Ann Thorac Surg 2004;77:53-60
© 2004 The Society of Thoracic Surgeons
Original article: cardiovascular
Echocardiographic analysis of ventricular geometry and function during repair of congenital septal defects
Joseph P. Hart, MDa,
Santos E. Cabreriza, BAa,
Rowan F. Walsh, MDa,
Beth F. Printz, MD, PhDb,
Brianne F. Blumenthal, BAa,
David K. Park, BSa,
April J. Zhu, BSa,
Cecily G. Gallup, BAa,
Alan D. Weinberg, MSc,
Daphne T. Hsu, MDb,
Ralph S. Mosca, MDa,a,
Jan M. Quaegebeur, MDa,
Henry M. Spotnitz, MDa*
a Department of Surgery, Columbia College of Physicians and Surgeons, New York, New York, USA
b Department of Pediatrics, Columbia College of Physicians and Surgeons, New York, New York, USA
c Department of Biostatistics, Columbia University College of Physicians and Surgeons, New York, New York, USA
Accepted for publication June 23, 2003.
* Address reprint requests to Dr Spotnitz, Department of Surgery, Columbia University College of Physicians & Surgeons, 622 W 168th St, PH 14-103, 14th Fl, New York, NY 10032, USA.
e-mail: hms2{at}columbia.edu
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Abstract
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BACKGROUND: This study investigated changes in left ventricular (LV) geometry and systolic function after corrective surgery for atrial (ASD) and ventricular septal defects (VSD).
METHODS: Transesophageal LV short-axis echocardiograms were recorded before and after operative repair of ASD (n = 11) and VSD (n = 7). Preload was measured using LV end-diastolic area indexed for body surface area. Measurements of septal-freewall (D1) and anterior-posterior (D2) endocardial diameters were used to assess LV symmetry from D1/D2. Systolic indices included stroke area, area ejection fraction, and fractional shortening.
RESULTS: Preload, stroke area, area ejection fraction, and fractional shortening of D1 increased after ASD repair but decreased after VSD repair (p < 0.05). End-diastolic symmetry increased after ASD closure and decreased after VSD closure (p < 0.05). Increases in stroke area and ejection fraction after ASD correction primarily reflected increased shortening of D1. A positive correlation was found overall between percent change in end-diastolic area (EDA) and percent change in area ejection fraction (r2 = 0.80, p < 0.0001, n = 18).
CONCLUSIONS: Preload was the primary determinant of changes in LV function in this series of ASD and VSD repairs. Intraoperative changes in position of the interventricular septum affected systolic and diastolic LV symmetry and septal free wall shortening. Additional studies are needed to define changes in afterload and contractility as well as diastolic compliance and systolic mechanics.
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Introduction
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Open-heart surgery for congenital heart disease (CHD) began with closure of an atrial septal defect by John Gibbon in 1953 [1]. Subsequently, the complexity and results of surgery for CHD have advanced dramatically. Correction of uncomplicated lesions is carried out in infants and children, with outcomes often superior to those observed in surgery for acquired heart disease. In comparison with adult surgery, less is known about changes in ventricular function related to surgical correction of CHD. Transesophageal echocardiography (TEE) has become a standard tool for cardiac monitoring in children, and has been employed for quantitative measurements. The purpose of the present investigation was to define quantitative changes in functional geometry during corrective surgery for CHD.
We believe that definition of perioperative changes in functional geometry will improve understanding of the efficacy of surgery and lead to more precise studies of global and regional systolic and diastolic mechanics.
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Patients and methods
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Patients
This study was approved by the Columbia University Institutional Review Board in January 1997. Informed consent was obtained from the patient or patient's legal guardian. Procedures followed were in accordance with "Columbia University Good Clinical Practice Guidelines." Eighteen patients were studied between 1997 and 2001 at the Children's Hospital of New York-Presbyterian. Patients underwent surgical correction of either atrial septal defect (ASD; n = 11) or ventricular septal defect (VSD; n = 7). Diagnostic workup included transthoracic two-dimensional echo and echo-Doppler. Cardiac catheterization was not performed for straightforward lesions. Median age was 2.6 years. Group characteristics are presented in Table 1.
