Ann Thorac Surg 1997;63:1691-1700
© 1997 The Society of Thoracic Surgeons
Original Article: Cardiovascular
Effect of Surgical Reconstruction on Flow Profiles in the Aorta Using Magnetic Resonance Blood Tagging
Mark A. Fogel, MD,
Paul M. Weinberg, MD,
Alison K. Hoydu, PhD,
Anne M. Hubbard, MD,
Jack Rychik, MD,
Marshall L. Jacobs, MD,
Kenneth E. Fellows, MD,
John Haselgrove, PhD
Division of Cardiology, Department of Pediatrics, Department of Radiology, and Division of Cardiovascular Surgery, Department of Surgery, The Children's Hospital of Philadelphia, and Departments of Pediatrics, Radiology, and Surgery, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Accepted for publication December 23, 1996.
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Abstract
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Background. The aorta that has undergone an aorta–pulmonary artery anastomosis may not exhibit the same velocity profile as the nonreconstructed aorta, whose velocity profile is thought to be uniform across the vessel diameter (plug flow). This may have an impact on fluid dynamics and will alter Doppler flow calculations. Our objective was to determine the impact of surgical reconstruction on the velocity and flow profiles of the reconstructed ascending and descending aorta.
Methods. Using a magnetic resonance imaging tagging technique that labels flowing blood (bolus tagging), we studied 22 patients (mean age, 8.6 ± 4.7 years) who had had a Fontan procedure. A cine sequence labeled the blood and acquired the image after 20 ms in the middle of the ascending aorta and behind the left atrium in the descending aorta. The repetition time was 50 ms.
Results. The reconstructed ascending aorta displayed a velocity profile skewed anteriorly, whereas in the nonreconstructed aorta, the velocity profile was flat. Reconstructed aortas also displayed flows that were higher anteriorly, took a longer time to reach maximum velocity, and were less like "plug" flow than the nonreconstructed aorta. The descending aorta, regardless of whether aortic reconstruction was present, displayed velocity profiles (at various phases of systole) skewed posteriorly.
Conclusions. The reconstructed aorta displays disturbed flow, and the velocities across the ascending aortic diameter are more varied than those in aortas without reconstruction and are skewed anteriorly. The descending aortic velocity profile in children is skewed posteriorly, regardless of whether aortic reconstruction is present. This information may help design and build a "better" aortic reconstruction.
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Introduction
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Although the shape of the velocity profile in the normal aorta is debatable [1–11], most investigators agree that flow in the ascending and descending aorta is generally axisymmetric across the vessel diameter (plug flow). These studies used hot-film anemometers, Doppler techniques, swirling echo contrast, and magnetic resonance imaging phase-encoded velocity mapping to determine the velocity profile. The shape of the velocity profile is important in fluid dynamics for efficient mass transfer of blood and has implications for cardiac output calculations by Doppler techniques [2, 6, 8].
Some patients who undergo the Fontan procedure require a previous aorta–pulmonary artery anastomosis with aortic arch augmentation to achieve adequate ventricular outflow (eg, patients with hypoplastic left heart syndrome). This manipulation may have effects on the velocity profile by changing aortic geometry and adding nonelastic materials to a normally elastic wall. This change may not be energy efficient and could affect the long-term functioning of the single ventricle and alter flow calculations.
This study uses magnetic resonance imaging blood labeling (bolus tagging) [12–17] to visualize flow patterns across the ascending and descending aortic diameter in both reconstructed aortas (neo-aorta) and aortas without reconstruction. Patients in both groups had a Fontan operation to isolate the effect of surgical reconstruction on the flow pattern (as opposed to using "normal" children in the nonreconstructed group). We address in vivo velocity profile alterations in the aorta, quantify this change, and discuss its implications.
