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Thoracic Imaging |
1 From the Department of Radiology, Hospital Calmette, University Center of Lille, Boulevard Jules Leclerc, 59037 Lille Cedex, France (M.R.J., N.B., P.D., J.R.); and Department of Medical Statistics, University of Lille, France (A.D., V.D.). Received February 20, 2004; revision requested April 30; revision received June 11; accepted July 21. Address correspondence to M.R.J. (e-mail: mremy-jardin@chru-lille.fr).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: For this review, neither institutional board approval nor informed consent was required. Thirty-six consecutive patients, including 22 patients (four men, 18 women; mean age, 46.0 years) with chronic thromboembolic pulmonary hypertension (group 1) and 14 patients (five men, nine women; mean age, 63.0 years) with primary pulmonary hypertension (group 2), underwent multisection spiral CT angiography of the pulmonary and systemic circulations with a four– (n = 17) or 16– (n = 19) detector row scanner. CT angiograms were assessed for the presence of abnormal bronchial and/or nonbronchial systemic arteries, CT features of pulmonary hypertension, and right ventricular dysfunction. Vascular and parenchymal signs of chronic pulmonary embolism were specifically analyzed on CT angiograms of group 1 patients. Comparative analyses were performed by using the 
2 or the Fisher exact test for categoric data. An unpaired bilateral Wilcoxon rank sum test was used for continuous data. A 2 goodness-of-fit test was used to compare observed proportions with equal proportions.
RESULTS: The degree of pulmonary hypertension was comparable in groups 1 and 2. Abnormally enlarged systemic arteries were identified in 16 (73%) of 22 patients from group 1 and in two (14%) of 14 patients from group 2 (P = .002). The systemic collateral supply in group 1 comprised enlargement of both bronchial and nonbronchial systemic arteries in nine (56%) of the 16 patients; the remaining seven patients had an exclusive enlargement of bronchial systemic arteries (n = 6, 38%) or nonbronchial (n = 1, 6%) systemic arteries. A total of 31 enlarged nonbronchial systemic arteries were depicted, including 13 inferior phrenic arteries, 10 intercostal arteries, seven internal mammary arteries, and one lateral thoracic artery. The mean ± standard deviation of abnormal nonbronchial systemic arteries per patient was 1.4 ± 1.9. No relationship was found between the mean number of abnormally enlarged nonbronchial systemic arteries and the CT angiographic features of chronic pulmonary embolism.
CONCLUSION: These results demonstrate the higher frequency of abnormally enlarged bronchial and nonbronchial systemic arteries in patients who have chronic thromboembolic pulmonary hypertension compared with patients who have primary pulmonary hypertension; this finding could help distinguish these two entities on CT angiograms.
© RSNA, 2005
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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According to the diagnostic approach to pulmonary hypertension that was proposed in 1997 by Reaside and Peacock (5), the ability to differentiate between chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension relies mainly on ventilation-perfusion scanning and pulmonary angiography. Computed tomography (CT), which enables recognition of chronically obstructed vessels, has been introduced into the diagnostic workup of patients with chronic thromboembolism; CT can also be used to exclude competing diagnoses and to confirm surgical accessibility of obstructed vessels (6–12). Although the diagnosis of chronic thromboembolic disease at CT relies on precise vascular features, sometimes the distinction between thromboembolic pulmonary hypertension and primary pulmonary hypertension may be difficult to make because in situ pulmonary artery thrombosis in patients with primary pulmonary hypertension may mimic pulmonary artery occlusions caused by thrombotic material of embolic origin (13–16). In chronic thromboembolic disease, the bronchial circulation is markedly increased as a result of the development of systemic-to-pulmonary anastomoses, which help to maintain pulmonary blood flow (17–19). Thus, the purpose of this study was to compare retrospectively the frequency of systemic collateral supply in patients who have chronic thromboembolic pulmonary hypertension with the frequency of systemic collateral supply in patients who have primary pulmonary hypertension by using multi–detector row helical CT angiography.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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For this retrospective study, we searched the computer database of the Department of Thoracic Imaging to identify patients who had chronic thromboembolic (group 1, n = 22) or primary (group 2, n = 14) pulmonary hypertension without associated chronic or acute lung diseases and who had undergone multi–detector row helical CT angiography of the thoracic vessels between December 2000 and March 2003. For all patients included in this study, the diagnostic tests that were used to assess primary pulmonary hypertension included a detailed history and physical examination, pulmonary function testing, perfusion scanning, helical CT, and, in patients with abnormal findings at lung scanning, pulmonary angiography. Serologic tests were performed to exclude collagen vascular diseases and human immunodeficiency virus infection. In this subset of patients, the diagnosis of primary pulmonary hypertension was made when other causes of pulmonary hypertension were ruled out, including cardiac, hepatic, and chronic lung diseases. The diagnosis of chronic thromboembolic pulmonary hypertension was made on the basis of at least one segmental perfusion defect at perfusion lung scanning; findings were confirmed in all patients by identifying the major CT criterion for chronic thromboembolic disease, namely, the presence of retracted embolic material (9–12).
