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Clinical Investigations: PULMONARY CIRCULATION |

Clinical Outcome After a Negative Spiral CT Pulmonary Angiographic Finding in an Inpatient Population From Cardiology and Pneumology Wards* FREE TO VIEW

Katia Bourriot, MD; Thierry Couffinhal, MD, PhD; Virginie Bernard, MD; Michel Montaudon, MD; Jacques Bonnet, MD; François Laurent, MD
Author and Funding Information

*From the Service de Cardiologie (Drs. Bourriot, Couffinhal, Bernard, and Bonnet), Hôpital Cardiologique du Haut-Lévêque, Pessac; and Service de Radiologie (Drs. Montaudon and Laurent), Unité d’imagerie thoracique et cardio-vasculaire, Hôpital du Haut-Levêque, Pessac, France.

Correspondence to: Thierry Couffinhal, MD, PhD, Service des Maladies Cardiovasculaires, Hôpital Cardiologique du Haut-Lévêque, Avenue de Magellan, 33604 Pessac Cedex, France; e-mail: thierry.couffinhal@bordeaux.inserm.fr



Chest. 2003;123(2):359-365. doi:10.1378/chest.123.2.359
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Study objectives: The purpose of this study was to assess the clinical follow-up of a negative spiral CT (SCT) angiographic finding after a suspicion of acute pulmonary embolism (PE) in a population of inpatients with cardiac and/or respiratory disease. In this high-risk population, clinical findings suggestive of PE are frequently misleading.

Design: One hundred seventy-five consecutive patients hospitalized in cardiac and pneumology wards underwent SCT angiography for suspected PE over a 30-month period. Angiographic findings were positive in one third. For the 117 patients with negative SCT angiographic findings, a clinical follow-up during a minimum of 6 months was assessed, particularly in relation to recurrent thromboembolism, mortality, and cause of death.

Results: The mean ± SD follow-up was 21 ± 11.5 months, and five patients were unavailable for follow-up. Of the 117 patients with negative findings, 81 patients did not receive anticoagulant therapy and 46 patients received anticoagulation for cardiac disease or deep venous thrombosis. Twenty-two patients died during the follow-up period, 3 of them during the first 3 months following the initial event from an undetermined cause. In patients still alive, a new PE occurred in two cases. Patients with a poor cardiopulmonary reserve did not present any recurrent events. In this population, tests other than imaging (d-dimers, cardiac echocardiography, or venous ultrasound) contributed little to eliminate the diagnosis of PE.

Conclusions: Whether or not early deaths are considered or not to be related to a recurrent PE, the rate of recurrence after a negative SCT angiographic finding varied between 1.8% and 4.9%. SCT angiography can be used confidently to rule out significant PE, and may prevent further investigations and unnecessary treatment in an inpatient population with cardiac and/or respiratory diseases.

Pulmonary embolism (PE) is a severe frequent disease and one of the leading causes of mortality in hospitalized patients. The rate of recurrence after an initial episode of PE has been found to be 8% in patients treated with anticoagulant therapy, but may reach 30% in untreated patients.12 Establishing or ruling out the diagnosis of PE is difficult due to the lack of specificity of clinical findings and of most biological and imaging tests.35

For patients with cardiac or pulmonary disease, clinical findings suggestive of PE are frequently misleading because the same findings can often be related to an underlying disease. In this particular group of patients, to rule out an acute PE with confidence is of primary importance because recurrence can be severe due to the degraded cardiac or respiratory status.6

Today, spiral CT (SCT) and Doppler ultrasound of the leg veins are known to be a cost-effective strategy in the diagnosis of PE. The sensitivity and specificity of SCT have been studied compared to angiography or to a “gold standard” obtained with ventilation/perfusion scintigraphy and follow-up710 and have been shown to vary widely in published series.11 In addition, the clinical validity of a negative SCT finding has been examined in four studies with results similar to that of angiography.5,1215 However, in a systematic review of the sensitivity and specificity of SCT, Rathbun et al11 concluded that the use of SCT in the diagnosis of PE has not yet been adequately evaluated. The safety of withholding anticoagulant treatment in patients with negative SCT results is uncertain. She argues that in each of these studies, anticoagulant treatment was withheld only in selected patients and some patients underwent pulmonary angiography, and the population was not clearly characterized in any of these studies.