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Material and Methods
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We prospectively studied 22 patients with functional single ventricle (9 with a nonreconstructed aorta, 13 with a neo-aorta) who underwent Fontan reconstruction at The Children's Hospital of Philadelphia between June 1, 1994, and July 31, 1995. All values are mean ± standard deviation. Mean patient age was 8.6 ± 4.7 years (± the standard deviation) (range, 2 to 20 years; median age, 5 years), and mean age at operation was 2.7 ± 2.1 years. Mean time from operation was 4.1 ± 4.9 years (range, 1 week to 15 years), and mean heart rate was 96 ± 20 beats/min (median rate, 94 beats/min). All studies were adequate for interpretation.
Anatomic diagnoses, the presence or absence of aortic reconstruction, and ventricular morphology are outlined in Table 1
. All patients underwent echocardiography within 6 months of magnetic resonance imaging (10/22 within a week) and had qualitatively good ventricular shortening. None of the patients had semilunar valve stenosis, and all had either trace or no regurgitation. None had symptoms referable to the cardiovascular system. Seven patients were studied within 1 week of operation and were on a regimen of digoxin and captopril as routine postoperative medicines. Patients were in stable enough condition to undergo a 1-hour magnetic resonance imaging scan under sedation (if <7 years old). Informed consent was obtained from all. No patient had arrhythmias precluding imaging in the scanner.
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Magnetic Resonance Imaging
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If less than 7 years old, patients were sedated with chloral hydrate, Nembutal (pentobarbital sodium), or Demerol (meperidine hydrochloride) prior to imaging. All patients were monitored with pulse oximetry, nasal end-tidal carbon dioxide, electrocardiogram, and direct visualization by television. All patients tolerated sedation without incident.
Our study used a Siemens 1.5 Tesla Magnetom SP 63. The scanning protocol was as follows (Fig 1A): After coronal localizers, T1-weighted axial images spanning the entire thorax were acquired. These images evaluated cardiovascular anatomy and were used as localizers for subsequent magnetic resonance imaging tagging. A series of T1-weighted images were then acquired in an oblique sagittal plane to obtain images along the long axis of both the ascending and descending aorta parallel to flowing blood (see Fig 1A, top and lower left). These images ensured that the final blood-tagging sequence was performed in the center of the vessel. The effective repetition time was the R-R interval (range, 350 to 800 ms); the echo time, 15 ms; the number of excitations, 3; the image matrix size, 128 x 256 pixels, interpolated to 256 x 256; the field of view, 180 to 250 mm; and the slice thickness, 3 to 8 mm.
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Fig 1. . Magnetic resonance imaging protocol for bolus tag imaging and analysis. (A) Spin-echo images were obtained parallel to flow of blood in ascending aorta (AAo) and descending aorta (DAo) (upper and lower left). A tag was placed halfway between aortic valve and apex of aortic arch in AAo (lower middle and right) and halfway between apex of aortic arch and diaphragm in DAo (not shown) (see Fig 3A ). Arrowheads indicate tag placement and movement in blood vessel and arrows, initial site of tagging. (B) Nine images of bolus tagging in AAo of reconstructed aorta (Ao) obtained 50 ms apart (left). Blood flow displaces saturation band (arrowheads), whereas stationary structures maintain original site of tagging (arrows). Image analysis (right) shows only three positions across Ao for simplicity. (AW = anterior wall; LV = left ventricle; P = posterior; PW = posterior wall; RV = right ventricle; S = superior; Vent = ventricle.)
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Multiple prospectively triggered images were acquired (Fig 1B; see Fig 1A, lower middle and right) using the bolus tagging sequence [12–17]. This is a cine gradient-echo sequence that uses a "presaturation" radiofrequency pulse before every acquisition to produce saturated spins along a line designated by the user (a black stripe representing a signal void on the image). The tag was placed perpendicular to blood flow. The blood flow displaces the saturation band, whereas stationary structures (eg, chest wall and spine) maintain the saturation band at its original position. The displacement of the saturation band on the blood relative to the chest wall and spine allows calculation of velocity and flow (see Fig 1B). Each image represents blood displacement (by motion of the "black stripe") between the time of tagging and image acquisition. The repetition time was 50 ms; the echo time, 8 ms; the number of excitations, 1; the matrix size, 128 x 128, interpolated to 256 x 256; the slice thickness, 5 to 10 mm; the tag thickness, 1.5 to 2 mm; and the field of view, 180 to 250 mm (mean, 200 mm).