Median ages were ASD = 6.4 years and VSD = 0.9 years. Patients were anesthetized with isofluorane and supplemental agents as needed, or with a narcotic-based anesthesia (n = 5, all ASD patients). Ascending arch and bicaval venous cannulation for cardiopulmonary bypass and 1:1 blood cardioplegia were used in all cases.
Clinical electrocardiographic and echocardiographic data are summarized for each patient in Tables 2 and 3.
All ASDs had moderate to large shunts with right ventricular (RV) overload, as measured by echocardiography and echo-Doppler. Shunt size was not quantitated by oximetry. Nine patients had ostium secundum ASDs, and 2 had sinus venosus ASDs. All ASD patients were in normal sinus rhythm before and after cardiopulmonary bypass, except for ASD patient 1, who had postoperative atrial pacing for a slow junctional rhythm. QRS duration was 108 milliseconds or less. However, 6 patients had pre- and postoperative right ventricular conduction delay (RVCD), and 3 patients had only preoperative RVCD. One patient had right bundle branch block (RBBB) pre- but not postoperatively. None of the ASD patients had significant residual shunt postoperatively.
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Table 2. Pre- and Postoperative Electrocardiographic and Echocardiographic Data for Patients Undergoing ASD Repair
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Table 3. Pre- and Postoperative Electrocardiographic and Echocardiographic Data for Patients Undergoing VSD Repair
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All seven patients in the VSD group had moderate to large VSDs and left ventricular (LV) volume overload by echocardiography. One of the 7 patients underwent a previous Rastelli operation with RBBB pre- and postoperatively (VSD patient 5). Postoperatively, all VSD patients were in normal sinus rhythm with the exception of VSD patient 6, who was in sinus tachycardia. Ventricular septal defect patients 5 and 6 had postoperative RBBB. All repaired VSDs had no more than a very small residual VSD by postoperative echo.
Clinical data
A log of significant intraoperative events, including exogenous fluid administration, cardiac rhythm, and use of inotropic agents, was maintained and entered into a customized digital database in which patients were maintained anonymously and coded by study number.
Swan-Ganz catheters were not used intraoperatively. Central venous pressure, left atrial pressure, and pulmonary artery pressure, when needed for clinical management, were obtained by the surgical team by needle puncture, using a fluid-filled pressure monitoring system. These data were not recorded in our protocol.
Echocardiography
Intraoperative echocardiograms were recorded immediately before and immediately after cardiopulmonary bypass. Atrial septal defect patient 3 received Dobutamine at 5 µg/kg/min and was atrially paced. Transesophageal echocardiography was performed with either a Agilent Sonos 5500 (Ann Arbor, MI) or a VingMed CFM800 (GE, Milwaukee, WI) echocardiogram machine. Three ASD patients and 1 VSD patient were studied by hand held epicardial echocardiography performed by the attending surgeon with a sterile transducer. Gain, sector depth, and reject settings were set for optimal identification of endocardial and epicardial cardiac borders. Left ventricular short-axis cross sections were recorded on videotape for off-line analysis. All data were measured at end-expiration. All patients were in sinus rhythm without pulsus alternans during data recording.
Measurements
All videotapes were analyzed on a VingMed CFM800. Each source tape was calibrated. Areas and dimensions were analyzed by manual planimetry of endocardium and epicardium in accordance with the standards set by the American Society of Echocardiography [2]. End-diastolic area (EDA) was measured at the maximum ventricular cross section, coincident with the R-wave of the electrocardiogram. End-systolic area (ESA) was measured at the minimal area in the same cycle used to measure EDA. Each pair of measurements was repeated on three successive beats and averaged. Stroke area (SA), the difference between EDA and ESA, was a surrogate for stroke volume;
 | (1) |
Area ejection fraction (EFa) was calculated from SA and EDA as indicated in equation 2:
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D1 and D2 defined endocardial septal to free wall and anterior to posterior LV diameters (Fig 1). The ratio of D1 to D2 was assessed as an index of geometry. Fractional systolic shortening (FS) of these dimensions was also calculated:
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Fig 1. Representative end-diastolic transesophageal echocardiography image illustrates vectors utilized to measure D1 (perpendicular to the interventricular septum) and D2 (parallel to the septum).