For each patient, the mean pulmonary artery pressure was obtained at hemodynamic examination performed with a Swan-Ganz catheter (Edwards Lifesciences, Irvine, Calif). Because bronchial arterial circulation may develop as the consequence of a tobacco-related bronchial disease, care was taken to record the patients’ smoking habits. For every smoker, cigarette consumption was estimated in pack-years. Table 1 summarizes baseline clinical and hemodynamic data from the 36 patients included in the present study. The mean age of patients with primary pulmonary hypertension was 17 years older than that of patients with chronic thromboembolic pulmonary hypertension. No statistically significant difference was found in the mean pulmonary artery pressure between the two groups of patients (P = .58). The frequency of clinical signs of right ventricular dysfunction was significantly higher in patients with primary pulmonary hypertension than in patients with chronic thromboembolic pulmonary hypertension (P = .03).
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Patients received 80–100 mL of contrast material (iohexol, Omnipaque 300; Amersham Health, Carrigtohill, Ireland) with 300 mg of iodine per milliliter and an injection rate of 4 mL/sec. For the four–detector row scanner, the start delay was empirically chosen and varied between 18 and 22 seconds. For the 16–detector row scanner, the automatic bolus-triggering software program was systematically applied, with a circular region of interest positioned at the level of the ascending aorta and a threshold for triggering data acquisition preset at 100 HU.
From each data set, three series of images were systematically reconstructed as follows: contiguous 1-mm-thick transverse CT scans viewed at mediastinal and lung window settings, oblique coronal and sagittal maximum intensity projections, and volume-rendered images of the thoracic vascular structures. Transverse CT images were photographed at lung and mediastinal window settings; owing to the number of images generated from each data set, only one image every 2 mm was photographed with a photographic format of 20 images per film.
CT Image Interpretation
Image interpretation.—CT angiograms were analyzed retrospectively in consensus by two faculty radiologists (M.R.J. and J.R., with 15 and 20 years of experience, respectively) who were blinded to the severity of pulmonary hypertension. The CT images were reviewed as hard-copy images with the option of using a cine-mode display on the computer workstation, if needed.
Evaluation of bronchial and nonbronchial systemic arteries.—For each patient, the angiograms were assessed for enlarged (diameter larger than 1.5 mm) right and/or left bronchial arteries by identifying contrast material–enhanced small, round, or curvilinear structures in the mediastinum and by tracing these structures along the bilateral main bronchi (20–23). Enlargement of bronchial arteries was graded as moderate when the bronchial artery diameter was 2.0–4.0 mm. Enlargement of bronchial arteries was graded as marked when the bronchial artery diameter was larger than 4.0 mm. Diameter size was estimated by comparing CT angiograms with reference images of normal-sized, moderately enlarged, and markedly enlarged bronchial arteries on cross sections. The number of abnormally enlarged right and/or left bronchial arteries was systematically recorded.
Nonbronchial systemic arteries were defined as arteries that enter the parenchyma through the pulmonary ligament or through the adherent pleura; the course of these arteries is not parallel to that of the bronchi (24). Abnormal enlargement of one or several of the following arteries—namely, the branches of the subclavian and axillary arteries, particularly the internal thoracic artery and its branches, the intercostal arteries, and the inferior phrenic arteries—was considered to be suggestive of a nonbronchial systemic arterial supply. Abnormal enlargement of nonbronchial systemic arteries was defined as a nonbronchial systemic artery with a diameter larger than 4.0 mm on CT angiograms. Diameter size was estimated by comparing CT angiograms with reference images of normal-sized and enlarged nonbronchial systemic arteries on cross sections. In the absence of reference data, no attempt was made to grade the severity of nonbronchial systemic artery enlargement. The presence of CT features suggestive of a nonbronchial systemic arterial supply was recorded for each hemithorax in each patient.