This sequence produced multiple images at different phases of the cardiac cycle referenced to the QRS (see Fig 1B, left). Phase encoding occurred 17 ms after the tag and frequency encoding, 20 ms after the tag. Tags were created at intervals of 50 ms (repetition time, 50 ms) starting 1.2 ms after the R wave.
Along the ascending aorta, the tag was positioned halfway between the semilunar valve and the apex of the aortic arch (Fig 2A; see Fig 1). In the descending aorta, the tag was positioned halfway between the apex of the aortic arch and the diaphragm (Fig 3A).
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Fig 2. . Bolus tagging in ascending aorta (AAo). (A) Velocity profile (arrowheads) in reconstructed aorta (Ao) (anterior skew) and Ao without reconstruction (flat profile). Representative velocity profiles extracted from images of (B) reconstructed Ao and (C) nonreconstructed Ao. These graphs of velocity versus position across AAo (1 = most posterior and 12 = most anterior) display the family of curves representing phases of systole and some in diastole (each curve represents a different phase with 1 at R wave). Representative velocity maps from images of (D) reconstructed Ao and (E) nonreconstructed Ao. These graphs of velocity versus phase (1 at R wave) display the family of curves representing the 12 positions across AAo diameter with 1 as most posterior and 12, most anterior. The thickness of the family of curves at each phase is a measure of how "pluglike" the flow is. Note how thick the family of curves is in reconstructed Ao, and they peak later in systole than in nonreconstructed Ao.
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Fig 3. . Bolus tagging in descending aorta (DAo). (A) Nine images of bolus tagging in DAo obtained 50 ms apart (left) and enlargement demonstrating posterior skew found in both reconstructed and nonreconstructed aortas (right). Arrowheads indicate tag in DAo and arrows, initial site of tagging. Representative velocity profiles extracted from images of (B) reconstructed aorta and (C) nonreconstructed aorta. These graphs of velocity versus position across DAo (1 = most posterior and 12 = most anterior) display the family of curves representing phases of systole and some in diastole (each curve represents a different phase with 1 at R wave). Note the posterior skew of both. Representative velocity maps from images of (D) reconstructed aorta and (E) nonreconstructed aorta. These graphs of velocity versus phase (1 at R wave) display the family of curves representing the 12 positions across DAo diameter with 1 as most posterior and 12, most anterior. Note how solid black lines (the more posterior positions) dominate the area with high velocities. (AAo = ascending aorta.)
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The bolus tagging technique was used because it directly visualizes the velocity profile, although it yields information in only one plane. Phase-encoded velocity mapping does provide a flow profile in cross-sectional area, but it does not directly visualize it. Further, the following drawbacks to phase-encoded velocity mapping were considered: it is operator dependent in terms of assigning a region of interest; blood vessels coursing near the vessel under study can cause artifactual results; and it does not have the spatial resolution that the bolus tagging technique has (as programmed on our Siemens SP 63), which becomes especially important in children.
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Image and Data Analysis
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Images were analyzed using the Volumetric Image Display and Analysis (VIDA) program [18] on a Sun SPARC 10 workstation (Sun Microsystems). On each image (phase of systole), the operator used a mouse to trace the following features: aortic anterior and posterior walls; the original site of tag placement ("baseline"); and the position of the tag moved by blood flow ("flow curve"). Computer-aided enhancement of the initial tracing of the baseline and flow curve chose the center of the saturation band by finding the local pixel of least intensity. Twelve streamlines were calculated and drawn by computer at equally spaced points across the aortic diameter from the weighted averages of the anterior and posterior walls drawn by the operator.
For each phase of systole, the distance moved by the tagged blood along each of the 12 streamlines was measured and the velocity along each streamline was calculated as follows (see Fig 1B):
Flow was calculated using these values, and results mirrored the velocity data (Appendix 1).