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Statistical analysis
Paired t tests as well as linear regression models were used to analyze pre/post data. All data were analyzed using SAS system software (SAS Institute Inc, Cary, NC). Significance was defined as a p value less than 0.05.
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Results
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Representative transesophageal echocardiograms during ASD closure are presented in Figure 2.
Postoperatively, end-diastolic septal flattening decreases, and LV symmetry and ejection fraction increase. Representative echocardiograms during VSD repair are illustrated in Figure 3.
Septal hypertrophy is apparent. End-diastolic area and ejection fraction decrease after repair, whereas septal flattening and asymmetry increase.
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Fig 2. Representative TEE short-axis LV images immediately before and after CPB for ASD closure. Prerepair images are on the left and postrepair images are on the right. Upper panels contain end-diastolic images and lower panels contain end-systolic images. The RV is oriented to the left in each image. Septal flattening results in an elliptical LV prerepair. This resolves after ASD closure. Planimetry demonstrates increased postoperative EFa in this patient. (ASD = atrial septal defect; CPB = cardiopulmonary bypass; EFa = area ejection fraction; LV = left ventricular; TEE = transesophageal echocardiography.)
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Fig 3. Representative epicardial short-axis LV images immediately before and after CPB for VSD closure. Prerepair images are on the left and postrepair images are on the right. Upper panels contain end-diastolic images and lower panels contain end-systolic images. The septum appears hypertrophied. After VSD closure, there is a decrease in both LV geometry and EDA. Planimetry demonstrates decreased postoperative EFa in this patient. (CPB = cardiopulmonary bypass; EDA = end-diastolic area; EFa = area ejection fraction; LV = left ventricular; VSD = ventricular septal defect.)
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Figure 4
illustrates ASD geometry over time and comparison of TEE with transthoracic echo. Transthoracic images were obtained a few days before and several months after repair. Transesophageal echocardigraphy was obtained immediately before and after cardiopulmonary bypass (CPB). Partial resolution of septal flattening is apparent postoperatively in both sets of images.
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Fig 4. Time course of LV geometry before and after ASD closure. Panel 1 was obtained by transthoracic echocardiography 1 week preoperatively. Panels 2 and 3 were obtained by intraoperative TEE immediately before and after cardiopulmonary bypass (CPB) for ASD closure. Panel 4 was obtained by transthoracic echocardiography 5 months postoperatively. Septal distortion seen in the first two panels is improved immediately and late after surgery. (ASD = atrial septal defect; CPB = cardiopulmonary bypass; EFa = area ejection fraction; LV = left ventricular; TEE = transesophageal echocardiography.)
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Average results for geometry and functional data are presented in Table 4
and Figures 5 and 6.
In the ASD group, EDA, stroke area, and ejection fraction all increased significantly after repair. In the VSD group, EDA, stroke area, and ejection fraction all decreased significantly. In Figure 7,
the postoperative percent change in EDA (expressed as a percent of the preoperative value) is plotted against the postoperative percent change in ejection fraction. This reveals a strong positive correlation between EDA and ejection fraction for the 18 patients studied. This regression equation is 
EFa = -0.01 + 0.86(%EDA) (r2 = 0.80 and p < 0.0001).
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Fig 5. Perioperative EDA changes. Brackets indicate standard errors. The CHD groups are defined on the x-axis. Prerepair data are represented by black bars; postrepair data are represented by white bars. *p less than 0.05 versus prerepair within the same group. EDA increased significantly in the ASD group and fell in the VSD group. (ASD = atrial septal defect; CHD = congenital heart disease; EDA = end-diastolic area; VSD = ventricular septal defect.)
