difference between the epicardial and endocardial volumes multiplied by the specific gravity of myocardium (1.04 g/mL).

Data analysis/statistics
The echocardiographic parameters were nonindexed and indexed for body surface area. The preoperative echocardiographic measurements were compared with the nonsurvivors in the two-ventricle repair group of patients of Rhodes and associates [3], using unpaired two-tailed Student’s t test, with p < 0.05 being significant. The Rhodes discriminating score [6] was calculated for each study patient using the formula: 14.0 (BSA) + 0.943 (ROOTi) + 4.78 (LAxHt) + 0.157 (MVAi) - 12.03, where BSA = body surface area, ROOTi = aortic root dimension indexed to body surface area, LAxHt = long-axis dimension of the heart, and MVA = indexed MV area. Similarly, the presence and number of the following risk factors were determined for each patient: LV long-axis/heart long-axis ratio <= 0.8, indexed aortic root diameter <= 3.5 cm/m2, indexed MV area <= 4.75 cm2/m2, and indexed LV mass <= 35 g/m2.

Because data for MV diameter were not included in the paper of Rhodes and associates [3], we used the published data of Ludman and associates [7] from two groups of patients (a group of neonates with normal heart and another group with significant right ventricular volume overload). Other measured echocardiographic dimensions for both preoperative and the two postoperative study groups were compared with the predicted normal for body surface area of Hanseus and associates [6]. LV volumes were compared with normals of Lange and associates [8] that used the formula EDV = 65.1 x 1.219 (BSA). Differences in measured preoperative and postoperative parameters were assessed using paired two-tailed Student’s t test, with p <= 0.05 being significant.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
Of a total of 72 cases reviewed, 8 infants (6 boys, 2 girls) satisfied the selection criteria. Mean age at diagnosis was 18 days (range 1–48 days), whereas the mean weight was 3.5 kg (range 2.7–4.3 kg). Presenting signs and symptoms included low cardiac output (6 patients), cyanosis (1 patient), and heart murmur (1 patient). All had associated structural cardiac anomalies (Table 1), with 4 having doppler evidence of mild valvar AS. Seven of 8 had either an atrial septal defect or patent foramen ovale; 1 patient was thought to have prenatal closure of the foramen ovale. One patient manifested with the Shone’s complex of CoA, mild AS, and parachute MV. Six of 8 were on prostaglandin infusion during preoperative evaluation. All had surgery soon after diagnosis (mean age at surgery 20 days; range 2–60 days), which consisted of repair of CoA (extended end-to-end anastomosis, 6 patients; subclavian flap aortoplasty, 2 patients) with an attendant ligation of a ductus arteriosus. Thoracotomy was done in 5 patients, whereas a sternotomy was used in 3 patients who required concomitant cardiopulmonary bypass and intracardiac repairs. The severity of coarctation or hypoplasia of the aortic arch was not a factor in the choice of the chest incision. Concomitant initial intracardiac operations were patch closure of large ventricular septal defect (1 patient), staged snare closure of atrial septal defect with baffling of right pulmonary veins to left atrium (1 patient), and creation of fenestrated atrial septal defect with a snare in a patient with intact atrial septum.


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  		Table 1. Patient Diagnoses and Type of Initial and Subsequent Operations

 
The preoperative echocardiographic data of the 8 study patients were compared with the 14 patients of Rhodes and associates [3], who did not survive the two-ventricle repair for critical AS (Table 2). The two groups were similar in body surface area, indexed MV area, and indexed LV length. The study patients had significantly smaller indexed end-diastolic volume and LV mass but significantly larger indexed aortic root. There was a trend towards a larger indexed aortic annulus, although the difference was not statistically significant. Of note, the short-axis view showed the LV cavity to have a flattened shape (Fig 1B), not spheroidal as is commonly seen in critical AS. Although the MV area on short-axis view was similar to the nonsurvivor group of Rhodes and associates [3], the preoperative MV annulus diameter measured at the four-chamber view (11.7 ± 1.8 mm, range 9–14 mm) did not differ significantly from groups of infants of Ludman and associates [7] with normal heart (10.1 ± 1.5 mm) and with significant right ventricular volume overload (10.1 ± 1.5 mm). The presence of satisfactory mitral diameter, in spite of small annular area, suggests that flattening, similarly observed in the LV cavity also occurs in the mitral valve.


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  		Table 2. Comparisons of Echocardiographic Measurements

 
Calculation for Rhodes’ discriminating score (Table 3) showed that all 8 patients had values <= -0.35, which would have been invariably predictive of death with the two-ventricle repair. Analysis of the various Rhodes risk factors (Table 3) revealed that all 8 had two or more factors present, which, similarly, would have meant nonsurvival for all with the two-ventricle repair. The aortic root risk factor contributed the least, with only two patients having a critically small value.