Because of differing heart rates and a temporal resolution of 50 ms, the phase of systole was standardized as a percentage of systole from the R wave to the flow tag returning to baseline (<20 mL/s of flow). The position across the aortic diameter was standardized as a percentage of the aortic diameter from the posterior to the anterior wall.
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Velocity Parameters
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For each phase of systole, the greatest velocity of any streamline was determined. Maximum velocity was the highest of these values. The phase of systole (percent) at which maximum velocity occurred as well as its position across the aorta (percent) was also calculated.
As a measure of how much the velocity profile mirrored "plug flow," the standard deviation of all velocities across the aorta at each phase of systole was determined (ie, the lower the standard deviation, the more "flat" or like "plug flow" it was). The greatest standard deviation throughout systole as well as the phase at which it occurred was then calculated.
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Statistical Analysis
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The two-way, unpaired Student t test compared means between the patients with nonreconstructed aortas and those with neo-aortas. The two-way, paired Student t test determined differences between variables in the ascending and descending aorta in a given patient. Interobserver variability was determined by the coefficient of variation. Statistical analysis was performed using JMP version 3.1.4 (SAS Institute, Cary, NC). All values are shown as the mean ± the standard deviation. Significance was defined as a p value of less than 0.05.
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Results
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Cardiac index for patients with and without aortic reconstruction was 3.0 ± 0.91 L•min-1•m-2 and 3.14 ± 0.76 L•min-1•m-2, respectively (p = not significant). Interobserver variability for tracking the tag (15/22 patients) had a coefficient of variation of 7.2% ± 3.3%.
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Ascending Aortic Flow-Velocity Profile and Flow Characteristics
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Figures 1 and 2A demonstrate the in vivo velocity profile. Velocity profiles plotted in different forms are shown in Figures 2B through 2E for both neo-aortas and nonreconstructed aortas. Velocity as a function of aortic diameter is displayed in Figures 2B and 2C for neo-aortas and nonreconstructed aortas, respectively. The flow profiles are qualitatively different. The neo-aortas demonstrated an anteriorly skewed velocity profile (higher velocities in the anterior aorta), whereas the nonreconstructed aortas had a flat and uniform velocity profile. Velocity as a function of time for each streamline is shown in Figures 2D and 2E for the neo-aortas and nonreconstructed aortas, respectively. Qualitatively, the neo-aortic maximum velocity peaked later in systole than that of the nonreconstructed aorta, and there was a greater variability of velocities across the diameter of the ascending neo-aorta (ie, the "thickness" of the family of lines in Figures 2D and 2E).
Table 2 quantitatively summarizes the velocity data of the ascending neo-aortas and nonreconstructed aortas. Maximum velocity was the same for the nonreconstructed aortas (86 ± 33 cm/s) and neo-aortas (91 ± 57 cm/s), although it took longer to reach this maximum velocity in the latter (57% ± 7% versus 47% ± 10%, respectively; p < 0.05). The position of maximum velocity was more anterior in neo-aortas than nonreconstructed aortas (70% ± 19% and 54% ± 18%, respectively, from the posterior wall (Figs 2A–2C). The maximum standard deviation of velocities across the aorta (how "pluglike" the flow is, or the "thickness" of the family of lines in Figs 2D and 2E) was significantly larger in neo-aortas than nonreconstructed aortas (28.4 ± 7.5 cm/s versus 21.0 ± 8.8 cm/s, p < 0.05), although the phase at which this occurred did not differ significantly.
The anterior skew to the velocity profile in the ascending neo-aorta was present with the "usable" semilunar valve anterior (eg, hypoplastic left heart syndrome) or posterior (eg, patients 14 and 15).
No differences in velocity profiles were noted within either group between functional single left and right ventricles (ie, in Table 1, patients 1 through 3 did not differ from patients 4 through 9 in the nonreconstructed aorta group, and patients 10 through 12 did not differ from patients 13 through 22 in the neo-aorta group).
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Descending Aortic Flow-Velocity Profile and Flow Characteristics
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Figure 3A demonstrates the in vivo velocity profile in the descending aorta. As with the ascending aorta, examples of the velocity profiles plotted in different forms are shown in Figures 3B through 3E for both neo-aortas and nonreconstructed aortas. Velocity as a function of aortic diameter is displayed in Figures 3B (neo-aorta) and 3C (nonreconstructed aorta). The flow profiles, depending on the phase of systole, are skewed posteriorly in both cases.
