Letters to the Editor
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Enhancement Characteristics of Pheochromocytomas
From Brigitte Happel, MD, and Gertraud Heinz-Peer, MD
Department of Radiology, University Hospital Vienna, Waehringer Guertel 18-20, 1080 Vienna, Austria
e-mail: brigitte.happel @meduniwien.ac.at
Editor:
In their article in the February 2005 issue of Radiology (1), Dr Szolar and colleagues stated that adrenal pheo- chromocytomas have a percentage en- hancement loss that is similar to that in adrenal metastases but is significantly less than that in adrenal adenomas at computed tomography (CT).
A total of 17 pheochromocytomas were included in their CT study. A ma- jor limitation of this study, however, was the small number of included pheo- chromocytomas.
Our unpublished experience in a large group of pheochromocytomas does not fully support these data. We examined 45 patients with 48 adrenal or extraadrenal pheochromocytomas be- tween 1995 and 2005 with magnetic resonance (MR) imaging. The protocol included transverse and coronal T2- weighted turbo spin-echo, chemical shift imaging, and T1-weighted fast low- angle shot three-dimensional sequences as a dynamic series. Until 1998, the de- layed series was performed 6 minutes after application of gadolinium-based contrast material, and after 1998, the delay was about 20 minutes.
Results of our MR imaging study show various enhancement patterns and washout characteristics of pheo- chromocytomas. In our study, 27% of the pheochromocytomas showed the typical and often-reported strong en- hancement and slow washout pattern.
A total of 16.5% of pheochromocy- tomas showed medium enhancement and slow washout, and 40% of pheo- chromocytomas demonstrated either medium or slow enhancement and rapid washout. These dynamic characteristics may also be seen in adenomas. Addi- tionally, 16.5% had strong contrast ma- terial uptake with rapid washout.
In contrast to the study results of Dr Szolar and colleagues, in our study the majority of pheochromocytomas dem- onstrated rapid washout at the delayed contrast-enhanced series, similar to be- nign lesions.
In addition, our results also confirm the findings and statements of Blake and coworkers (2) that pheochromocytomas currently remain imaging chameleons.
References
1. Szolar DH, Korobkin M, Reittner P, et al. Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT. Radiology 2005;234:479-485.
2. Blake MA, Kalra MK, Maher MM, et al. Pheochromocytoma: an imaging chameleon. RadioGraphics 2004;24(suppl 1):S87-S99.
Response
From
Dieter H. Szolar, MD, and Melvyn T. Korobkin, MD Diagnostikum Graz-Südwest and Medical School, Karl Franzens University Weblinger Gürtel 25, 8054 Graz, Austria e-mail: dieter.szolar @diagnostikum-graz.at
We thank Drs Happel and Heinz-Peer for their interest in our article and their com- ments. We agree that the number of pheochromocytomas was small (n = 17), and we acknowledged that limitation in the discussion section of our article (1).
Very few cases of contrast enhance- ment washout of adrenal pheochromo- cytomas have been documented. Caoili et al (2) reported that one patient with pheochromocytomas had a percentage enhancement washout in the range of that of adenomas. Blake et al (3) de- scribed the contrast material washout profiles in five patients and stated that the range of absolute washout percent- age was 35.9%-69.2% on 10-minute delayed CT scans with a relative wash- out percentage ranging from 15.5% to 83.3%. Unfortunately, the data for each of the five cases were not described. Nonetheless, the washout patterns were clearly variable, with some in the adenoma range and others in the non- adenoma range.
It is difficult to assess the data de- scribed in the letter by Drs Happel and Heinz-Peer. Their studies have used ga- dolinium-enhanced dynamic MR imag- ing rather than contrast-enhanced CT. They do not define the terms “slow washout” and “rapid washout” in quan- titative terms, so we cannot relate their observations to those reported in CT studies.
Krestin et al (4) first described the rapid contrast enhancement washout of adrenal nonadenomas compared with adenomas by using dynamic gadolin- ium-enhanced MR imaging, but authors of three separate subsequent articles could not confirm their results (5-7). The observations described in the cur- rent letter are extremely interesting, but until the specific technical details, definitions, and quantitative results are fully described in a published report, it is hard to integrate these observations with the published CT information.
References
1. Szolar DH, Korobkin M, Reittner P, et al. Adrenocortical carcinomas and adrenal pheochromocytomas: mass and enhancement loss evaluation at delayed contrast-enhanced CT. Radiology 2005;234:479-485.
