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1 Department of Radiology, Beth Israel Deaconess Medical Center and Harvard
Medical School, Boston, MA 02215.
2 Present address: Department of Diagnostic Radiology, School of Medicine, Keio
University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Received May 30, 2003;
accepted after revision July 24, 2003.
Supported by General Electric Yokagawa Medical Systems Educational
Fund.
Abstract
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MATERIALS AND METHODS. Twenty-seven patients with acute pulmonary embolism and 14 patients with chronic or recurrent pulmonary embolism were retrospectively identified from 700 consecutive patients with suspected pulmonary embolism. The case data for the patients were assessed by two thoracic radiologists whose final judgments were reached by consensus. On the MDCT pulmonary angiograms obtained in these patients, the bronchial arteries were assessed by finding enhancing, small, round or curvilinear structures within the mediastinum and tracing their paths along the bilateral main bronchi. Bronchial arteries with a diameter greater than 1.5 mm were considered to be dilated.
RESULTS. The diameters of the bronchial arteries in the group with chronic or recurrent pulmonary embolism were significantly larger than diameters of the bronchial arteries in the group with acute pulmonary embolism (p = 0.0002). Dilatation of bronchial arteries was observed in two of the 27 patients with acute pulmonary embolism and in seven of 14 patients with chronic or recurrent pulmonary embolism. This difference was statistically significant (p = 0.004). No dilated bronchial arteries were seen in patients who had acute pulmonary embolism but had no a history of deep venous thrombosis.
CONCLUSION. Acute pulmonary embolism did not appear to cause dilatation of bronchial arteries, whereas chronic or recurrent pulmonary embolism was frequently associated with dilated bronchial arteries. In patients in whom the distinction between acute and chronic or recurrent pulmonary embolism on MDCT pulmonary angiography is clinically unclear and in whom the bronchial arteries are dilated, a diagnosis of chronic or recurrent pulmonary embolism should be favored.
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The bronchial arteries usually arise from the aorta and intercostal arteries and drain into the left atrium via pulmonary veins and partly into the right atrium via the azygos vein [1]. These arteries have a maximum diameter of 1.5 mm and are rarely seen on helical CT [24]. Previous studies reported that dilated bronchial arteries become visible on helical CT angiography in patients with chronic pulmonary thromboembolism [2, 3]. Of particular interest is the finding that the response of the bronchial circulation to acute pulmonary embolism appears to be a decrease in flow rather than the expected increase in flow [5]. To date, however, CT findings of the bronchial arteries have not been reported in the setting of acute pulmonary embolism. Matsuda [6] reported the findings of bronchial arteriography in patients with pulmonary embolism at various stages although no bronchial-to-pulmonary arterial collaterals were detected at the acute stage.
Recent advances in CT technology have allowed the use of narrower collimation than that previously used; thus, the chest can be scanned in 12 sec with a 1.25-mm collimation using an eight-row MDCT scanner. MDCT increases image resolution and improves evaluation of tiny bronchial vessels. We hypothesized that with this technology, bronchial arteries would more frequently be visualized in greater detail than was possible on conventional CT, thereby allowing MDCT evaluation of patients with suspected pulmonary embolism. The purpose of our study was to identify the bronchial arteries on MDCT pulmonary angiography in patients with pulmonary embolism and to compare the bronchial arteries of patients with acute pulmonary embolism with those of patients with chronic or recurrent pulmonary embolism.
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Patients with MDCT pulmonary angiographic evidence of pulmonary embolism were categorized into two groups on the basis of a combination of MDCT pulmonary angiographic findings and the onset and duration of clinical symptoms. MDCT pulmonary angiographic findings considered characteristic of acute pulmonary embolism included partial or complete filling defects and railroad track signs [7]. MDCT pulmonary angiographic findings of chronic pulmonary embolism included the presence of complete filling defects at the level of stenosed pulmonary arteries, eccentric thrombi, evidence of recanalization, and arterial stenosis or web [7]. With regard to the onset and duration of symptoms, patients with an abrupt onset of symptoms that lasted 10 or fewer days were classified as having acute pulmonary embolism. Patients with a history of acute pulmonary embolism or symptoms that continued for longer than 1 month after the last embolic episode were categorized as having recurrent or chronic pulmonary embolism. Patients whose symptoms lasted 11 or more days were categorized as having subacute pulmonary embolism and were included in the chronic or recurrent pulmonary embolism group.
We retrospectively reviewed clinical histories to determine the principal reason that the patient underwent MDCT pulmonary angiography, history of present illness, medical history, and hospital course. Our institutional review board approved our retrospective review study of medical records and images without requiring informed consent from the patients.