Examples of the velocity–time courses for each streamline are shown in Figures 3D (neo-aorta) and 3E (nonreconstructed aorta). Maximum velocity is reached at the same phase (phase 5) in both. There is also no difference in the variability of velocities across the diameter of the descending aorta (ie, the "thickness" of the family of lines in Figures 3D and 3E) between the neo-aorta and the nonreconstructed aorta.
Table 2 summarizes quantitatively the velocity data of the descending neo-aorta and nonreconstructed aorta. Maximum velocity was significantly lower in the neo-aorta than the nonreconstructed aorta (94 ± 31 cm/s versus 118 ± 26 cm/s; p = 0.05), although time to reach maximum velocity was not significantly different, occurring just over halfway through systole. The position of maximum velocity was similar in both groups, occurring at about 40% of the aortic diameter (from the posterior wall). No differences between groups were noted in the maximum standard deviation of velocities ("thickness" of the family of curves in Figures 3D and 3E) or the time to reach this value (occurring approximately 70% through systole).
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Comparison Between Ascending and Descending Aorta
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In the nonreconstructed aorta, the maximum velocity in the descending aorta (118 ± 26 cm/s) was significantly greater than in the ascending aorta (86 ± 33 cm/s). This occurred significantly later in systole (60% ± 10%) than in the ascending aorta (47% ± 10%). The position of maximum velocity, however, was not different between the ascending and descending aorta. In the neo-aorta, unlike the nonreconstructed aorta, the maximum velocity was the same in the ascending and descending aorta, although the position of maximum velocity was significantly more anterior in the ascending (70% ± 19%) than descending aorta (39% ± 21%).
The maximum standard deviation of the velocities was the same in the ascending and descending aorta regardless of group, although the time to reach maximum standard deviation was significantly earlier in the ascending than descending aorta in both groups.
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Flow Data
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The flow data for the ascending and descending aorta are described in Appendix 2 and in general, mirror the velocity data. Even though the nonreconstructed descending aorta had a significantly higher velocity than the neo-aorta (see Table 2), the maximum flow was nearly identical to that of the neo-aorta (Table 3). Also, although maximum and average flows were not significantly different between the two groups, the ascending neo-aorta had significantly more anterior flow than the nonreconstructed aorta, which had flow equally distributed between anterior and posterior regions. In the descending aorta, depending on the systolic phase, both groups had more posterior than anterior flow.
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Comment
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The debate concerning the shape of the aortic velocity profile [1–11] is not an academic exercise. It has far-reaching implications for the energetics of the mass transfer of blood. If flow is thought of as an infinite amount of infinitesimally small streamlines, "plug" flow ("flat" profile), by definition, has all streamlines moving at the same velocity with little shear forces experienced between them. Of course, because of the "no-slip" condition (fluid particles next to the wall have a velocity of 0), a boundary layer forms near the vessel wall, with the resulting shear force at any point in the boundary layer given by the formula [19] 
rx = -µ (
V/r), where rx is the shear force/area, µ is the viscosity, and V/r is the slope of the axial velocity profile with respect to the radius. The smaller the slope of the axial velocity profile with respect to the radius (ie, the flatter the velocity profile), the less shear force, and therefore less energy loss, there is.
Variations in the velocity profile can cause artifacts in Doppler calculations [2, 6, 8]. For example, in measuring the velocity–time integral for cardiac output, a velocity is assigned for each time point and is assumed to be representative of the mean velocity for the entire cross-sectional area of the vessel. If the velocity profile is skewed, the velocity in the sample volume will not be representative of the mean velocity for the entire cross-sectional area of the vessel. Also, if the sample volume is placed over a skewed profile, the velocity–time integral (which involves tracing the outer border of the spectral recording) will be overestimated (because the highest velocity in the skewed profile will enter the calculation). The body of literature assumes a "flat" profile [2, 6, 8].