CT signs of pulmonary hypertension and right ventricular dysfunction.—The presence of pulmonary hypertension was suspected at CT angiography when the diameter of the pulmonary artery was larger than that of the aorta, with the concurrent presence of enlarged central and peripheral pulmonary arteries (8,25–29). Increased diameter of the right and left central pulmonary arteries—that is, a diameter larger than 1.6 cm measured in the scanning plane of the bifurcation of the main pulmonary artery—indicated enlarged central pulmonary arteries. Enlargement of peripheral pulmonary arteries was visually assessed by comparing the arterial diameter with the bronchial diameter at the level of segmental and subsegmental divisions; a pulmonary artery–to–accompanying bronchus ratio greater than 1.0 was indicative of enlarged peripheral pulmonary arteries.
The following CT signs of right ventricular dysfunction were systematically analyzed on non–electrocardiographically gated transverse sections (30–34): (a) dilatation of the right ventricle; (b) deviation of the interventricular septum toward the left ventricle; (c) abnormal thickening of the right ventricular wall (ie, a right ventricular wall thickness larger than 0.4 cm); (d) dilatation of the right atrium, inferior vena cava, and coronary sinus; and (e) reflux of contrast material into the inferior vena cava and hepatic veins. Dilatation of the right ventricle was noted when the right ventricle was wider than the left ventricle. In addition, the maximum (diastolic) transverse diameters in the short axis of the right and left ventricular cavities were measured on a single transverse image that was obtained at the plane of maximal visualization for each of the ventricular cavities; these measurements are further referred to as the right and left ventricular widths. Abnormal thickening of the right ventricular wall was measured on the transverse diastolic image of the right ventricle.
CT signs of chronic pulmonary embolism.—Two categories of CT features of chronic pulmonary embolism were analyzed, namely, the vascular and parenchymal signs of chronic pulmonary embolism (9–12,35). The vascular signs of chronic pulmonary embolism recorded in the present study include (a) organized embolic material, namely, partial or complete endoluminal filling defects; (b) retracted embolic material, namely, complete filling defects at the level of pulmonary artery stenosis, abrupt cut-offs, and narrowing; (c) recanalized embolic material, namely, webs, bands, or stenoses with poststenotic dilatation; and (d) calcified embolic material, namely, calcifications within filling defects. Each patient in group 1 had a variable combination of vascular features of chronic pulmonary artery; these vascular features were recorded as unilateral or bilateral findings involving the central (ie, mediastinal and/or lobar) pulmonary arteries, peripheral (ie, segmental and/or subsegmental) pulmonary artery branches, or both. The parenchymal signs of chronic pulmonary embolism that were evaluated include features of mosaic perfusion and sequelae of lung infarction. Mosaic perfusion was recognized on CT angiograms as sharply demarcated regions of decreased and increased attenuation and vascularity that often conformed to the boundaries of secondary pulmonary lobules without evidence of destruction or displacement of pulmonary vessels (36). Sequelae of lung infarction included pleural thickening, which is often seen with the concurrent presence of parenchymal scarring. Parenchymal scarring was recognized by the presence of wedge-shaped, pleural-based parenchymal areas of high attenuation.
