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DOI:10.2214/AJR.06.0572
AJR 2007; 188:1660-1664
© American Roentgen Ray Society

Clinical Observations

Gradual Pulmonary Artery Enhancement: New Sign of Septal Defects on CT

I-Chen Tsai1,2,3,4, Tain Lee1,2,3, Min-Chi Chen1, Yun-Ching Fu3,4,5, Sheng-Lin Jan2,5, Wei-Lin Tsai1,2,3,4 and Chung-Chi Wang6

1 Department of Radiology, 407, Taichung Veterans General Hospital, No. 160, Section 3, Taichung Harbor Rd., Taichung, Taiwan, R.O.C.
2 Faculty of Medicine, Medical College of Chung Shan Medical University, Taiwan, R.O.C.
3 Department of Medicine, National Yang Ming University, Taiwan, R.O.C.
4 Institute of Clinical Medicine, National Yang Ming University, Taiwan, R.O.C.
5 Section of Pediatric Cardiology, Department of Pediatrics, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C.
6 Section of Cardiovascular Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C.

Received April 27, 2006; accepted after revision October 31, 2006.

 
I.-C. Tsai and T. Lee contributed equally to this study.

Address correspondence to T. Lee (sillyduck{at}vghtc.gov.tw).


Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
OBJECTIVE. Hemodynamic information observed on serial images obtained with bolus tracking might help in diagnosing septal defects on CT. Our purpose was to qualitatively and quantitatively examine a new sign called gradual pulmonary artery enhancement.

CONCLUSION. Gradual pulmonary artery enhancement is a newly recognized CT sign that may be helpful in evaluating septal defects.

Keywords: cardiac imaging • congenital • CT angiography • CT • pediatric radiology • septal defects


Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Given its improved spatial and temporal resolution, scanning times, dose modulation, and capacity for ECG gating, MDCT is now widely used in cardiac applications. An example is the evaluation of patients with congenital heart diseases [1–4], many of whom have atrial septal defects (ASDs) or ventricular septal defects (VSDs).

Reports of using CT to diagnose septal defects have been based on direct visualization of the defects [1–3] or shunts [4]. However, these approaches require two-phase scanning or high-resolution imaging during motionless breath-holding. The former exposes patients to a twofold radiation dose, which is particularly harmful in pediatric populations. The latter requires the patient's cooperation, which young children sometimes cannot provide. Therefore, a new CT sign that is independent of these methods would be beneficial.

Because of the synchronization methods, such as bolus tracking [5], available with modern CT scanners, we can precisely time the arterial phase by observing each patient's hemodynamics. In our experience, serial CT images obtained with bolus tracking show a specific pattern that might be useful in diagnosing septal defects. The enhancement pattern—or time–attenuation relationship if put quantitatively—of the pulmonary artery differs in patients with and those without septal defects. Our purpose was to qualitatively and quantitatively examine the CT phenomenon of gradual pulmonary artery enhancement.


Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
For the study group, we retrospectively identified patients with an ASD, VSD, or both proven on echocardiography who were examined between July 2005 and June 2006. To focus on the effect of an isolated septal defect on the enhancement pattern, we excluded patients with a common atrioventricular canal (i.e., atrioventricular septal defect) because of the complex mixing hemodynamics caused by the endocardial cushion defect and valvular insufficiency, patients with other cardiovascular anomalies that could change their hemodynamics (e.g., pulmonary stenosis, patent ductus arteriosus), and patients with sinus venosus–type ASD because of its usual association with partial anomalous pulmonary venous return.

For the control group, we randomly selected patients with negative cardiac CT findings between January and June 2006. CT images and echocardiograms were carefully reviewed to exclude those with septal defects, motion impairment, and other structural anomalies (e.g., chamber dilatation, hypertrophy, aneurysm formation).

Given its retrospective design, the study was performed with a waiver from our institutional review board. All patients or their parents gave signed informed consent before undergoing CT.

Cardiac CT Protocol
Oral propranolol (Cardilol, Veteran's Pharmaceutical Factory), 0.5 mg/kg of body weight, was given 1 hour before scanning to reduce the patient's heart rate. CT was performed by using a 40-MDCT unit (Brilliance 40, Philips Medical Systems) with a dual-syringe injector (Stellant, Medrad). Parameters were tube voltage, 120 kV; weight-based effective tube current, 150–700 mAs per section; collimation, 40 x 0.625 mm; rotation time, 0.42 second; and pitch, 0.2 with retrospective ECG gating.

