Ann Thorac Surg 1998;65:503-508
© 1998 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Acute Changes in Preload, Afterload, and Systolic Function After Superior Cavopulmonary Connection
Mary T. Donofrio, MD,
Marshall L. Jacobs, MD,
Thomas L. Spray, MD,
Jack Rychik, MD
Division of Pediatric Cardiology, Department of Pediatrics, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA,
Division of Cardiothoracic Surgery, Department of Surgery, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
Accepted for publication July 14, 1997.
Dr Donofrio, Division of Pediatric Cardiology, Medical College of Virginia, Virginia Commonwealth University, 1200 E Broad St, Box 980342, Richmond, VA 23298 (e-mail: mdonofrio@gems.vcu.edu).
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Abstract
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Background. Superior cavopulmonary connection reduces the volume work of the single ventricle.
Methods. To determine the effects of superior cavopulmonary connection on preload, wall stress (or afterload), and systolic ventricular function, we studied 9 patients before and after operation, and at hospital discharge. Using echocardiography, preload was estimated by the ventricular end-diastolic area, and wall stress was calculated at end-systole and peak-systole. Ventricular function was represented by rate-corrected velocity of circumferential fiber shortening and fractional area change divided by rate-corrected ejection time.
Results. End-diastolic area and wall stress decreased postoperatively. Ventricular wall thickness increased with a concomitant decrease in cavity area. There was no change in mean blood pressure or heart rate or in rate-corrected velocity of circumferential fiber shortening or fractional area change divided by rate-corrected ejection time. These findings persisted at hospital discharge.
Conclusions. In single ventricles, superior cavopulmonary correction results in an immediate decrease in preload and afterload. The decrease in afterload results primarily from alterations in ventricular geometry. Although no improvement in systolic function was noted, diminished work related to the reduction in loading conditions may have beneficial long-term effects on preserving myocardial performance.
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Introduction
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The functional single ventricle, which pumps to both the systemic and pulmonary circulations, exists in a suboptimal physiologic state in which there is an increased volume load. Surgical intervention to redirect blood flow in such a way that the ventricle pumps to the systemic circulation alone reduces the volume load and theoretically results in a beneficial change in physiology. The superior cavopulmonary connection (SCPC) (bidirectional Glenn or hemi-Fontan operation) is an anastomosis of the superior vena cava to the right or left branch pulmonary artery. Because the operation enables a substantial proportion of the venous return to flow passively into the lungs, the ventricle pumps only to the body, and the volume load is reduced.
Previous investigators [1] [2] [3] [4] have demonstrated that a change in ventricular geometry occurs with volume reduction after SCPC. The present study was designed to assess the acute effects of SCPC on ventricular function and afterload (as reflected by myocardial wall stress). We hypothesized that because of the conservation of myocardial mass, an acute reduction in ventricular volume results in an immediate decrease in cavity size and a concomitant increase in wall thickness, which then causes an immediate reduction in myocardial wall stress, or afterload. In addition, these changes in loading conditions may have an effect on ventricular function and potentially improve myocardial performance. To test these hypotheses, we investigated the immediate postoperative changes in preload, afterload, and systolic ventricular function after SCPC in patients with a single ventricle.
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Material and Methods
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Over a 3-month period, all patients admitted to undergo SCPC at The Children’s Hospital of Philadelphia were studied. Prospective echocardiographic evaluation was performed immediately before SCPC, immediately after SCPC, and at the time of hospital discharge. Imaging was done with a Hewlett-Packard Sonos 2000 Echocardiograph (Andover, MA) and an appropriate transducer. Transesophageal imaging was carried out immediately before and after operation; transthoracic imaging was done at the time of discharge. Patients were included in the analysis only if adequate images of the ventricular short axis could be obtained. Studies were analyzed off-line with a Digisonics software package (Houston, TX) interfaced with a Summagraphics board (Seymour, CT) and a personal computer. Patients were excluded if the properties of the ventricle did not permit an estimation of meridional wall stress using Laplace’s law. More specifically, patients were included only if there was a uniform wall thickness (wall thickness of n ± 1 mm in four sampled quadrants), and the short-axis shape of the ventricle approximated a circle (the ratio of orthogonal diameters = 1 ± 0.1). No patient died during our evaluation period.
