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Attenuation of Acute and Chronic Pulmonary Emboli¹

¹ From the Departments of Thoracic Radiology and Statistics, Massachusetts General Hospital and Harvard Medical School, Founders 202, 55 Fruit St, Boston, MA 02115. From the 2003 RSNA Annual Meeting. Received February 27, 2004; revision requested May 5; final revision received July 7; accepted August 26. Address correspondence to C.W. (e-mail: cwittram@partners.org).

	ABSTRACT

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PURPOSE: To compare retrospectively the attenuation coefficients of acute and chronic pulmonary embolism (PE).

MATERIALS AND METHODS: Institutional review board approval was obtained, and informed consent was waived. The study was compliant with requirements of the Health Insurance Portability and Accountability Act. All patients with chronic PE, from July 2001 to January 2004, were identified via a radiology report search system; of the 39 identified, 25 were excluded because the thrombi were too small to measure or were obscured by streak artifacts or because there was no corroborative evidence of chronic PE. Of 27 consecutive patients with acute PE who were also identified, two were excluded because of streak artifacts. The final study group included six women and eight men with chronic PE (mean age, 50 years; range, 26–76 years) and 11 women and 14 men with acute PE (mean age, 61 years; range, 33–83 years) (P = .01 for age). Images were acquired with a four–detector row computed tomographic scanner and 1.25-mm collimation. Two readers made independent attenuation measurements of the largest thrombus in each patient at a workstation. Statistical analysis included calculation of means and standard deviations, the t test, and the Bland-Altman test.

RESULTS: Reader 1 found mean attenuation of 90 HU ± 30 (range, 54–155 HU) for chronic PE and 33 HU ± 15 (range, 6–63 HU) for acute PE (P < .001). Reader 2 found mean attenuation measurements of 83 HU ± 32 (range, 32–135 HU) for chronic PE and 33 HU ± 14 (range, 13–65 HU) for acute PE (P < .001). The mean attenuation for both readers was 33 HU for acute PE (95% confidence interval: 26, 41 HU) and 87 HU for chronic PE (95% confidence interval: 66, 107 HU). The Bland-Altman test demonstrated agreement between readers.

CONCLUSION: The mean attenuation measurement in chronic PE is significantly higher than in acute PE.

© RSNA, 2005

	INTRODUCTION

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Pulmonary embolism (PE) is the third most common acute cardiovascular disease, after myocardial infarction and stroke, and it leads to thousands of deaths each year because it often goes undetected (1). In a study performed to evaluate trends of inpatient thoracic radiology use over a decade at an academic medical center, Wittram et al (2) showed that use of computed tomography (CT) in the investigation of patients suspected of having thromboembolic disease has increased considerably (2). Although the use of ventilation-perfusion scintigraphy and pulmonary angiography has decreased, these imaging modalities still have roles in the evaluation of patients in whom PE is suspected.

Acute PE is often a complication of deep leg or pelvic vein thrombosis. Fragmentation and fibrinolysis cause dissolution of the vast majority of acute PE. Chronic PE persists in a number of patients, and it has been suggested that chronic PE results from individual variations in the fibrinolytic activity of pulmonary vessels (3). To our knowledge, the attenuation of chronic PE has not been measured. This information may help in differentiating acute from chronic thrombus at first encounter if old CT studies are not available. Thus, the purpose of our study was to compare retrospectively the attenuation coefficients of acute and chronic PE.

	MATERIALS AND METHODS

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Patients
Our institutional review board approved this retrospective study and waived informed consent. Our study was compliant with requirements of the Health Insurance Portability and Accountability Act. Between July 2001 and January 2004, all patients with a diagnosis of chronic PE or acute PE at CT pulmonary angiography were identified from our radiology information database search program (Folio, Woburn, Mass). The patients’ charts were collected consecutively on the basis of the report text, and they were reviewed by the first author (C.W.) for corroborative evidence (imaging or clinical data) to confirm the diagnosis of PE, which was assigned at CT. The corroborative criteria for chronic PE used in this study included acute PE at the same site for more than 3 months or chronic PE documented with CT or angiographic findings, a previous medical history of chronic PE, or a clinical history consistent with pulmonary arterial hypertension. Corroborative evidence of acute PE included no history of prior PE, with previous imaging findings—when available—negative for thromboembolism.