2. Caoili EM, Korobkin M, Francis IR, et al. Ad- renal masses: characterization with combined unenhanced and delayed enhanced CT. Radi- ology 2002;222:629-633.
3. Blake MA, Krishnamoorthy SK, Boland GW, et al. Low-density pheochromocytoma on CT:
a mimicker of adrenal adenoma. AJR Am J Roentgenol 2003;181:1663-1668.
4. Krestin GP, Steinbrich W, Friedman G. Adre- nal masses: evaluation with fast gradient-echo MR imaging and Gd-DTPA-enhanced dynamic studies. Radiology 1989;171:675-680.
5. Korobkin M, Lombardi TJ, Aisen AM, et al. Characterization of adrenal masses with chemical shift and gadolinium-enhanced MR imaging. Radiology 1995;197:411-418.
6. Reinig JW, Stutley JE, Leonhardt CM, et al. Differentiation of adrenal masses with MR imaging: comparison of techniques. Radiology 1994;192:41-46.
7. Semelka RC, Shoenut JP, Lawrence PH, et al. Evaluation of adrenal masses with gadolinium enhancement and fat-suppressed MR imag- ing. J Magn Reson Imaging 1993;3:337-343.
Prediction of Pulmonary Function in COPD on the Basis of CT Measurements of Bronchial Wall Thickness
From
Maarten Nieber, MSc, Hein Putter, PhD, Jan Stolk, MD, Johan H. C. Reiber, PhD, and Berend C. Stoel, PhD
Department of Radiology, Image Processing, Leiden University Medical Center Albinusdreef 2, 2333 ZA Leiden, the Netherlands e-mail: m.nieber@lumc.nl
Editor:
With the latest technical advances in computed tomography (CT), in vivo measurements of human airway dimen- sions, such as lumen area and wall thickness, have now become feasible even for small bronchi. Authors of re- cent studies have explored the correla- tions between these bronchial dimen- sions and pulmonary function. In this respect, we read with interest the arti- cle by Dr Orlandi and colleagues (1), in the February 2005 issue of Radiology, on the associations between wall thick- ening and lung function in chronic ob- structive pulmonary disease (COPD). They assessed wall thickening by mea- suring percentage wall area (PWA) and wall thickness-to-diameter ratio (TDR) and subsequently normalized PWA for body weight. In a multiple regression
analysis they found that a combination of PWA, TDR, and PWA per kilogram of body weight could significantly pre- dict gas exchange (diffusing capacity of the lung for carbon monoxide [DLco]) and airway obstruction (forced expira- tory volume in 1 second-vital capacity ratio [FEV1/VC]) (both expressed as percentage of predicted value). How- ever, it is unclear why these three pa- rameters were included in the analysis, as they basically measure the same fea- ture (ie, wall thickness relative to lumen size). Moreover, the inclusion of highly correlated predictors such as PWA and TDR is undesirable, since it causes un- stable regression coefficient estimates (2). Stable estimates of regression coef- ficients and their confidence intervals are essential for the interpretation of a model, but these were not provided by the authors.
However, our main concern is that the authors probably have introduced a confounder. The normalization of PWA to body weight suggests that weight was associated with airway dimensions (the authors did not elucidate this matter). By entering both original PWA and weight-normalized PWA as predictor variables, it is likely that a confound- ing factor has been introduced, as an association between body weight and DLCO (or FEV1/VC) could explain the association found by means of the mul- tiple regression. A relationship be- tween body weight and DLCO and FEV1/VC is conceivable, since weight loss is related to the progression of COPD (3). We suggest that the au- thors test whether the combination of PWA, PWA normalized to body weight, and weight significantly im- proves the prediction compared with a model that includes only weight.
References
1. Orlandi I, Moroni C, Camiciottoli G, et al. Chronic obstructive pulmonary disease: thin- section CT measurement of airway wall thick- ness and lung attenuation. Radiology 2005; 234(2):604-610.
2. Harrell FE. Regression modeling strategies. New York, NY: Springer, 2001.
3. Wilson DO, Rogers RM, Wright EC, An- thonisen NR. Body weight in chronic obstruc-
tive pulmonary disease. The National Insti- tutes of Health Intermittent Positive-Pressure Breathing Trial. Am Rev Respir Dis 1989; 139(6):1435-1438.