Patients
A total of 11 patients with a functional single ventricle were identified. Two were excluded for the criteria already discussed; thus the data of 9 patients were analyzed. Diagnoses included hypoplastic left heart syndrome (n = 4), double-outlet right ventricle (n = 2), unbalanced atrioventricular canal (n = 1), and tricuspid atresia (n = 2). Six had previously undergone a Norwood repair, 2 had systemic–pulmonary artery shunts, and 1 had a pulmonary artery band. The age at operation was 9.6 ± 6.4 months. Initial postoperative echocardiograms were made within 1 hour after operation in all patients, and discharge studies were done at a mean of 8 ± 5 days after operation. Initial postoperative medications included low-dose dobutamine hydrochloride (2µg · kg-1 · min-1) in 5 patients, and discharge medications included digoxin and furosemide in 5 patients and Lasix alone in 4 patients.
Echocardiographic Calculations
Preload was estimated as the end-diastolic area (EDA) measured in the short-axis projection just beneath the atrioventricular valve. Afterload, or meridional wall stress, was calculated at both end-systole and peak-systole using images taken from the short-axis projection (Fig 1). Using a modification of the formula of Grossman and colleagues [5] [6], wall stress was calculated by the following equation: 
, where P = pressure in millimeters of mercury, Ai = ventricular cavity inner area in square centimeters, and Ao = ventricular outer area in square centimeters [7] (see Appendix 1 for derivation of this formula). For calculation of wall stress at end-systole, the mean cuff blood pressure obtained by Dinamap was used to estimate end-systolic cavity pressure. Investigators have shown that mean aortic pressure correlates with end-systolic pressure obtained at cardiac catheterization [8] and that mean blood pressure correlates with end-systolic pressure determined by interpolation of tomometric carotid Doppler pulse tracings using the systolic and diastolic pressures determined simultaneously by Dinamap [9].
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Echocardiographic transesophageal image (A) before superior cavopulmonary connection and (B) immediately after the operation. Note reduction in cavity size and increase in wall thickness that occur immediately after operation. (Cavity = ventricular inner cavity; PW = posterior wall.)
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Ventricular inner and outer areas were measured at end-systole, which was timed by phonocardiographic semilunar valve closure. For calculations at peak-systole, the systolic cuff blood pressure was used as an estimation of the peak cavity pressure. Ventricular areas were measured at end-diastole because it is assumed that peak-systolic wall stress occurs around the time of isovolumic contraction [10] [11].
Measured variables of systolic function included the rate-corrected velocity of circumferential fiber shortening (VCFc) 
, where Ced = ventricular circumference at end-diastole, Ces = circumference at end-systole, ET = ejection time, and RR = electrocardiographic R-R interval) and the percent fractional area change divided by the rate-corrected ejection time (%FAC/ETc) 
, where Aed = ventricular area at end-diastole, Aes = area at end-systole, and ET and RR are as just identified). Ejection time was defined as the duration of time the systemic semilunar valve was open and was determined by measurement of the M-mode images taken through the plane of the valve.
Statistical Analysis
All measurements were made three times, and the average was used for calculations. The preoperative and postoperative studies were analyzed in random order to diminish observer bias. Statistical analysis was performed with a Wilcoxon signed-rank test, and significance was defined as a p value of less than 0.05. All results are expressed as the mean ± the standard error.
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Results
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Hemodynamic Data
There was no change in mean heart rate, diastolic blood pressure, and mean blood pressure after SCPC. Systolic blood pressure decreased significantly (p < 0.01) (Table 1).
Preload
The mean EDA decreased by 34% immediately after operation (p < 0.01). This change persisted, with no difference noted between the immediate postoperative area and the area at hospital discharge (Table 2; Fig 2). In 1 patient, the EDA increased slightly immediately after SCPC, but by hospital discharge, it had decreased significantly (Fig 3).