We studied only Fontan patients who by necessity underwent midline sternotomy and circulatory arrest to make the two groups comparable to observe the effects of surgical reconstruction.
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Ascending Aorta-Velocity Profile and Flow Characteristics
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Our study clearly demonstrated substantial differences between nonreconstructed aorta and neo-aorta. Although maximum flow and velocity as well as average flow in the ascending aorta were not different between the groups, the neo-aorta differed from the nonreconstructed aorta in both temporal and spatial distribution of velocity and flow. Temporally, the time to maximum velocity was longer and the time to highest anterior flow rate, greater in the neo-aorta than the nonreconstructed aorta. This delay in developing the full velocity profile and flow may be evidence that the ventricle is having difficulty ejecting blood into the neo-aorta. Both groups had the same cardiac index (which removes the variable of ventricular performance), and there was no difference between aortas with different ventricular morphology within each group.
Spatially, in the neo-aorta, the position of maximum velocity was more anterior, the maximum standard deviations of the velocities were greater (ie, less "pluglike"), there was greater anterior flow, and there were greater maximum and minimum anterior flow rates than in the nonreconstructed aorta. This altered flow in the ascending neo-aorta may be the cause of energy inefficiency (by the loss of "plug" flow) and may have an impact on the long-term functioning of the single ventricle. This may be the reason why our laboratory has observed altered ventricular strain and wall motion in Fontan patients [20, 21] compared with the normal ventricle. In addition, the altered flow may affect systemic venous pathway flow if the adaptations necessary to pump in a nonuniform manner have an effect on ventricular compliance, as it has been demonstrated that systemic venous pathway flow is in large part due to diastolic filling [22, 23].
The differences between the neo-aorta and the nonreconstructed aorta may be due to the aortic reconstruction itself. All patients with a neo-aorta had homograft material, which augmented the aortic arch. It may be necessary to change the biomaterial or the arch geometry to mimic the flow in a nonreconstructed aorta to maximize energy efficiency. Alternatively, the anterior skew of the velocity profile in the ascending neo-aorta may be due to the ventriculoarterial spatial relationships (the "usable" semilunar valve in many cases is the pulmonary valve, which is anterior). We observed, however, that even when the "usable" semilunar valve was posterior (eg, patient 14 and 15), there was an anterior skew. Further, our study made use of only single ventricles in comparing neo-aortas and nonreconstructed aorta, and various ventricular morphologies made no difference in the velocity profile. This negates the possibility that contraction patterns causing a streaming effect from both a mechanical and electrophysiologic standpoint may be different. Differences, therefore, between neo-aorta and nonreconstructed aorta were due only to the reconstruction.
In this study we examined the velocity and flow profiles of the neo-aorta and nonreconstructed aorta in pediatric patients. Previous studies have examined adults [1–4, 6, 7] or used animals [5, 8–11]. These studies provided conflicting results for the velocity profile shape in the ascending aorta [1]. Some observed a flat ("plug" flow) [8, 9, 11] and axisymmetric profile. Others demonstrated a parabolic [4, 24] or skewed profile [3, 5–7, 10] mostly along the posterior wall [1, 3, 5, 7]. Our data in the nonreconstructed ascending aorta are consistent with a flat velocity profile, as in true normals. The flow curves in some instances appear skewed posteriorly because the posterior wall has the greatest curvature (the anterior wall has the least curvature). In a "flat" velocity profile (ie, all streamlines moving at the same velocity), the tag along the posterior wall (greatest curvature) must bend further along the curvature than the tag along the anterior wall. This may explain the posterior skewness observed by other investigators.
Changing the velocity profile shape and attempting to simulate the nonreconstructed aorta may be achieved by altering the native aorta–pulmonary artery anastomotic geometry (eg, tapering the connection, making the diameter smaller proximally) or changing the biomaterial used, as already mentioned. The single-ventricle heart may then pump more efficiently and prolong the life of the ventricle.