Response
From Gianna Camiciottoli, MD,* Ilaria Orlandi, MD,+ Stefano Diciotti, PhD,* and Mario Mascalchi, MD, PhD+ Respiratory Medicine Unit, Department of Critical Care,* Radiodiagnostic Section, Department of Clinical Physiopathology,* Department of Electronics and Telecommunications,* University of Florence, Viale Morgagni 85, 50134 Florence, Italy e-mail: m.mascalchi@dfc.unifi.it
We thank Dr Nieber and colleagues for their interest in the article we recently published in Radiology (1), which dem- onstrated that use of a combination of PWA, TDR, and PWA normalized for body weight predicted airway obstruc- tion, as measured with FEV1/VC, and gas exchange impairment, as measured with DLCO, in 42 patients with COPD and that this prediction was stronger in the subgroup of 20 patients with clinical features of chronic bronchitis.
They wondered why we included in the analysis three parameters-namely, PWA, TDR, and PWA per kilogram of body weight-that basically measure the same feature (wall thickness relative to lumen size). Admittedly, despite sev- eral precautions in the measurements of the airways on thin-section CT images, including selection of round bronchi with an external diameter of greater than 2 mm and a maximum diameter- to-minimum diameter ratio less than 1.5, neither PWA nor TDR stands alone as a perfect measurement, because bronchial wall thickness is probably overestimated on CT scans owing to in- accuracies in boundary detection and inclusion of adjacent peribronchial in- terstitium (2). As a matter of fact, like in other studies (2,3), we measured both.
However, the main concern Dr Nieber and colleagues had was the in-
troduction of a confounder, namely body weight, in the analysis we per- formed. In particular, they speculated that the association between body weight loss and functional parameters as DLCO or FEV1/VC in patients with COPD could explain the association found at multiple regression analysis. Actually, the correlations between FEV1/VC and body weight (r = 0.30, P = . 051) and between DLco and body weight (r = 0.30, P = . 049) were weak in the 42 patients with COPD with mod- erate functional impairment we exam- ined. No correlation was observed in the two subgroups of patients with or those without chronic bronchitis.
At multivariate analysis the combi- nation of PWA, PWA normalized to body weight, and weight did not sub- stantially improve the prediction of air- way obstruction and gas exchange in the 42 patients with COPD (R values range, 0.32-0.49) and notably in the subgroup of 20 patients with chronic bronchitis (R values range, 0.30-0.51) compared with that obtained with the model in- cluding PWA, TDR, and PWA per kilo- gram of body weight (1).
References
1. Orlandi I, Moroni C, Camiciottoli G, et al. Chronic obstructive pulmonary disease: thin- section CT measurement of airway wall thick- ness and lung attenuation. Radiology 2005; 234:604-610.
2. Awadh N, Muller N, Park CS, et al. Airway wall thickness in patients with near fatal asthma and control groups: assessment with high resolution computed tomography scan. Thorax 1998;53:248-253.
3. Nakano Y, Muro S, Sakai H, et al. Computed tomographic measurements of airway dimen- sions and emphysema in smokers. Am J Re- spir Crit Care Med 2000;162:1102-1108.
Regarding Trends in Recall, Biopsy, and Positive Biopsy Rates for Screening Mammography
From Richard L. Ellis, MD
Norma J. Vinger Center for Breast Care, Gundersen Lutheran Medical
Center EB1-002, 1900 South Avenue, La Crosse, WI 54601
e-mail: rlellis@gundluth.org
Editor:
I read with interest the article by Dr Gur and colleagues, entitled “Trends in Re- call, Biopsy, and Positive Biopsy Rates for Screening Mammography in an Aca- demic Practice” (1), in the May 2005 issue of Radiology. The authors should be applauded for their efforts and will- ingness to share their performance data for recall, biopsy, and positive biopsy rates for screening mammography, as well as the number of cancers detected for each quarter (nine consecutive cal- endar quarters). However, I could not help but wonder why the authors did not include the mean and median size of the invasive cancers detected with screening mammography. The mean and median tumor size for invasive can- cers detected with screening should be considered the first order of business when trying to determine if a radiology group and/or its individual members are having an impact on morbidity and mortality from breast cancer (2-6).