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Changes in mean ventricular end-diastolic area (preload) after superior cavopulmonary connection. (D/C = at hospital discharge; NS = not significant; Post = immediately after operation; Pre = before operation; * = p < 0.01.)
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Changes in ventricular end-diastolic area (preload) for individual patients after superior cavopulmonary connection. Eight of the 9 patients had an immediate decrease after operation, and before hospital discharge, all patients had a decrease from the preoperative value. (D/C = at hospital discharge; Post = immediately after operation; Pre = before operation.)
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Afterload
Mean end-systolic and peak-systolic wall stress decreased immediately after operation. End-systolic wall stress fell by 30% (p < 0.01) and peak-systolic wall stress, by 48% (p < 0.01). These changes persisted at hospital discharge (Fig 4; see Table 2). For individual patients, both end-systolic and peak-systolic wall stress decreased immediately after SCPC (Fig 5).
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Changes in (A) mean end-systolic wall stress and (B) mean peak-systolic wall stress after superior cavopulmonary connection. (D/C = at hospital discharge; NS = not significant; Post = immediately after operation; Pre = before operation; * = p < 0.01.)
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Changes in end-systolic wall stress for individual patients after superior cavopulmonary connection. All patients had an immediate decrease after operation. Similar data were obtained for peak-systolic wall stress (not displayed). (D/C = at hospital discharge; Post = immediately after operation; Pre = before operation.)
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To determine which variables led to the changes in end-systolic wall stress, the ventricular end-systolic cavity area and the wall thickness were analyzed independently. Cavity area decreased by 28% immediately after operation (p < 0.01), and wall thickness increased by 32% (p < 0.01). These changes persisted at hospital discharge (Fig 6; see Table 2). As stated previously, the systolic blood pressure decreased after operation. The mean blood pressure, which is the measure used in the calculation of end-systolic wall stress, did not change. In the single patient who did not have a decrease in EDA until hospital discharge, end-systolic area and wall stress both decreased immediately after operation. There was an immediate decrease in systolic blood pressure and no change in mean blood pressure in this patient.
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Changes in (A) mean end-systolic cavity area and (B) mean wall thickness after superior cavopulmonary connection. (D/C = at hospital discharge; NS = not significant; Post = immediately after operation; Pre = before operation; * = p < 0.01.)
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Ventricular Function
Neither the VCFc nor %FAC/ETc changed significantly after surgical intervention. There was a trend in the data, however, in that the mean VCFc improved steadily (Fig 7; see Table 2). Individual patient data showed a variable response (Fig 8).
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Changes in two variables indicative of systolic function after superior cavopulmonary connection: (A) rate-corrected velocity of circumferential fiber shortening and (B) percent fractional area change divided by rate-corrected ejection time. (D/C = at hospital discharge; NS = not significant; Post = immediately after operation; Pre = before operation.)
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Changes in velocity of circumferential fiber shortening in individual patients after superior cavopulmonary connection. Note the wide variation in response. (D/C = at hospital discharge; Post = immediately after operation; Pre = before operation.)
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Subgroup Analysis
In the comparison of patient subgroups on the basis of previous operation (Norwood versus other) and medications administered (dobutamine versus no dobutamine and digoxin versus no digoxin), no differences were noted in the documented changes in EDA, wall stress, and measures of systolic function after SCPC.
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Comment
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Reduction of the volume load in the single-ventricle heart has been reported to occur immediately after cavopulmonary connection [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12]. In the present study, the decrease in preload is represented by the immediate decrease in EDA. In addition to the peak-systolic myocardial wall stress, the end-systolic wall stress, or afterload, decreased concomitantly because of the diminution in cavity size and the increase in wall thickness. Surprisingly, the mean blood pressure did not change despite elimination of the systemic runoff from an aorta–pulmonary artery shunt in 8 patients. These findings suggest that the primary cause of the reduced end-systolic wall stress is the change in ventricular geometry associated with the volume-unloading surgical procedure rather than a decrease in systemic vascular resistance.