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Descending Aorta-Velocity Profile and Flow Characteristics
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It could be argued that because the ascending neo-aortic flow is different from that of the nonreconstructed aorta, the downstream descending neo-aortic flow should also be different. The degree to which this effect is manifested is also a consideration. Because the innominate, left carotid, and left subclavian arteries are between the ascending and descending aortic tagging levels, ascending aortic effects may not be manifested in the descending aorta.
The most striking finding is that flow in the descending aorta is not "pluglike" in either group; in fact, both groups displayed velocity profiles skewed posteriorly at various systolic phases. Flow in the anterior aorta was slightly less than half (46%) of the total flow over all of systole, yet there were phases where flow was only 33% to 35% in the anterior descending aorta. The velocity profile qualitatively (see Figs 3A through 3C) and quantitatively is consistent with more flow posteriorly (eg, the position of the maximum velocity was 39% to 43% from the posterior wall). This was most pronounced at the end of the second third of systole.
Some [11] have argued that the curvature of the aortic arch and its branching vessels at its apex may play a role in forming the velocity profile of the descending aorta. Chandran [1] noted that secondary flows and vortices exist in the descending aorta and possibly are caused by this curvature and vessel branching. This may be the origin of the posterior skew we noted in our two-dimensional study. Using a conical hot-film probe, Falsetti and colleagues [11], however, found the velocity pattern in the ascending and descending aorta similar in dogs except that the velocity profile displayed "a little more rounding." Although Seed and Wood [10] did not measure the velocity profile in the anteroposterior plane of the descending aorta, measurement of the right-left plane with a hot-film constant-temperature probe displayed a "blunt" or flat profile with slightly higher velocities toward the right. Rieu and co-workers [7] using pulsed Doppler velocimetry, also found a "blunted" profile in an elastic model of the descending aorta, although the diagrams displayed velocity profiles skewed posteriorly at certain phases of systole.
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Comparison Between Ascending and Descending Aorta
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There was an acceleration of velocity from the ascending to descending aorta in the nonreconstructed aorta that was not present in the neo-aorta. Nevertheless, the maximum standard deviation of velocities was found to be the same between the ascending and descending aorta regardless of group. This absence of acceleration in the descending neo-aorta (which is not found in the nonreconstructed aorta) may be due to the geometry of the neo-aortic arch or the biomaterials used.
As would be expected, maximum and average flows in the ascending aorta were significantly greater than those in the descending aorta because of diversion of blood to the innominate, carotid, and subclavian arteries.
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Limitations
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Our temporal resolution was 50 ms (20 Hz). Any flow-related events that took place more quickly and did not remain for more than 30 ms would not be imaged. Further, if any flow-related events took place between tagging levels and did not manifest themselves at those levels, they also would not have been imaged. We doubt that this has substantially affected our results or conclusions.
We conservatively estimated subpixel tracking of the tag at 
pixel. Spatial resolution of our images was about 0.8 mm for a 128 x 128 matrix and a mean field of view of 200 mm. For velocities of approximately 100 cm/s, this yields an error of about 4%. An unexpected phenomenon of less than 1 mm would not have been imaged. We also would expect that if the error rate in tracking the tag were too high, there would be a lot of noise in the velocity profile; this was not observed (see Figs 1–3). Again, we doubt that this substantially affected our results or conclusions.
Our study was a two-dimensional one. As Chandran [1] and others [25] have noted, a full three-dimensional description of the flow is necessary because of helical and secondary flow patterns. We chose the bolus tagging technique because it directly visualizes the velocity profile at the cost of obtaining data in one plane. A full three-dimensional description of this flow is our next logical step.
Finally, our observations do not necessarily lead to the conclusion that the neo-aorta group has more complications than the nonreconstructed aorta group. This requires long-term follow-up with multiple matched variables, such as age and ventricular morphology.
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Conclusion
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Patients with neo-aortas display disturbed flow, and velocities across the vessel diameter are more varied (skewed anterior) than in patients with a nonreconstructed aorta. The descending aortic velocity profile in children is skewed posteriorly, regardless of whether the aortic arch is reconstructed or not. We speculate that this information may help design and build a "better" aortic reconstruction by varying the geometry and materials of the reconstruction to more closely mimic "plug" flow.