The primary purpose of screening mammography is to reduce mortality from breast cancer. Prognostic indicators for breast cancer survival include tumor size, tumor type, tumor grade, mammo- graphic presentation, regional lymph node status, and metastatic disease. However, tumor size is recognized as act- ing as a governor that directly influences the other prognostic indicators. It is criti- cal to understand that invasive breast car- cinoma must be detected at an early phase of its natural history, allowing the disease to be interrupted prior to the de- velopment of regional or systemic meta- static disease, in order to have the great- est effect on reducing breast cancer mortality. Provided with this information, it would be of much interest if Dr Gur and colleagues would share the mean and me- dian size of the invasive cancers detected with screening mammography from their recent report.
References
1. Gur D, Wallace LP, Klym AH, et al. Trends in recall, biopsy, and positive biopsy rates for
screening mammography in an academic practice. Radiology 2005;235(2):396-401.
2. Michaelson JS, Satija S, Kopans D, et al. Gauging the impact of breast carcinoma screening in terms of tumor size and death rate. Cancer 2003;98(10):2114-2124.
3. Michaelson JS, Silverstein M, Wyatt J, et al. Predicting the survival of patients with breast carcinoma using tumor size. Cancer 2002; 95(4):713-723.
4. Tabar L, Duffy SW, Vitak B, Chen HH, Pre- vost TC. The natural history of breast carcinoma: what have we learned from screening? Cancer 1999;86(3):449-462.
5. Tabar L, Vitak B, Chen HH, Yen MF, Duffy SW, Smith RA. Beyond randomized con- trolled trials: organized mammographic screening substantially reduces breast carci- noma mortality. Cancer 2001;91(9):1724- 1731.
6. Leung JW. Screening mammography reduces morbidity of breast cancer treatment. AJR Am J Roentgenol 2005;184(5):1508-1509.
Response
From
David Gur, ScD, Amy H. Klym, BS, and Jules H. Sumkin, DO
Department of Radiology, University of Pittsburgh, 300 Halket Street, Suite 4200, Pittsburgh, PA 15213- 3180
e-mail: gurd@upmc.edu
We thank Dr Ellis for his comments. We agree that tumor size is an impor- tant parameter that correlates with ulti- mate prognosis, and on average, the “earlier” (and the “smaller”) at detec- tion the better the expected outcome. However, this was not the purpose of our study. Our study was not designed to address efficacy of screening in terms of possible morbidity or mortality, and the time frame of our study does not allow for such an experimental assess- ment for several years to come. Rather our study was designed to review possi- ble trends, if any, related to operational variables, each having a well-defined bi- nary outcome associated with it- namely, a decision to recall (or not), a decision to biopsy (or not), and the out- come of these biopsies in terms of being positive for cancer (or not). These data
allowed us to analyze simple operational trends and summarize their impact in terms of “attributable detection.” Since cancer detection rates remained sub- stantially unchanged despite an increas- ing trend in the number of biopsies per- formed (in particular those related to microcalcification clusters), we expect to have very low statistical power to detect small changes, if any, in average tumor size of the invasive component of cancers in this limited study. In addi- tion, we caution that one-dimensional tumor size measurements may not be as precise as one would hope for this pur- pose. As important perhaps, a one-di- mensional measure of “size” is not likely to be the optimal measurement, nor the most sensitive one, to assess trends or as a predictive measure of outcome. With that being said, for those who un- derwent stereotactic vacuum-assisted core biopsies and/or US-guided core bi- opsies followed by surgical removal of the tumor, the average reported tumor “size” (“largest one dimension of the in- vasive component”) as provided in pa- thology reports was 12.0 mm (median, 11.0 mm; range, 1.0-40.0 mm), and no significant trend was observed during the period in question.
Attenuation of Acute and Chronic Clots
From Rocco Cobelli, MD, Maurizio Zompatori, MD, Nicola Sverzellati, MD, and Gabriele Levrini, MD Department of Clinical Sciences, Section of Radiology, University of Parma, Via Gramsci 14, Parma 43100, Italy e-mail: cobellirocco@hotmail.com
Editor:
We read with interest the article by Dr Wittram and colleagues, in the June 2005 issue of Radiology, about the pos- sibility to distinguish between acute and chronic pulmonary embolism through the evaluation of the attenuation of the clots with contrast material-enhanced computed tomography (CT) (1).
In our opinion, some points of this
work are not completely clear. In partic- ular, the authors report the mean atten- uation of acute clots to be 33 HU; this value is hardly correct, because the blood itself has an attenuation of 20-30 HU (2,3). The intravascular clots are mainly composed of red blood cells and fibrin, so their hematocrit level is higher than is that of the circulating blood and consequently, their attenuation is higher (3). If the reported mean attenu- ation of the acute clots is correct, this implies that probably all of the patients were anemic.