In a study by Suga and associates [13] using an isolated ventricular preparation, end-systolic cavity volume was shown to be dependent on end-systolic pressure when end-diastolic volume and contractility were held constant. In our study, the end-diastolic and end-systolic volumes decreased, and the end-systolic pressure, as estimated by the mean blood pressure, remained constant. These data suggest that the contractility increased after SCPC. The VCFc and %FAC/ETc did not change significantly, but the trend in the data suggests that myocardial shortening did improve. When using VCFc and %FAC/ETc as measures of contractility, it must be kept in mind that these variables are preload independent only under restricted physiologic conditions [6]. No study has determined if VCFc and %FAC/ETc are independent of the changes in preload that occur as a result of redirection of the circulation after SCPC.
Peak-systolic wall stress has been indicated to be a stimulus for myocardial hypertrophy [5] [14]. In this study, both peak-systolic and end-systolic wall stress decreased after SCPC. The final palliative operation for patients with a functional single ventricle is the Fontan operation (superior and inferior venae cavae–pulmonary artery connection). Many reports [15] [16] have shown that the Fontan operation is not well tolerated in patients with myocardial hypertrophy and ventricular dysfunction. It follows that early removal of the volume load and reduction in peak myocardial wall stress with the SCPC may decrease the stimulus for ventricular hypertrophy and improve the outcome of the Fontan operation in patients with a single ventricle.
Limitations
Determination of meridional wall stress in this group of patients is a representation of the total wall stress in all planes. In addition, the mean blood pressure is only an estimate of the true ventricular end-systolic cavity pressure. The measurements obtained are helpful, however, if they are used not to determine the absolute value of myocardial wall stress but to assess the change in each patient that occurs with surgical intervention using the data from each patient as its own control. Calculation of ventricular volumes in diastole and instantaneous wall stress in multiple planes throughout the cardiac cycle would be needed to determine the overall effects of SCPC. In addition, long-term follow-up is necessary to discover whether the changes noted persist beyond the study period.
Conclusions
Superior cavopulmonary connection results in an immediate and persistent decrease in end-diastolic cavity area (or preload), peak myocardial wall stress, and end-systolic wall stress (or afterload). The decrease in end-systolic wall stress results from alterations in ventricular geometry as represented by the decrease in cavity size and the concomitant increase in wall thickness. Though SCPC did not result in a significant improvement in measured variables of systolic function, there was a trend in the data suggesting that there may be improvement after surgical intervention. In addition, the decrease in end-systolic cavity area with no change in end-systolic pressure suggests improved contractility. We believe that early performance of SCPC to reduce ventricular volume load and decrease peak-systolic and end-systolic wall stress before separating the circulation completely with the Fontan operation is a beneficial procedure that results in favorable physiology and may ultimately improve myocardial performance and affect the long-term survival of patients with a single ventricle.
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Acknowledgments
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We extend sincere thanks to Dr Meryl Cohen and Dr Alexa Hogarty for their assistance in acquiring the images in these patients.
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Appendix 1
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Calculation of Wall Stress
Formula of Grossman and colleagues [5] [6] for wall stress:
where WS = wall stress in grams per square centimeter, 1.35 = the conversion factor to change millimeters of mercury into grams per square centimeter, P = ventricular cavity pressure in millimeters of mercury, d = ventricular cavity internal diameter, and h = ventricular wall thickness.
For the ventricular short axis (note, for a circle, Area = pi x radius2):
where Ai = ventricular short-axis inner area, 
= pi, and d = ventricular cavity short-axis diameter, and
where Ao = ventricular short-axis outer area, = pi, D = ventricular short-axis outer diameter.
Because D = d + 2h for the ventricular short axis,
By manipulating Ai and Ao to solve for d and h,
Substituting into the formula of Grossman and colleagues,
Solving,
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References
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Abstract
Introduction