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Appendix 1. Flow Calculations
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To determine flow, the flow curve (the stripe moved by the motion of the blood) was interpolated to yield 24 points across the vessel wall. By determining with a planimeter the area between flow curve and baseline (the initial position of tagging) in the aorta, the volume swept by rotating this area 180 degrees around the center of the vessel yielded the volume of blood crossing the initial saturation plane at the time of image generation (eg, at each measured phase). The following formula was used:
where Di and Di+1 are the distances (centimeters) the flow curve has traveled at positions i and i + 1, Aodia is the aortic diameter (centimeters), and Ri and Ri+1 are the distances (centimeters) from the center of the aorta at positions i and i + 1. Flow is then calculated by dividing the volume of blood by the time between tagging and image acquisition:
Stroke volume (milliliters) was calculated by summing the flow at all phases (milliliters per millisecond) and multiplying by the time (milliseconds) between images:
The cardiac index was calculated by multiplying the stroke volume times the heart rate and dividing by the body surface area.
Flow Parameters
Flow at each measured phase of systole was calculated as just shown. The maximum flow rate as well as the average flow rate throughout systole was then determined.
As another gauge of how "pluglike" the flow was, the aorta was divided into anterior and posterior regions (six anterior streamlines and six posterior streamlines), and flow in the anterior aorta was calculated as a percentage of the total flow at each phase of systole. Summing the flow in the anterior aorta over all systole calculated the total amount of anterior flow. We then examined each phase of systole to obtain the maximum and minimum anterior flow rates and the phase in which they occurred (standardized as a percentage).
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Appendix 2. Quantitative Flow Results
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Flow results are shown in Table 3.
Ascending Aorta
In the ascending aorta, the maximum and average flows did not differ significantly between the neo-aorta and the nonreconstructed aorta. However, there was a significantly higher amount of total flow over all systole in the anterior neo-aorta (65% ± 15%), whereas in the nonreconstructed aorta, flow was equally divided between the anterior and posterior portions of the vessel (48% ± 12% of flow in the anterior nonreconstructed aorta). Further, at any measured phase of systole, the neo-aorta consistently demonstrated greater maximum and minimum anterior flow rates than the nonreconstructed aorta. The maximum anterior flow rate occurred significantly later in systole in the neo-aorta.
Descending Aorta
As with the ascending aorta, the maximum and average flows in the descending aorta did not differ significantly between the neo-aorta and the nonreconstructed aorta. Further, the total amount of flow across all of systole in the anterior descending aorta did not differ between the two groups (approximately 46% of the flow). In addition, the maximum and minimum flow rates in the anterior descending aorta at any given phase of systole did not differ between the neo-aorta and nonreconstructed aorta, although these ranged from 59% to 33% respectively in the neo-aorta and from 55% to 35% in the nonreconstructed aorta. The phase of maximum anterior descending aortic flow occurred earlier than the phase of minimum anterior descending aortic flow (48% and 55% through systole versus 67% and 69%, respectively) but did not differ significantly between the two groups.
Comparison Between Ascending and Descending Aorta
Both the maximum and average flow rates were significantly greater in the ascending aorta than the descending aorta regardless of type (neo-aorta versus nonreconstructed aorta). In the neo-aorta, however, the total anterior flow rate and the maximum and minimum anterior flow rates were significantly greater in the ascending than the descending aorta. Also in that group, the phase of minimum anterior flow rate occurred earlier in the ascending aorta than in the descending aorta. The phase of maximum flow rate, however, occurred later in the ascending aorta than in the descending aorta. This did not hold true for the nonreconstructed aorta.
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Acknowledgments
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We thank Brent Baxter, MS, for his invaluable technical support and John Hoford, BS, for his programming expertise.
Doctor Fogel has been funded through a fellowship grant of the Southeastern Pennsylvania affiliate of the American Heart Association.
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Footnotes
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Address reprint requests to Dr Fogel, Division of Cardiology, The Children's Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104.
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Abstract
Introduction