MDCT Technique
All patients were imaged on an eight-row MDCT scanner (LightSpeed; General
Electric Medical Systems, Milwaukee, WI). Gantry rotation time was 0.5 sec.
The imaging parameters were 1.25-mm collimation. with a pitch of 13.5 used in
fast mode. With these protocols, the chest can be scanned in 12 sec. The
direction of scanning used in all patients was from the lung base to the lung
apex. During the examination, 75100 mL of 68% ioversol solution
(Optiray 320 [320 mg I/mL], Mallinckrodt Medical, St. Louis, MO) was injected
IV with an automated injector (EnVision, Medrad, Pittsburgh, PA) at a rate of
3.5 mL/sec. Scanning delay was 2025 sec. Axial images were
reconstructed with intervals of 0.6 mm.
Image Analysis
Images were interpreted on a PACS (picture archiving and communication
system) (PathSpeed, General Electric Medical Systems). All cases were reviewed
by two thoracic radiologists who each had more than 5 years' clinical
experience and who reached conclusions by consensus. Images were reviewed
using a combined cine stack with static one-on-one viewing. All MDCT pulmonary
angiograms were displayed on mediastinal window settings (window level
setting, 40 H; window width setting, 350 H). The location of a clot was
recorded as being in the main, lobar, or segmental pulmonary arteries of the
right or left lung on the angiograms. For each patient, the angiograms were
assessed for visible bronchial arteries by finding enhancing, small, round or
curvilinear structures in the mediastinum and tracing them along the bilateral
main bronchi [3,
4,
12]. Other high-density
structures, such as calcified lymph nodes or calcified bronchial wall
cartilage, were distinguished from bronchial arteries by changing the window
level or width setting or tracing the continuity. Because we reviewed MDCT
pulmonary angiograms in patients with suspected pulmonary embolism, the
scanned area covered the aortic arch through the descending aorta at the level
of diaphragm.
In terms of the total number of bronchial arteries, we determined the four branches according to the classification of Kasai and Chiba [13]right superior, right inferior, left superior, and left inferior that passed on the superior or inferior wall of the corresponding bronchusand recorded the number of bronchial arteries. The most proximal site from the origin of bronchial arteries was measured. We did not count the common trunk (i.e., the single bronchial artery that supplies lungs bilaterally) as one bronchial artery, and both bronchial arteries were measured at the site after branching because we could not always find the common trunk itself. The intercostobronchial artery, which is often identified as the right bronchial artery, was measured at the proximal site where the bronchial artery branches away from the intercostal artery. Bronchial arteries with a diameter greater than 1.5 mm were considered to be dilated [3, 14, 15].
Statistical Analysis
A two-tailed Fisher's exact test was used to assess the difference between
the dilated bronchial arteries in the acute pulmonary embolism group and those
in the chronic or recurrent pulmonary embolism group. Student's t
test was used to assess the differences between the two groups in the diameter
and numbers of bronchial arteries observed on MDCT scans. A p value
of less than 0.05 was considered statistically significant.
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We identified 91 bronchial arteries in 27 patients with acute pulmonary embolism. We identified 41 right and 50 left bronchial arteries. In the chronic or recurrent pulmonary embolism group, 50 bronchial arteries were identified in 14 patients26 right and 24 left bronchial arteries. The mean number of bronchial arteries revealed on MDCT was 3.4 in patients with acute pulmonary embolism and 3.6 in patients with chronic or recurrent pulmonary embolism. The number of bronchial arteries observed on MDCT scans in the two groups was not significantly different (p = 0.4).
The diameter of bronchial arteries varied from 0.7 to 1.9 mm (mean ± SD, 1.1 ± 0.3 mm) in the acute pulmonary embolism group, whereas the diameter of bronchial arteries varied from 0.6 to 2.8 mm (mean, 1.4 ± 0.5 mm) in the chronic or recurrent pulmonary embolism group. The diameter of the bronchial arteries in the chronic or recurrent pulmonary embolism group was significantly larger than the diameter in the acute pulmonary embolism group (p = 0.0002).
Dilatation of bronchial arteries was observed in two (7%) of the 27 patients with acute pulmonary embolism and seven (50%) of the 14 patients with chronic or recurrent pulmonary embolism (Figs. 1A, 1B, 1C, 2A, 2B, 2C, 3A, 3B, 3C). This difference was statistically significant (p = 0.004). In the acute pulmonary embolism group, a clot was observed in the main pulmonary artery in both patients with dilated bronchial arteries. Moreover, both of these patients showed evidence of deep venous thrombosis. Among patients with chronic or recurrent pulmonary embolism who had dilated bronchial arteries, one had a clot in the main pulmonary artery, three had a clot in the lobar artery, and two had a clot in the segmental artery. In one patient with suspected recurrent pulmonary embolism, dilated bronchial arteries were seen but showed no evidence of pulmonary embolism.