Thirty-nine patients with chronic PE were identified; 20 were excluded because the lesions were too small to measure (ie, not present on three consecutive images or too small to allow the area of the region of interest [ROI] to be half the diameter of the thrombus being measured), two were excluded due to streak artifacts, and three were excluded because there were no imaging findings or history to confirm a diagnosis of chronic PE. Thus, 14 patients with chronic PE were available for our study (six women, eight men; age range, 26–76 years; mean age, 50 years). Twenty-seven consecutive patients with acute PE were identified, but two were excluded because of streak artifacts, leaving 25 patients with acute PE in our study (11 women, 14 men; age range, 33–83 years; mean age, 61 years). The two-tailed t test was performed with SAS software (version 8; SAS Institute, Cary, NC) and demonstrated a significant difference in age (P = .01) but not sex between the two groups.

CT Technique
A multi–detector row CT scanner (four rows of detectors) (LightSpeed; GE Medical Systems, Milwaukee, Wis) was used to acquire the images. Images were acquired from 2 cm below the lowest hemidiaphragm to the top of the aortic arch, in a caudocranial direction. The imaging field of view used was the widest rib-to-rib distance acquired in apnea after inspiration. For intravenous access, an antecubital vein was used, with 135 mL of ioxilan (300 mg iodine per milliliter) injected through an 18-gauge catheter at a rate of 4 mL/sec. Images were acquired with the following settings: collimation and reconstruction width, 1.25 mm; table speed, 7.5 mm per rotation; pitch, 6:1; peak voltage, 120 kVp; amperage, 300 mA; and tube rotation time, 0.8 second. Image acquisition was started 20 seconds after commencement of the intravenous contrast medium injection, and a standard algorithm was used.

Diagnostic Criteria of PE
Both acute and chronic PE were identified as intraluminal filling defects that demonstrated a sharp interface with intravascular contrast material (C.W.). The diagnostic criteria for acute PE included (a) complete arterial occlusion with failure to opacify the entire lumen—the artery may be enlarged compared with pulmonary arteries of the same order of branching (4–6), (b) a central arterial filling defect surrounded by intravascular contrast material (4), and (c) a peripheral intraluminal filling defect that forms acute angles with the arterial wall (5,6).

The diagnostic criteria for chronic PE included (a) complete occlusion of a vessel smaller than pulmonary arteries of the same order of branching (5,6), (b) a peripheral eccentric filling defect that forms obtuse angles with the vessel wall (5,6), (c) contrast material flowing through apparently thick-walled arteries that are smaller due to recanalization (5,6), (d) a web or band within a contrast material–filled artery (5,6), and (e) an intraluminal filling defect with morphologic features of acute PE, which has been present for more than 3 months.

Measurements
The images were viewed at a picture archiving and communication system, with an IMPAX monitor (version 4.1; Agfa, Teterboro, NJ). Images were displayed with three gray scales for interpretation of the lung window (window width, 1500 HU; window level, –600 HU), mediastinal window (window width, 350 HU; window level, 40 HU), and PE-specific settings (window width, 700 HU; window level, 100 HU).

Two radiologists (C.W. and M.M.M., with 8 and 2 years of experience, respectively, in thoracic radiology interpretation) independently measured attenuation in Hounsfield units. They identified the largest diameter thrombus for an individual patient and measured the ROI from the middle image of three that demonstrated the thrombus. The ROI diameter was selected to be half the diameter of the thrombus being measured and positioned so as to avoid streak artifacts.

Each reader independently selected the largest image of the main pulmonary artery, used a circular ROI approximately half the diameter of the main pulmonary artery—away from streak artifacts—and recorded the area of the ROI and the mean attenuation for the pulmonary artery. Other CT findings of PE were read by consensus. The additional findings of chronic PE included enlarged main pulmonary artery and collateral bronchial artery, mosaic lung attenuation, and pericardial effusion (7). The additional findings of acute PE included a right ventricle short axis larger than left ventricle short axis, consolidation or ground-glass opacification peripheral to PE, atelectasis, mosaic attenuation, and pleural effusion.

Statistical Analysis
Statistical analysis included the calculation of means and standard deviations, and ² and two-tailed t tests were performed with SAS software (version 8; SAS Institute). P values less than .05 were considered to indicate statistical significance. The Bland-Altman test was used to analyze the degree of measurement agreement between readers.