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Fig 6. Similar to Figure 5, indicating effects of surgery on intraoperative area ejection fraction. EFa increased significantly after CPB in the ASD group and decreased in the VSD group. (ASD = atrial septal defect; CPB = cardiopulmonary bypass; EFa = area ejection fraction; VSD = ventricular septal defect.)
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Fig 7. Change in EDA, as a percent of preoperative EDA along the x-axis is related to change in EFa, as a percent of preoperative EFa on the y-axis. A linear relationship exists for the combined data from 18 patients (r2 = 0.80, p < 0.0001). Group means are represented by large open symbols, with brackets indicating group standard errors. There is a significant linear correlation between changes in ejection fraction and EDA. (EDA = end-diastolic area; EFa = area ejection fraction.)
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After ASD closure, end-diastolic symmetry (D1/D2) increased from 0.66 ± 0.03 to 0.74 ± 0.03 (p < 0.01). The absolute values of both D1 and D2 increased significantly. Fractional shortening of D1 increased, but D2 did not (Table 4).
After VSD closure, end-diastolic symmetry decreased from 0.7 ± 0.04 to 0.64 ± 0.05 (p < 0.05). The absolute values of both D1 and D2 decreased significantly. Similar to the ASD group, there was a significant decrease in postoperative fractional shortening of D1 but not D2 in the VSD group.
Heart rate and peak systolic arterial blood pressure did not change significantly after CPB in either group (Table 4).
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Comment
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The important determinants of LV systolic function are preload, afterload, and contractility. The effects of these factors on LV ejection fraction in experimental animals were documented by Palacios and associates 1984 [3]. Increases in preload and contractility increased ejection fraction, whereas increases in afterload reduced ejection fraction. Heart rate secondarily affects stroke volume through diastolic filling time, diastolic relaxation, and viscosity. Rate alone can increase cardiac output by increasing the number of stroke volumes per unit time. Synchrony of contraction also affects LV function, as shown in studies of idiopathic hypertrophic subaortic stenosis [4] and biventricular pacing [5]. Thus, rhythm changes like atrioventricular block, bundle branch block, and temporary ventricular pacing can alter ventricular function.
The utility of ejection fraction as an index of function is diminished by its multiple determinants. It is generally agreed that an increase in ejection fraction can be interpreted as an increase in intrinsic contractility only under a very limited set of conditions. Furthermore, in congenital heart disease, RV function can affect LV function, through pressure gradients across the interventricular septum, as well as by position, contraction, and shape of the septum. In addition, transseptal pressure gradients can alter LV compliance [6].
Accurate determination of systolic and diastolic mechanics of correction of congenital heart disease is a complex task, which was not the objective of this study. The purpose of this study was to obtain preliminary echo data studies in order to define questions that require focused investigation with more sophisticated methods. Quantitative echo studies have proved valuable for this purpose in the past in studies of valvular heart disease. For example, studies of techniques of mitral valve repair accelerated after early data showed large, acute reductions of ejection fraction unique to valve replacement for chronic mitral regurgitation [7, 8].
Even the modest objectives of the present study required careful selection to obtain patients in whom the pathophysiology was primarily attributable to the lesion of interest, not confounded by simultaneous correction of other lesions, including mitral or aortic insufficiency. Studies were also scrutinized to eliminate patients with functionally significant postoperative shunts or ventricular pacing. The results obtained demonstrate an important association between changes in preload and changes in postoperative ejection fraction. This relation (Fig 7), not defined previously, suggests but does not prove that changes in afterload and contractility were not major determinants of function in this series. Furthermore, the data imply important preload reserve after VSD correction. Figure 7 implies that an increase in LV end-diastolic volume alone could produce an increase in postoperative LV ejection fraction of 30% after VSD repair. Of course, this would only be true if the RV is capable of supporting increased flow. If RV failure or elevated pulmonary vascular resistance limited this reserve in practice, nitric oxide may facilitate increased LV preload and limit the need for inotropic agents. This must be regarded purely as speculation until additional data are obtained.