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  		Table 3. Rhodes Discriminating Scores and Risk Factors in 8 Study Patients

 
All study patients survived the operation, and have been followed for 1.1–6.7 years (mean 3.1 years). All are doing well, in spite of 7 of 8 requiring additional operations (Table 1) at a mean age of 5 months (range 1–12 months). Three patients underwent resection of sub-AS: discrete subaortic membrane in 2 and attempted fibromuscular resection in 1. The latter underwent modified Konno operation. No patient had the Ross operation. In 2 patients with atrial septal defect, 1 had patch closure with a snare during initial surgery, with the small residual defect surgically closed during a subsequent sub-AS resection. Another patient had closure of the atrial septal defect with a fenestration as a subsequent surgery followed by fenestration closure.

The earliest postoperative echocardiograms (Table 4) that could be analyzed for this study were performed at a mean age of 41 days (range 8–92 days). The most recent echocardiograms (Table 4, Fig 2) were performed at a mean age of 2.2 years (range 1.0–6.2 years). Changes in cardiac configuration observed in the early postoperative period included statistically significant increases in MV diameter and area, LV dimension, area, and volume. In the most recent postoperative studies, there were significant increases in LV length, diastolic dimension, four-chamber view LV area, and volumes. Likewise, the ratio of LV apex-to-heart length increased markedly, suggesting a shift of the cardiac apex towards the normally dominant LV. Furthermore, there was a significant increase in MV diameter, indexed MV area, and LV mass. The nonindexed aortic annular and aortic root dimensions increased over time, although there were no significant differences in values when indexed to surface area, suggesting appropriate growth of this part of the heart with increase in body size.


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  		Table 4. Comparison of Preoperative With Latest Postoperative Echocardiographic Parameters in 8 Study Patients

 


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  		Fig 2. Apical four-chamber view. Preoperatively (A), the left ventricle was very small, with the apex formed by the right ventricle. One and a half years postoperatively (B), the left ventricle had enlarged and had formed the cardiac apex. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
For certain heart defects, concern about adequacy of LV size to sustain the systemic circulation has been controversial [3, 9–11]. In the presence of mitral or aortic atresia, a two-ventricle repair is not feasible. Depending on institutional experience, a sequence of palliation culminating in a modified Fontan procedure, cardiac transplantation, or no treatment may be chosen. In right ventricular volume overload, as seen in total anomalous pulmonary venous connection, marked hypoplasia of LV may occur but has always been considered compatible with life [12].

The choice of operation is less definite if the hypoplastic LV is associated with severe aortic valve stenosis. A higher mortality is observed when severe AS occurs in association with a small LV cavity [13, 14]. Critical limits of associated cardiac anomalies in severe infant aortic valve stenosis have been proposed to identify those with poor prognosis when biventricular repair is chosen: LV end-diastolic volume < 20 mL/m2, aortic annulus size < 6. 0 mm, LV length < 25 mm, MV annulus diameter < 11 mm, cardiac apex formed by the right ventricle (RV), presence of endocardial fibroelastosis, and Rhodes’ equation for a discriminating score for survival and sum of certain variables for LV hypoplasia [3, 10, 13–16].

CoA can be associated with a hypoplastic LV. As many as 45% of 123 infants with CoA were identified as having a small LV in a postmortem study [1]. Only 20% of these autopsy cases had associated aortic valve stenosis of any severity.

Aortic root diameter appeared to have the least involvement in assessment for survival in a two-ventricle repair, and aortic root greater than 6 mm suggests that the left heart can grow satisfactorily over time. A small subaortic outflow tract could be a factor, but this has been shown to grow rapidly after repair of interrupted aortic arch with ventricular septal defect [17].

The preoperative mean indexed MV area of the study patients was significantly smaller than the nonsurviving patients of Rhodes and associates [3]. These values may have been affected by the methods used to measure MV area. Rhodes and associates [3] calculated MV area based on an assumed ellipsoid shape and utilizing orthogonal diameters. We opted to perform planimetry for precise circumference delineation because 2 study patients with markedly dilated coronary sinus and large left superior vena cava had a straightened posterior MV annular border resulting in a nonellipsoid annulus. Furthermore, in some patients the MV annulus appeared to have a crescentic shape rather than ellipsoidal. The present study has shown that the MV diameter at four-chamber view, which represents the longer diameter of the MV annulus, is a very reliable two-dimensional echocardiographic parameter for adequacy of the valve. This has been shown as a reliable predictor by Ludman and associates [7] for identifying hypoplastic left heart syndrome, and by Parsons and associates [18] to identify patients who will survive surgery for isolated aortic valve stenosis. With the availability of the Ross-Konno procedure [19] for reconstruction of the LV outflow tract, the mitral valve becomes the limiting factor for these patients [20].

In critical AS, the markedly increased cavitary stress that results from the obstructive valve may be a determinant in retaining the ellipsoidal or globular LV shape. In our study patients, the flattened LV cavity appears similar to conditions associated with marked RV volume overload. This distorted LV configuration contributed to diastolic dimensions and planimetered short-axis areas that are much smaller than predicted. Thus, variables that are dependent on short-axis dimensions and LV length, namely, LV volume and mass, may be affected, resulting in values that are smaller than predicted.