	RESULTS

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Chronic PE
Review of the charts of patients in the chronic PE group revealed previous imaging with CT pulmonary angiography in five of 14 patients and contrast material–enhanced CT with 5-mm collimation in two of 14 who demonstrated acute PE in the same region as those with chronic PE. The interval from previous CT to CT pulmonary angiography ranged from 3 months to 4 years 11 months (mean, 1 year 1 week). In one additional patient, chronic PE was diagnosed at CT pulmonary angiography 2 months before CT pulmonary angiography was performed in this study. In two more patients, pulmonary angiograms that confirmed chronic PE were obtained 5 and 7 weeks after the study CT pulmonary angiograms were obtained. The remaining four of 14 patients underwent no prior or subsequent imaging to confirm chronic PE in our institution; of these, three had a medical history of chronic PE, and one a long history consistent with pulmonary arterial hypertension.

The emboli in the patients with chronic PE were identified on the right side within the apical segmental artery in the upper lobe in one patient, the upper lobe artery in one, the interlobar artery in two, the lower lobe pulmonary artery in three (Fig 1), the posterior basal segmental artery in the lower lobe in three (Fig 2), and the medial basal segmental artery in the lower lobe in one. One embolus was located in the left pulmonary artery, one in the interlobar artery, and another within the posterior basal segment arteries in the left lower lobe. Other findings of chronic thromboembolic disease included an enlarged main pulmonary artery in 10 patients, collateral bronchial artery enlargement in nine, mosaic lung attenuation in seven, and pericardial effusion in five.

View larger version (74K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Contrast-enhanced transverse CT scan of a 61-year-old man with chronic PE in the right lower lobe pulmonary artery. Chronic PE is characterized by formation of obtuse angles with the vessel wall. The circular ROI measurement was 84 HU.

View larger version (74K): [in this window] [in a new window] [Download PPT slide]   Figure 2. Contrast-enhanced transverse CT scan of a 54-year-old man with chronic PE in the left lower lobe, posterior basal segment. Chronic PE is characterized by complete occlusion of a vessel that is smaller than pulmonary arteries of the same order of branching in the other lung. The circular ROI measurement was 78 HU.

The emboli in patients in the acute PE group that were identified on the right side affected the right pulmonary artery in one patient, the apical segment artery in the upper lobe in one, a subsegmental artery in the upper lobe in one, the interlobar artery in one, the lower lobe artery in four, the posterior basal segment artery in the lower lobe in three, and a subsegmental artery in the lower lobe in three. On the left side, acute PE was identified in a subsegmental artery in the left upper lobe in one patient, the interlobar artery in three, the lower lobe artery in two (Fig 3), the lateral basal segment artery in the lower lobe in two, the posterior basal segment artery in the left lower lobe in two, and a subsegmental artery in the lower lobe in one. The additional CT findings in acute PE included a right ventricle short axis larger than the left ventricle short axis in two patients, consolidation or ground-glass opacification peripheral to PE in seven, atelectasis peripheral to PE in nine, mosaic attenuation in one, and pleural effusion in 11.

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 3. Contrast-enhanced transverse CT scan of a 54-year-old man with acute PE in the left lower lobe pulmonary artery. Acute PE is characterized by the formation of acute angles with the vessel wall. The circular ROI measurement was 12 HU.

View larger version (22K): [in this window] [in a new window] [Download PPT slide]   Figure 4. Graph shows the mean and the upper and lower 95% CIs in patients with chronic PE (CPE) and acute PE (APE). There is no overlap in values.

View larger version (23K): [in this window] [in a new window] [Download PPT slide]   Figure 5. Graph shows Bland-Altman test agreement between readers. SD = standard deviation.

	DISCUSSION

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The morphologic outcome of acute PE has been previously evaluated (10). Remy-Jardin et al (10) reviewed findings in 62 patients who were referred to a cardiac intensive care unit with massive acute PE, received anticoagulation therapy, and underwent follow-up CT pulmonary angiography after a mean interval of 11 months. The CT pulmonary angiograms demonstrated that 30 patients (48%) had complete resolution of acute PE and 32 (52%) had incomplete resolution, with a significant difference in the severity of PE between the two groups.