The chronic clots are reported to have very high attenuation (87 HU ± 30 [standard deviation]); the authors are not able to explain this, since they did not perform unenhanced CT. In our opinion, the high attenuation of the clots is caused by the vascularization or by the calcification (the authors do not describe the presence of calcification in the zone of the clots in which they place the region of interest) of the clots them- selves. It is not probable for the high attenuation to be due to the hemoglobin concentration of the chronic clots; in fact, in the first period after the embolus constitution, the clot has a high concen- tration of the protein fraction of hemo- globin and, therefore, an elevated atten- uation level. But, in a second period, the attenuation decreases because of the progressive breakdown of red blood cells and the removal of cell elements, predominantly proteins, by means of phagocytes action. Because the chronic clots mentioned in the article are prob- ably old and in an advanced phase of reorganization in which they appear vascularized, it is improbable that the finding of elevated attenuation is justi- fied by the presence of a high concentra- tion of hemoglobin.
In the January-February issue of the Journal of Computer Assisted Tomogra- phy, our team reported (2) the results of a study in which we evaluated the percentage of cases in which emboli can be detected on unenhanced CT scans. The main difference between our study and that of Dr Wittram and colleagues refers to the attenuation evaluation of the clots, which we performed exclu- sively on the unenhanced CT scans. In
our results, the mean attenuation of the clots that appeared hyperattenuating on the unenhanced scans and were, also in accordance with their morphologic fea- tures, classified as strongly probably acute, was reported to be 74.25 HU ± 10.07 (95% confidence interval [mean ± confidence interval]: 74.25 ± 4.93). These results, which are very different from the findings reported by Dr Wit- tram and colleagues, confirm the data reported in other articles in which the attenuation of acute clots was evalu- ated. The emboli that appeared to be hypoattenuating and were character- ized by means of a morphologic appear- ance that was strongly evocative of chronic pulmonary embolism had a value of 27.7 HU ± 11.69 (mean ± 95% confidence interval: 27.7 ± 11.45), with a range of 21-46 HU. We considered this value to be evocative for chronic thrombosis, a condition in which the clot is in an advanced reorganizing phase and the hemoglobin content is low.
In conclusion, we think the article by Dr Wittram and colleagues is very interesting but contains some limita- tions; the authors evaluated the attenu- ation of clots only at contrast-enhanced CT. In our opinion, this fact may cause pitfalls in the densitometric analysis of acute clots and prevent a correct evalu- ation of the attenuation of chronic clots. We therefore suggest, in every CT ex- amination performed in patients sus- pected of having chronic pulmonary em- bolism, obtaining an unenhanced CT scan, with the aim of differentiating chronic from acute clots.
References
1. Wittram C, Maher MM, Halpern EF, Shepard JO. Attenuation of acute and chronic pulmo- nary emboli. Radiology 2005;235(3):1050- 1054.
2. Cobelli R, Zompatori M, De Luca G, Chiari G, Bresciani P, Marcato C. Clinical usefulness of computed tomography study without contrast injection in the evaluation of acute pulmonary embolism. J Comput Assist Tomogr 2005; 29(1):6-12.
3. New PF, Aronow S. Attenuation measure- ments of whole blood and blood fractions in computed tomography. Radiology 1976;121: 635-640.
Response
From Conrad Wittram, MB, ChB,* Eugene Mark, MD,+ Michael M. Maher, MD,* and Joanne O. Shepard, MD* Departments of Radiology* and Pa- thology,+ Massachusetts General Hospital and Harvard Medical School Founders Building, Room 202, 55 Fruit Street, Boston, MA 02114 e-mail: cwittram@partners.org
To address the first issue, in response to the letter by Dr Cobelli and colleagues, a review of the histologic background of venous thromboembolism is appropri- ate: An acute thrombus is formed from fibrin, platelets, neutrophils, and red blood cells, and as the cells necrose, swelling often occurs. Activation of the fibrinolytic pathways can lead to rapid total lysis of acute emboli. When this is incomplete, endothelial cells become activated, and sprouts with irregular clefts lined by endothelial cells develop within a few days. A general rule of thumb is that cellular penetration can advance at the rate of approximately 1 mm per day, depending on conditions. Fibroblastic proliferation occurs with and adjacent to capillary formation. Re- ticulin may be detected after about 4 days and collagen in 5-10 days and thereafter hemosiderin may appear at about 1 week, which is later than the 2 days it takes to appear after bleeding into skin or meninges. Fibrocytic prolif- eration reaches a maximum at about 4 weeks, and at this time elastin may be present. Remodeling gradually trans- forms the clot into compartments; this process can continue for longer than a year (1). An acute thrombus has a CT attenuation value that is dependant largely on the proportions of red blood cells, with its hemoglobin and iron moi- ety, and fibrin. It is therefore of no sur- prise that the Hounsfield unit value of acute pulmonary embolism in our study (2) is similar to previously published at- tenuation measurements of whole blood (3). Clot contraction, and a possible in- crease in thrombus attenuation owing to an increase in hemoglobin and iron
moiety concentration, can only occur af- ter capillary formation and fibroblastic proliferation.