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To our knowledge, no data are available on the measurements of bronchial arterial blood flow in humans, but several animal studies on the effects of acute pulmonary artery obstruction have been reported. Williams and Towbin [17] studied a dog model and found that bronchial arterial flow decreased during the 24 hr after pulmonary artery snaring. Also using a dog model, Jindal et al. [18] reported that bronchial flow decreased after acute pulmonary artery occlusion.
From the findings reported by these researchers, acute pulmonary embolism does not appear to cause bronchial dilatation, and our data support their results. We found dilatation of bronchial arteries in 50% of the group of patients with chronic or recurrent pulmonary embolism, a finding that also supports the results of previous reports [3]. Distinguishing acute from chronic pulmonary embolism on MDCT pulmonary angiography is not always possible [19]. It is vital to differentiate patients with chronic or recurrent pulmonary embolism from those with acute pulmonary embolism because patients with chronic pulmonary embolism might benefit from pulmonary thromboendarterectomy and patients with recurrent pulmonary embolism might be candidates for the insertion of an inferior vena caval filter [20]. Signs such as a crescent-shaped thrombus adhering to the arterial wall, a thrombus containing calcifications, and recanalization are useful in diagnosing chronic pulmonary embolism [7]. In some patients, dilated bronchial arteries that supply the lungs can be observed on CT scans [3].
Our study showed that dilatation of bronchial arteries was seen only in two patients (7%) with acute pulmonary embolism who also had a history of deep venous thrombosis. On the other hand, only one of 25 patients with acute pulmonary embolism without dilated bronchial arteries had a history of deep venous thrombosis. Pulmonary embolism and deep venous thrombosis should be considered part of the same pathologic process because more than 90% of pulmonary emboli arise from deep venous thrombosis of the lower extremities [20]. In a study by Moser et al. [21], nearly 40% of patients with deep venous thrombosis who had no symptoms of pulmonary embolism exhibited evidence of pulmonary embolism on ventilationperfusion scans and chest radiographs. In light of these facts, our two patients with dilated bronchial arteries who were placed in the acute pulmonary embolism group possibly had chronic or recurrent cases of pulmonary embolism. The significant incidence of dilated bronchial arteries among patients in the chronic or recurrent pulmonary embolism group suggests the possibility that dilated bronchial arteries may be useful for determining whether a patient is presenting with acute or chronic pulmonary embolism. However, the retrospective nature of our study limited our ability to determine the clinical impact of this finding. Future prospective studies are necessary to investigate this possibility.
There are additional limitations to our study. Because we did not have any patients who underwent conventional angiography, we could not confirm the accuracy of our findings with a "gold standard." However, because we identified the bronchial arteries on the basis of data presented in previous reports [24, 15], we believe that our observations of bronchial arteries (using the combined cine stack with static one-on-one viewing on a PACS) were still reasonably accurate. Our study included few cases of chronic or recurrent pulmonary embolism, but both chronic cases and recurrent cases of this disease are relatively rare [22].
Although the MDCT angiograms were obtained on state-of-the-art equipment, we were limited to 1.25-mm collimation by the design of our scanner. Using MDCT with a collimation of less than 1 mm may enhance the characterization of the bronchial arterial system and may be helpful in future studies. The dilatation of bronchial arteries may be an indication of increased pulmonary artery pressures in the patients with chronic pulmonary embolism. Because of the retrospective design of our study, we did not have the pulmonary arterial pressures for these patients and did not study the findings related to elevated pressures on the MDCT scans. Prospective studies correlating bronchial arterial findings with pulmonary arterial pressures could prove useful.
In conclusion, acute pulmonary embolism did not appear to cause dilatation of bronchial arteries, whereas chronic or recurrent pulmonary embolism was frequently associated with dilated bronchial arteries. If the distinction between acute and chronic or recurrent pulmonary embolism on MDCT pulmonary angiograms is clinically unclear in a patient with dilated bronchial arteries, the diagnosis of chronic or recurrent pulmonary embolism should be favored. The performance of prospective studies could help to determine the predictive value and clinical significance of dilated bronchial arteries in patients with pulmonary embolism.
Acknowledgments
We thank Donna Wolfe for editorial assistance.
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