The attenuation in patients with acute PE has been measured previously (11). By using 3-mm collimation CT pulmonary angiography, Cham et al (11) found a mean attenuation of 49 HU in patients with acute PE (95% CI: 44 HU, 34 HU). Unlike in that study, all our patients underwent imaging with 1.25-mm collimation. In addition, we used strict criteria to ensure that partial volume artifact did not affect measurements by using the middle image of three that demonstrated thrombus. In our study, we found a mean attenuation of 33 HU ± 15 in patients with acute PE.

To our knowledge, attenuation in patients with chronic PE has not been previously reported. We calculated the mean attenuation in patients with chronic PE to be 87 HU ± 30. This value was significantly higher than the mean for patients with acute PE (P < .001). Although there was some overlap between chronic and acute PE for individual results, this overlap was not reflected in the lower and upper 95% CIs for the two groups. The reasons for the higher attenuation in patients with chronic PE compared with those with acute PE are likely related to enhancement of organizing thrombus, retraction of thrombus with concentration of hemoglobin and its iron moiety, and possibly, calcium deposition. Paydarfar et al (12) used preoperative contrast-enhanced magnetic resonance (MR) imaging to evaluate 15 consecutive patients with intraluminal cardiac masses. Contrast enhancement on MR images was seen in three of the patients with subsequently proved organized thrombus (12). These findings support our observations and our hypothesis that enhancement is seen in patients with chronic PE.

Limitations of this study include the fact that the diagnoses of acute and chronic PE were not confirmed with the reference standard, pulmonary angiography, in the vast majority of cases. The reason is that in practice, within our institution, conventional angiography is used to confirm or refute PE in patients with indeterminate findings at CT pulmonary angiography, and both the acute and chronic PE groups in our study had imaging or clinical evidence to corroborate the CT findings. Also, in a study conducted to evaluate chronic PE detection, Bergin et al (13) demonstrated that CT pulmonary angiography was more accurate than angiography in depicting central vessel disease.

A second limitation of our study is that only one PE was measured per patient. The study was designed this way, to optimize the ability to measure the thrombus by selecting the largest thrombus. A third limitation is the relatively small number of patients with chronic PE examined, an unavoidable consequence of applying our strict measurement criteria to these patients. A fourth limitation is that unenhanced CT was not performed just prior to contrast-enhanced CT. We assume that the higher attenuation values seen in patients with chronic PE are most likely due to enhancement of organizing thrombus; however, without unenhanced CT, it is impossible to be certain if they are due to hemoglobin-iron concentration from clot retraction or calcium deposition.

The finding of enhancement in patients with chronic PE raises the problem of differentiating between PE and an uncommon cause of an intraluminal arterial filling defect, a primary pulmonary artery sarcoma (14,15). Both chronic PE and pulmonary artery sarcoma can demonstrate contrast enhancement, although other findings may permit differentiation between the two entities. Signs that suggest a pulmonary artery sarcoma at CT pulmonary angiography include a lobulated mass that forms acute angles with its vessel wall, vascular distention, and local extravascular spread (14–16). Chronic PE often forms obtuse angles with the adjacent arterial wall (5,6). To differentiate between acute PE and pulmonary artery sarcoma, as both can form acute angles with the vessel wall, pulmonary artery sarcomas demonstrate enhancement (14,15), whereas acute PE does not. If uncertainty remains in the differentiation between PE and vascular tumor, angiographically guided biopsy may be necessary.

In summary, knowing the attenuation range for acute PE may be useful in the incremental evaluation of a pulmonary artery filling defect and may aid in differentiating between acute PE and flow artifact. This study demonstrates that chronic PE has a higher mean attenuation than acute PE, and we believe this difference is likely due to enhancement of organizing thrombus.

	FOOTNOTES

 
Abbreviations: CI = confidence interval, PE = pulmonary embolism, ROI = region of interest

Authors stated no financial relationship to disclose.

Author contributions: Guarantor of integrity of entire study, C.W.; study concepts and design, C.W.; literature research, C.W.; clinical and experimental studies, C.W., M.M.M.; data acquisition, C.W., M.M.M.; data analysis/interpretation, all authors; statistical analysis, C.W., E.F.H.; manuscript preparation, definition of intellectual content, and editing, C.W.; manuscript revision/review, C.W., M.M.M., J.O.S.; manuscript final version approval, C.W.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 

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