The second issue is that our institu- tion does not perform unenhanced CT prior to CT pulmonary angiography, be- cause this is considered unnecessary and an insensitive test for this indica- tion. In the population we studied, cal- cium deposition in chronic thrombus was not obvious on CT scans (2). Within our discussion we clearly state, “The reasons for the higher attenuation in patients with chronic PE [pulmonary embolism] compared with those with acute PE are likely related to enhance- ment of organizing thrombus, retraction of thrombus with concentration of he- moglobin and its iron moiety, and possi- bly, calcium deposition” (2).
The third issue relates to a variance of results between the article by Dr Co- belli and colleagues (4) and our work (2). In our study, corroborative evi- dence of acute and chronic pulmonary embolism from the clinical history or imaging was a selection criterion, 1.25-mm section thickness was used in all cases, there were two readers, and contrast material was used to define the clot margins (2); the article by Dr Co- belli and colleagues did not address these four important methodologic points (4). Dr Cobelli and colleagues measured thrombus attenuation values on unenhanced CT scans; of 51 cases, they found 10 clots that demonstrated hyperattenuation, five with hypoattenu- ation, six with mixed attenuation, and 30 with isoattenuation with respect to blood. One obvious question is, in the 30 cases that demonstrated a thrombus that was isoattenuating with respect to blood, how can one accurately measure something one cannot see? The article by Dr Cobelli and colleagues is entitled “Clinical Usefulness of Computed To- mography Study without Contrast Injec- tion in the Evaluation of Acute Pulmo- nary Embolism,” and in the materials and methods of this article they de- scribe imaging patients with “the clinical suspicion of pulmonary embolism.” There is no stratification into acute or chronic embolism or corroborative evi- dence of acute or chronic emboli. They
interpret their results by stating that thrombi that demonstrate hyperattenu- ation are acute and that thrombi that demonstrate hypoattenuation with re- spect to blood are chronic. These con- clusions cannot be made from their re- sults, as clinical, imaging, or histologic corroborative evidence of thrombus age was not present within their study (4). In the conclusion of their letter to us, Dr Cobelli and colleagues state, “We there- fore suggest, in every CT examination performed in patients suspected of hav- ing chronic pulmonary embolism, ob- taining an unenhanced CT scan, with the aim of differentiating chronic from acute clots.” However, their study did not evaluate chronic pulmonary emboli
(4). In conclusion, the article by Dr Co- belli and colleagues is interesting in the fact that pulmonary emboli can be iden- tified on 41% of unenhanced CT scans in a retrospective study. However, one is uncertain of the age of the thrombo- emboli that the authors investigated, and therefore the Hounsfield unit values found in the article by Dr Cobelli and colleagues are called into question. The purpose of our work was to compare the attenuation values of acute and chronic emboli corroborated with clini- cal and imaging evidence; the results are derived from in situ acute and chronic thromboemboli on contrast-en- hanced CT scans and are therefore of substantial practical value.
References
1. Zollinger HU. Histologisch altersbestimmung von thrombosen und embolien. Virchows Arch 1963;336:220-237.
2. Wittram C, Maher MM, Halpern EF, Shepard JA. Attenuation of acute and chronic pulmo- nary emboli. Radiology 2005;235:1050-1054.
3. New PF, Aronow S. Attenuation measure- ments of whole blood and blood fractions in computed tomography. Radiology 1976;121: 635-640.
4. Cobelli R, Zompatori M, De Luca G, Chiari G, Bresciani P, Marcato C. Clinical usefulness of computed tomography study without contrast injection in the evaluation of acute pulmonary embolism. J Comput Assist Tomogr 2005;29: 6-12.