Statistical Analysis
Statistical analysis was performed with commercially available software (SAS, version 8; SAS Institute, Cary, NC). Results are expressed as frequencies and percentages for categoric variables and as means ± standard deviations for numeric variables. Comparative analyses were performed by using the 2 or the Fisher exact test for categoric data. An unpaired bilateral Wilcoxon rank sum test was used for continuous data. A 2 goodness-of-fit test was used to compare observed proportions with equal proportions. A P value of less than .05 indicated a statistically significant difference.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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In the clinical context of chronic thromboembolic pulmonary hypertension, systemic artery dilatation was a frequent finding. Abnormal enlargement of bronchial arteries was identified in 15 (68%) of the 22 investigated patients. This frequency is comparable with frequencies observed at CT angiography in previous studies of patients with chronic thromboembolic pulmonary hypertension; in these studies, frequencies of abnormal enlargement of bronchial arteries varied between 50% and 61% (8,10,20,38). In our study, enlargement of bronchial arteries was observed with the concurrent presence of nonbronchial systemic arteries in nine of 15 patients, whereas enlargement of bronchial arteries was an isolated CT finding in the remaining six of 15 patients. In group 1, CT angiography enabled the identification of abnormally enlarged nonbronchial systemic arteries in 10 (45%) of 22 patients, a finding not previously reported in cases of chronic thromboembolic pulmonary hypertension. The most frequently depicted abnormal nonbronchial systemic arteries were the inferior phrenic, intercostal, and internal mammary arteries, with a mean of 1.4 abnormal nonbronchial systemic arteries per patient. Despite the lack of CT angiographic demonstration of systemic nonbronchial-to-pulmonary artery shunts, one can hypothesize that the nonbronchial systemic collateral supply participate in the shunt between the systemic and pulmonary circulations known to develop in chronic thromboembolic disease. After direct catheterization of the right and left ventricles of the heart and by using a contrast medium dilution method, Endrys et al (37) found a mean shunt volume of 29.8% ± 18.6 for systemic blood flow. By examining 17 patients with magnetic resonance imaging, Ley et al (39) found a mean shunt volume of 36.2%; both investigators refer to this shunt volume as the "bronchopulmonary" collateral shunt.
Bilateral enlargement of bronchial and/or nonbronchial systemic arteries was found in 60% and 70% of patients, respectively, a finding that is concordant with the notion that thromboembolic pulmonary hypertension is a bilateral disease (40). Because the role of the bronchial collateral supply in chronic thromboembolic disease is well established, we searched for potential relationships between the enlargement of bronchial and nonbronchial systemic arteries and the anatomic characteristics of chronic pulmonary embolism. By using the mean number of abnormally enlarged bronchial and/or nonbronchial systemic arteries as the main criterion, we failed to demonstrate any relationship with CT angiographic characteristics of chronic thromboembolic disease; in particular, we were unable to demonstrate any relationship between the presence of areas of mosaic perfusion and abnormally enlarged bronchial and/or nonbronchial systemic arteries. These regional attenuation differences, including regional hypoattenuating and hyperattenuating areas that are often sharply demarcated, have been described as characteristic findings in chronic pulmonary embolism (9,36). Whereras hypoattenuation is related to either distal vasculopathy in nonobstructed areas or hypoperfusion distal to occluded vessels, the increase in lung attenuation of adjacent areas has been related to the redistribution of blood flow through open vessels and to the development of collateral blood flow (41). The lack of statistically significant relationships must be interpreted while acknowledging the technical limitations of CT in demonstrating subtle morphologic changes in peripheral pulmonary arteries.
Several other limitations of this study deserve mention. First, none of our patients underwent conventional angiography of systemic arteries, so we could not confirm the accuracy of the CT angiographic depiction of abnormal systemic collateral supply with a standard of reference. Second, our analysis was based on small groups of patients, a limitation that is directly linked to the fact that chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension are rare entities. Third, we did not include an evaluation of interobserver agreement in the detection of systemic arteries. The consensus reading of CT angiograms, however, was based on well-validated criteria for the depiction of dilated bronchial arteries (20,21), and we based our description of abnormally enlarged nonbronchial systemic arteries on CT features of obvious arterial enlargement. The latter criterion may have added another potential bias in our results, namely, the risk of underestimating nonbronchial systemic artery involvement in chronic thromboembolic pulmonary hypertension.
In conclusion, our findings demonstrate a higher frequency of abnormally enlarged bronchial and nonbronchial systemic arteries in patients who had chronic thromboembolic pulmonary hypertension compared with patients who had primary pulmonary hypertension; these findings could help distinguish between these two entities on CT angiograms.
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FOOTNOTES |
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Author contributions: Guarantors of integrity of entire study, M.R.J., J.R.; study concepts, J.R.; study design, M.R.J., J.R.; literature research, M.R.J., J.R.; clinical studies, N.B., P.D.; data acquisition, N.B., P.D.; data analysis/interpretation, M.R.J.; statistical analysis, V.D., A.D.; manuscript preparation, definition of intellectual content, and editing, M.R.J.; manuscript revision/review, M.R.J., J.R.; manuscript final version approval, M.R.J.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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) lateral to the main pulmonary artery is related to the patient’s history of coronary artery bypass surgery.