Our data also emphasize the importance of dynamics of the interventricular septum, with end-diastolic shape and D1 fractional shortening increasing postoperatively in ASD patients and decreasing in VSD patients. These directional changes parallel changes in EDA, emphasizing the importance of preload on shape and regional function. The importance of preload is further implied by the observation in ASD repair that when changes in fractional shortening were asymmetrical, changes in fractional shortening occurred in parallel with changes in the length of the end-diastolic diameter.
Surgical closure of the interatrial communication in ASD eliminates the left to right shunt, increasing left ventricular flow and decreasing the attendant RV volume overload. Closure of the atrial septum restores the possibility of physiologic transseptal LV-RV pressure gradients, end-diastolic pressure in the LV normally exceeding that in the RV. Measurements of left atrial or LV pressures postoperatively are not available for our patients.
In VSD, closure of the interventricular communication decreases the left to right shunt. Left ventricular inflow is reduced by removal of the shunt, thereby reducing preload. We believe that reduction in LV preload was the primary cause of reduced postoperative SA in this study, but other factors could be involved, including adverse effects of the septal patch on afterload and regional contractility.
Previous studies have examined ventricular function during CHD surgery utilizing conductance ventriculography or sonomicrometry. One conductance study of a variety of defects demonstrated reduced contractility and no change in diastolic properties [9]. Conductance and sonomicrometry have been used independently to demonstrate benefical effects of modified ultrafiltration on systolic and diastolic properties [10, 11]. Colan and del Nido have noted difficulties with conductance in CHD [12], and our laboratory has noted many problems with conductance [13–15]. Our preference for echocardiographic measurements is based on the ability to measure internal and external dimensions and wall thickness simultaneously [7, 16–22]. We also prefer to insert pressure catheters whenever possible through an existing cardioplegia site and retrograde across the aortic valve and into the LV [23].
Sectioning planes available with TEE are limited when compared with hand-held transducers, and this causes short-axis distortion in some patients. This distortion results in underestimation of D1, but the problem applies equally to systolic and diastolic measurements and does not cause errors in calculation of changes in ejection fraction or fractional shortening (Blumenthal and associates, unpublished observations). This allows TEE and epicardial echo measurements to be combined, if proper sectioning techniques are utilized.
The potential foreshortening of D1 in TEE leads us to interpret cautiously a postoperative D1/D2 ratio in the ASD group of less than 1. The normal left ventricle is circular in cross section, with a minor semiaxis ratio of 1.0. A postoperative D1/D2 of less than 1 (0.74 in this study) could imply residual wall stresses that would lead to gradual remodeling over time. Stimulated by this observation, late follow-up studies in our laboratory indeed confirm that LV shape continues to normalize for many months after ASD repair.
Future studies of effects of surgery in congenital heart disease would be enhanced by analysis of diastolic compliance, systolic function curves, and septal mechanics. These measurements require pressure and flow meter data. Comparison studies with nonsurgical groups, including patients undergoing ASD closure in the catheterization laboratory and with robotic techniques, are also in progress in our laboratory.
We conclude that TEE is useful for intraoperative study of LV geometry in repair of ASD and VSD. Our data emphasize a strong overall correlation of changes in preload with changes in ejection fraction, both values increasing after ASD repair and decreasing after VSD repair. Both groups manifest asymmetrical changes in shape and fractional shortening, which occur predominantly along the diameter perpendicular to the interventricular septum. Additional studies are needed to define the impact of asymmetrical diastolic geometry on regional systolic function and to further define changes in systolic and diastolic function of the LV and RV.
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Acknowledgments
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The authors gratefully acknowledge the assistance of the skillful clinical team at New York Presbyterian Hospital, without whom this study would not be possible. In particular, we wish to thank Rozelle Corda, NP, the clinical perfusion team, and our pediatric cardiology group, led by Welton Gersony, MD, for their invaluable assistance. We also thank Alan Weinberg for assistance with statistical analysis and May Deutsch for assistance with manuscript preparation. This work was supported by National Institutes of Health grant R01 HL 48109.
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References
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Abstract
Introduction