Scanning proceeded craniocaudally from 0.5 cm below the carina through the heart. Bolus tracking was performed 5 seconds after the injection of contrast material, and serial images were obtained in the ascending aorta at the level of the carina. Parameters were 120 kV, 20 mAs per section, and cycle time of 1.26 seconds, which the scanner limited to multiples of the subsequent rotation time (0.42 second).


Figure 1
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  		Fig. 1 —7-year-old boy with Kawasaki disease and negative cardiac CT. Measurement of CT attenuation values on serial bolus-tracking images obtained at level of carina. A and B are 1-cm2 regions of interest in main pulmonary artery and ascending aorta. Software generated time–attenuation curve. We recorded CT numbers at every second for further analysis.

 
After the region of interest in the ascending aorta reached 150 H, scanning was started after a 5-second postthreshold delay. If patients could hold their breath as instructed, scanning was done with breath-holding; if not, scanning was done with the patient breathing freely. Doses of contrast medium were 100 mL for patients weighing more than 50 kg and 2 mL/kg for those weighing less than 50 kg. We administered a saline chaser bolus that was 30% of the volume of the contrast agent. The flow rate was determined as the volume of contrast agent divided by the scanning time in seconds plus 8.

The pediatric injection protocol was based on the contrast-covering time described elsewhere [6]. With bolus tracking, the contrast-covering time allowed us to adjust the duration of the injection of contrast material to cover the scanning area after the bolus arrived at the ascending aorta. The duration was designed to cover the postthreshold delay and scanning time with a 3-second margin of safety. Thus, scanning occurred in the middle of the injection and good enhancement was ensured.

Analysis of Time–Attenuation Parameters
Serial tracker images were loaded onto a dedicated CT workstation for time–attenuation analysis (Test Injection Bolus Timing, Extended Brilliance Workspace; Philips Medical Systems), and CT attenuation values were measured (Fig. 1). Data were recorded and quantitatively analyzed (Excel 2000, Microsoft).

To quantify enhancement patterns of the pulmonary artery, we calculated the maximal slope of pulmonary artery enhancement (MSPA), the time to MSPA (tMSPA), the area between the curves of the pulmonary artery and the aorta (ABC), and the mean ratio of pulmonary artery and aortic enhancement (PA/AO).

Study Group Versus Control Group
We compared demographic data and time–attenuation parameters of the study and control groups.

Subgroups of Septal Defects Versus Control Group
Septal defects were categorized according to the type of shunt diagnosed on echocardiography. Group 1 was ASD, group 2 was VSD, and group 3 was coexistent ASD and VSD. Time–attenuation parameters of these subgroups were compared with those of the control group to detect trends. Time–attenuation curves obtained in the study and control groups and in the three subgroups were subjectively and qualitatively analyzed. For this analysis, two cardiac radiologists, each of whom interpreted more than 400 cardiac CT studies per year, interpreted the findings in consensus.

Comparison of Small and Large Defects
We separated patients by the mean size of their ASDs. Groups 1a and 1b had defects smaller and larger, respectively, than the mean for the entire study group. We compared their demographic data, size of ASDs, and time–attenuation parameters to determine the effect of ASD size on the time–attenuation parameters. We repeated this analysis in patients with VSDs. Groups 2a and 2b consisted of patients with VSDs smaller or larger, respectively, than the mean.

Statistics
Statistical analysis was performed by using statistical (SPSS version 11.5 for Microsoft Windows) and spreadsheet (Excel 2000) software. Demographic data, injection parameters, MSPA values, tMSPA values, ABC values, and PA/AO values were compared among groups by using a two-tailed independent Student's t test. Sex distribution was compared by using a chi-square test. Differences with p ≤ 0.05 were statistically significant.


Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Patient Demographics
Twenty-two patients with septal defects formed the study group. According to their echocardiographic results, 12 patients had ASDs, six had VSDs, and four had both. All ASDs were the ostium secundum type, and all VSDs were the perimembranous type. Three patients with tetralogy of Fallot were excluded because of combined pulmonary stenosis. Two patients with common atrioventricular canal were excluded because they had endocardial cushion defects and valvular insufficiency. The control group contained 21 patients. Demographic data of the groups did not significantly differ (Table 1).


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  		TABLE 1: Results of Comparisons

 

Study Group Versus Control Group
Compared with the control group, study patients had smaller MSPAs, ABCs, and PA/AO values and longer tMSPA values (Table 1).