The observed rapid increase in LV cavitary size soon after surgery suggests that LV hypoplasia resulted from decreased preload and markedly increased right ventricular volume. Adequate LV cavitary size can be attained after normalization of cardiac loading conditions, as observed in total anomalous pulmonary venous connection, atrial septal defect, and unbalanced atrioventricular canal defect [21]. Minich and associates [22] also observed similar normalization of echocardiographic parameters in non-apex-forming ventricles, including 3 patients with CoA.

The postoperative recovery of this subset of patients required lengthy hospitalization, indicating prolonged LV adaptation time. Early in the postoperative course, a foramen ovale or an atrial septal defect may need to be left open or surgically created to allow left atrial shunting because of a noncompliant ventricle. Subsequently, the defect in the atrial septum could be closed. Further operations may be needed for other associated cardiac lesions, including subAS.

In conclusion, despite severe LV hypoplasia associated with CoA, repair that allows for two functioning ventricles is possible in selected cases. The prognostic criteria for LV hypoplasia in critical AS may not be applicable to severe CoA in the newborn. These infants represent a separate subgroup of patients that may do well after CoA repair if the aortic root and MV diameters are of reasonable size and not significantly obstructed. Relief of CoA may result in growth of the very small LV.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Bharati S, Lev M. The Pathology of Congenital Heart Disease. Armonk, NY: Futura Publishing Co., 1996:677–710, 765–85, 1247–49.
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  7. Ludman P., Foale R., Alexander N., Nihoyannopoulos P. Cross sectional echocardiographic identification of hypoplastic left heart syndrome and differentiation from other causes of right ventricular overload. Br Heart J 1990;63:355-361.[Abstract/Free Full Text]
  8. Lange P.E., Onnasch D., Farr F.L., Heintzen P.H. Angiographic left ventricular volume determination. Accuracy as determined from human casts, and clinical application. Eur J Cardiol 1978;8:449-476.[Medline]
  9. Latson L.A., Cheatham J.P., Gutgesell H.P. Relation of the echocardiographic estimate of left ventricular size to mortality in infants with severe left ventricular outflow tract obstruction. Am J Cardiol 1981;49:887-891.
  10. Keane J.F., Norwood W.I., Bernhard W.F. Surgery for aortic stenosis in infancy. Circulation 1983;68(Suppl III):46.
  11. Page D.A., Levine M.M. Left ventricular growth in a patient with critical coarctation of aorta and hypoplastic left ventricle. Ped Cardiol 1995;16:176-178.
  12. Graham T.P., Jr, Jarmakani J.M., Canent C.V., Jr Left heart volume characteristics with a right volume overload. Total anomalous pulmonary venous connection and large atrial septal defect. Circulation 1972;45:389-396.[Abstract/Free Full Text]
  13. Leung M.P., McKay R., Smith A., Anderson R.H., Arnold R. Critical aortic stenosis in early infancy. Anatomic and echocardiographic substrates of successful open valvotomy. J Thorac Cardiovasc Surg 1991;101:526-535.[Abstract]
  14. Karl T.R., Sano S., Brawn W.J., Mee R.B.B. Critical aortic stenosis in the first month of life. Ann Thorac Surg 1990;50:105-109.[Abstract]
  15. Pelech A.N., Dyck J.D., Trusler G.A., et al. Critical aortic stenosis. Survival and management. J Thorac Cardiovasc Surg 1987;94:510-517.[Abstract]
  16. Gatzoulis M.A., Rigby M.L., Shinebourne E.A., Redington A.N. Contemporary results of balloon valvuloplasty and surgical valvotomy for congenital aortic stenosis. Br Heart J 1995;73:66-69.
  17. Serraf A., Lacour-Gayet F., Robotin M., et al. Repair of interrupted aortic arch. J Thorac Cardiovasc Surg 1996;112:1150-1160.[Abstract/Free Full Text]
  18. Parsons M.K., Moreau G.A., Graham T.P., Jr, Johns J.A., Boucek R.J., Jr Echocardiographic estimation of critical left ventricular size in infants with isolated aortic valve stenosis. J Am Coll Cardiol 1991;18:1049-1055.[Abstract]
  19. Reddy V.M., Rajasinghe H.A., Teitel D.F., Haas G.S., Hanley F.L. Aortoventriculoplasty with the pulmonary autograft. J Thorac Cardiovasc Surg 1996;111:158-167.[Abstract/Free Full Text]
  20. Silverman N.H., McElhinney D.B. Which two ventricles can-not be used for a biventricular repair? . Ann Thorac Surg 1998;66:634-640.[Abstract/Free Full Text]
  21. Phoon C.K.L., Silverman N.H. Conditions with right ventricular pressure and volume overload, and a small left ventricle. J Am Coll Cardiol 1997;30:1547-1553.[Abstract]
  22. Minich L.L., Tani L.Y., Hawkins J.A., Shaddy R.E. Possibility of postnatal left ventricular growth in selected infants with non-apex-forming left ventricles. Am Heart J 1997;133:570-574.[Medline]
Accepted for publication March 13, 1999.


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