Subgroups of Septal Defects Versus Control Group
Figure 2A, 2B, 2C, 2D shows the results of our comparison of time–attenuation parameters. On subjective inspection of the curves in the control group, pulmonary artery enhancement showed a pattern of early rising with a subsequent plateau (Fig. 3A). The enhancement curves were increasingly smooth in patients with ASDs, VSDs, and coexistent ASDs and VSDs. With ASDs, the curve only slightly differed from the control curve, with a loss of early rising enhancement (Fig. 3B). With VSDs, the pulmonary artery and aortic enhancement curves were close (Fig. 3C); and with coexistent ASDs and VSDs, they almost overlapped (Fig. 3D). Because transit times differed among individuals, averaging the data within a group smoothed the pattern.


Figure 2
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  		Fig. 2A —Comparison of time–attenuation parameters among control group and subgroups. MSPA = maximal slope of pulmonary enhancement, ASD = atrial septal defect, VSD = ventricular septal defect, bar = mean ± 1 SD. Across groups, MSPA values are decreasing (A), time to MSPA (tMSPA) values are lengthening (B), area between curves of pulmonary artery and aorta values are decreasing (C), and mean ratio of pulmonary artery and aortic enhancement (PA/AO) values are decreasing (D).

 

Figure 3
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  		Fig. 2B —Comparison of time–attenuation parameters among control group and subgroups. MSPA = maximal slope of pulmonary enhancement, ASD = atrial septal defect, VSD = ventricular septal defect, bar = mean ± 1 SD. Across groups, MSPA values are decreasing (A), time to MSPA (tMSPA) values are lengthening (B), area between curves of pulmonary artery and aorta values are decreasing (C), and mean ratio of pulmonary artery and aortic enhancement (PA/AO) values are decreasing (D).

 

Figure 4
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  		Fig. 2C —Comparison of time–attenuation parameters among control group and subgroups. MSPA = maximal slope of pulmonary enhancement, ASD = atrial septal defect, VSD = ventricular septal defect, bar = mean ± 1 SD. Across groups, MSPA values are decreasing (A), time to MSPA (tMSPA) values are lengthening (B), area between curves of pulmonary artery and aorta values are decreasing (C), and mean ratio of pulmonary artery and aortic enhancement (PA/AO) values are decreasing (D).

 

Figure 5
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  		Fig. 2D —Comparison of time–attenuation parameters among control group and subgroups. MSPA = maximal slope of pulmonary enhancement, ASD = atrial septal defect, VSD = ventricular septal defect, bar = mean ± 1 SD. Across groups, MSPA values are decreasing (A), time to MSPA (tMSPA) values are lengthening (B), area between curves of pulmonary artery and aorta values are decreasing (C), and mean ratio of pulmonary artery and aortic enhancement (PA/AO) values are decreasing (D).

 

Figure 6
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  		Fig. 3A —Time–attenuation curves in control group and subgroups. Aorta = {diamondsuit}, pulmonary artery = {blacksquare}. Control curves show typical pulmonary artery enhancement pattern with early rising and subsequent plateau. Time–attenuation parameters, including maximal slope of pulmonary enhancement (MSPA), time to maximal slope of pulmonary enhancement (tMSPA), area between curves of pulmonary artery and aorta (ABC), and mean ratio of pulmonary artery and aortic enhancement (PA/AO), are illustrated.

 

Figure 7
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  		Fig. 3B —Time–attenuation curves in control group and subgroups. Aorta = {diamondsuit}, pulmonary artery = {blacksquare}. Curves for patient with atrial septal defect (ASD) show loss of early rising pattern.

 

Figure 8
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  		Fig. 3C —Time–attenuation curves in control group and subgroups. Aorta = {diamondsuit}, pulmonary artery = {blacksquare}. Curves for patient with ventricular septal defect (VSD) show loss of both early rising pattern and subsequent plateau. Enhancement curves for pulmonary artery and aorta are closer than in B.

 

Figure 9
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  		Fig. 3D —Time–attenuation curves in control group and subgroups. Aorta = {diamondsuit}, pulmonary artery = {blacksquare}. Curves for patient with ASD and VSD show nearly overlapping enhancement curves for pulmonary artery and aorta. This finding indicates large shunt volume between left and right sides of heart.

 
Comparison of Small and Large Defects
ASDs had a mean size of 10.9 mm. Therefore, eight patients were in group 1a and four in group 1b (Table 1). Demographic data did not differ between the groups. However, tMSPA values were longer and MSPA, ABC, and PA/AO values were smaller in group 1b than in group 1a.

VSDs had a mean size of 10.0 mm. Therefore, three patients were in group 2a and three in group 2b (Table 1). Their demographic data were not significantly different. ABC and PA/AO values were smaller in group 2b than in group 2a. MSPA and tMSPA values were similar.


Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
We describe a new CT sign of septal defects called gradual pulmonary artery enhancement. In qualitative terms, imaging in patients with septal defects showed gradual pulmonary artery enhancement during bolus tracking, which differed from the fast enhancement and plateau observed in control subjects. In quantitative terms, patients with septal defects had significantly decreased MSPA, ABC, and PA/AO values and increased tMSPA values.

Gradual pulmonary artery enhancement is related to left–right cardiac shunting. During the injection of contrast material, nonopacified blood from the left side of the heart enters the right side and dilutes enhancement of the pulmonary artery, smoothing the enhancement curve. With different types or sizes of shunts, the curve shows different extents of flattening. With this new sign, we can diagnose septal defects by assessing hemodynamic information obtained during bolus tracking even when the defect is not directly visualized on subsequent CT arteriography. Most important, this sign is derived from information already embedded in the routine CT arteriogram, and the patient is not exposed to the high radiation dose of two-phase scanning [4].

When CT arteriography is performed with bolus tracking at the level of the ascending aorta and pulmonary artery, gradual pulmonary artery enhancement can aid image interpretation. For example, it can help in differentiating causes of pulmonary artery dilatation during CT pulmonary angiography even if the protocol is not designed for visualizing septal defects. We have encountered several young women patients with dilated pulmonary arteries and no pulmonary embolism but a positive gradual pulmonary artery enhancement sign. Given this sign and their ages and presentations, ASD was suspected and confirmed on echocardiography. The validity of this sign in protocols other than electrocardiographically gated cardiac CT with ß-blockade needs confirmation because differences in cardiac output might also alter the pulmonary artery enhancement pattern.

In the comparison of small and large VSDs, MSPA and tMSPA values overlapped and did not significantly differ. Because of the large pressure gradient in VSDs (even small ones), shunt flow is assumed to be so large that the MSPA and tMSPA are pushed to the edge, and they no longer reflect changes in shunt size. However, ABC and PA/AO values can still reflect differences in shunt sizes. All four parameters may be useful for detecting septal defects, but ABC and PA/AO values might be best because they help in differentiating small and large VSDs.

Our study had limitations. First, because of the small sample size, we included only patients with ostium secundum–type ASD or perimembranous VSD. We could not analyze relationships among locations and time–attenuation parameters of the septal defects. Because secundum-type ASDs and perimembranous VSD are the defects most often encountered in practice, our study reflected real clinical situations. Second, we did not statistically compare subgroups with the control group. In the ideal situation, a least-significant-differences test is used to compare multiple groups. However, because CT is currently not the primary technique used to evaluate isolated septal defects (partly because of its radiation), our cases were limited. Because of the small sample size, significant differences would not have been detected in all comparisons if the least-significant-differences test had been applied, although the mean time–attenuation parameters did show a typical trend.

In conclusion, gradual pulmonary artery enhancement is a newly recognized CT sign that may be helpful in evaluating septal defects. Large prospective studies are needed to quantify shunt flow and to explore the accuracy of this sign.


References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Mochizuki T, Ohtani T, Higashino H, et al. Tricuspid atresia with atrial septal defect, ventricular septal defect, and right ventricular hypoplasia demonstrated by multidetector computed tomography. Circulation 2000;102 :E164 –E165[Medline]
  2. Goo HW, Park IS, Ko JK, Kim YH, Seo DM, Park JJ. Computed tomography for the diagnosis of congenital heart disease in pediatric and adult patients. Int J Cardiovasc Imaging2005; 21:347 –365[CrossRef][Medline]
  3. Goo HW, Park IS, Ko JK, et al. CT of congenital heart disease: normal anatomy and typical pathologic conditions. RadioGraphics 2003;23 [spec no]:S147 –S165[Abstract/Free Full Text]
  4. Funabashi N, Asano M, Sekine T, Nakayama T, Komuro I. Direction, location, and size of shunt flow in congenital heart disease evaluated by ECG-gated multislice computed tomography. Int J Cardiol 2006; 112:399 –404[CrossRef][Medline]
  5. Cademartiri F, Nieman K, van der Lugt A, et al. Intravenous contrast material administration at 16-detector row helical CT coronary angiography: test bolus versus bolus-tracking technique. Radiology 2004;233 : 817–823[Abstract/Free Full Text]
  6. Tsai I-C, Lee T, Chen M-C, Tsai W-L, Lin P-C, Liao W-C. Homogeneous enhancement in pediatric thoracic CT aortography using a novel and reproducible method: contrast-covering time. AJR2007; 188:1131 –1137[Abstract/Free Full Text]

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