In the present study, we assessed clinical outcome following a negative SCT finding to rule out PE in a high-risk group of patients of whom 70% have a known cardiorespiratory disease and 36% have an inadequate cardiorespiratory reserve. The recurrence of PE was analyzed by a long-term follow-up in this particular cohort of patients.

Patients

One hundred seventeen consecutive patients with a clinical suspicion of PE who had negative SCT findings for PE were considered for the study. They were recruited in our institution from June 1996 to December 1998. In the same time period, 58 patients (prevalence of PE, 33%) were found to have positive SCT findings (n = 54) or a diagnosis of PE based on angiography (n = 4). All were hospitalized patients in cardiology and pneumology wards. Eighty-two patients (70%) had a known respiratory or cardiac disease at the time of the SCT and were already investigated for this. For one third of patients, suspicion of PE was considered at some point during hospitalization; for two thirds, suspicion of PE was the reason for hospitalization. Thirty-five patients (30%) were included in a previous study comparing SCT and ventilation/perfusion scintigraphy in the diagnosis of PE.16 All patients underwent both SCT and color Doppler ultrasound of the legs and d-dimer test. Previous anticoagulation therapy at the time of hospital admission was also noted.

Data Collection

Data were collected by a physician and included age, sex, clinical symptoms and physical signs (thoracic pain, dyspnea, cough, malaise, tachycardia, signs of venous thrombosis… ), risk factors (previous emboli, cancer, cardiac disease, COPD, coagulation disorders, previous surgery or immobilization), results of ECG, chest radiography, and other tests. Based on clinical findings, results of ECG, blood gas analysis, and chest radiography, a clinical probability of PE was established retrospectively by one investigator aware of the results following criteria previously described, and included three levels: high, intermediate, and low.35 Comorbid diseases were considered present if they were documented in a cardiovascular or pneumologic department and if they occurred within 3 months prior to study entry. Ischemic heart disease was defined by a history of myocardial infarction or coronary heart disease documented by a coronarography showing at least a vessel stenosis > 50%. Left-sided congestive heart failure was defined by a history of congestive heart failure and a systolic dysfunction on echocardiography with an ejection fraction < 40%. Atrial fibrillation was considered after a second episode. Pulmonary hypertension was defined as a systolic pulmonary arterial pressure ≥ 40 mm Hg measured by echocardiography. COPD was defined by the presence of a history or findings on chest radiography. History of COPD was defined by the presence of a history of chronic bronchitis and/or emphysema not reversed by or incompletely reversed by bronchodilatation. During pulmonary function tests, FVC at 1 s was ≤ 80% than predicted in all our patients meeting the definition of COPD.6

Cardiorespiratory reserve was defined as inadequate if a patient presented one of the following: pulmonary edema, right ventricular failure, hypotension (systolic pressure < 90 mm Hg), syncope, acute tachyarrhythmias, or respiratory failure shown by severely abnormal spirometry (FEV1 < 1.0 L or vital capacity < 1.5 L) or blood gas measurements (Po2 < 50 mm Hg or Pco2 > 45 mm Hg on room air).17

Technical Considerations
Spiral CT:

CT scans were acquired with a Sonatom 4+S scanner (Siemens Medical Systems; Erlangen, Germany) scanner. A contrast-enhanced CT evaluation of the pulmonary arteries was performed from the level of the aortic arch to at least 2 cm below the level of the pulmonary veins. Scans were acquired during suspended inspiration or shallow breathing, depending on the patient’s ability to hold his or her breath during the acquisition time. Technical parameters included 3-mm (n = 35) or 2-mm collimation (n = 82), 1.8 to 2.0 pitch 120 kilovolts, 170 mA, and 0.75-s scan time. Images were reconstructed at 2-mm intervals with the use of a standard algorithm and an field of view adapted to the size of the patient. Contrast material was injected at 4 to 5 mL/s with a power injector (Medrad; Pittsburgh, PA) through an 18- to 20-gauge catheter into the antecubital fossa. The injected arm was placed at the patient’s side to eliminate kinking of the subclavian vein at the thoracic inlet during injection, and the other arm was placed above the patient’s head. A total volume of 120 to 150 mL of nonionic contrast material (Omnipaque 240; Nycomed Ingenor; Paris, France) was injected. A timing bolus was not used, and scanning began 12 to 15 s after the initiation of injection. The scan delay and arm position allowed direct visualization of the IV site of the first phase of injection and minimized the risk of interstitial injection. Images were viewed at settings for pulmonary vasculature (window width, 350 to 400 Hounsfield units [HU]; window level, 50 HU) and lung parenchyma (window width, 1,200 HU; window level, 700 HU) on hard copies. The entire examination could be reviewed on a workstation. The presence or absence of an occlusive or nonocclusive clot in the main, lobar, segmental, and subsegmental arteries was recorded on a study data sheet. SCT studies were categorized as follows: (1) positive for PE if a clot was observed, (2) negative for PE if no clot was observed, or (3) indeterminate if poor examination, inadequate enhancement, or motion artifacts precluded confident interpretation of the study. Acute PE was diagnosed if a normal-sized or enlarged pulmonary artery was obstructed completely by an enhancing thrombus, or if nonocclusive filling defects were apparent centrally in the vessel. The initial reading was used to assess the need for further investigations. Subsequently, the images were independently interpreted by the second radiologist to confirm the first interpretation. Consensus was obtained between readers in case of discordance. Interobserver agreement between readings calculated with the κ statistic was excellent (0.72).16

Doppler Ultrasound:

All ultrasound examinations were performed by experienced radiologists or cardiologists with a Doppler ultrasound scanner (Elegra; Siemens Medical Systems) by means of 7.5-MHz and 3.5-MHz linear display probes. The veins of both legs were examined with color or duplex sonography, from the calf to the inferior vena cava. The criterion for deep venous thrombosis was the presence of an intraluminal thrombus or incomplete compressibility of the veins, or both.

Cardiac Echocardiography:

Transthoracic Doppler echocardiography (Sequoïa; Acuson; Mountain View, CA) was performed at the time of the suspicion of PE by experienced cardiologists. Assessment of right ventricular measures, wall motion, and calculation of the pulmonary artery systolic pressure were done as described previously.18

d-Dimers:

All patients included underwent blood sampling and d-dimer testing at emergency hospital admission or at the time of PE suspicion. d-Dimer levels were measured the same day using rapid enzyme-linked immunosorbent assay on plasma (Asserachrom D-Di Diagnostica Stago; Asnière, France). d-Dimer test results were considered positive at > 500 ng/mL.

Clinical Follow-up and Outcome

Patients were followed up by their family physicians and were systematically interviewed by telephone (at least once) by one of the study coordinators with a standardized questionnaire to determine a recurrence of PE events. They were all contacted between March 2000 and May 2000. The family physician was contacted whenever a possible event was disclosed in the interim history, and the medical charts were reviewed if a patient was readmitted to a hospital for any cause. For each abnormal event, data noted were clinical findings and results of tests, the eventual date and cause of death, whether anticoagulation was performed, and its duration. For patients who died, the cause of death was ascertained using the death certificate. However, 47% of the patients underwent at least one consultation or hospitalization within 3 months after the initial event with one of the investigators for cardiologic or pneumologic pathology. Duration of follow-up was calculated from the date of the negative SCT finding to the date the patient was contacted by phone or the date of death.

Characteristics of the Population

One hundred seventy-five patients underwent SCT pulmonary angiography; findings were positive in one third, attesting to a high-risk group. The population studied included 117 patients with negative SCT findings, 69 women and 48 men hospitalized in cardiology (n = 79) and pneumology wards (n = 38). The mean ± SD age was 65.0 ± 16.4 years (range, 19 to 93 years). Eighty-two patients (70%) had a known cardiac or respiratory disease (Table 1 ).

The clinical probability for the diagnosis of PE was considered low for 36 patients (31%), intermediate for 39 patients (33%), and high for 42 patients (36%). Risk factors for thromboembolic disease were present in 81 patients (69.2%), including cardiac disease (29%), previous thromboembolic disease (16.2%), cancer (12%), COPD (9.4%), coagulation disorders (0.85%), and others (1.7%) [Table 1]. Follow-up was performed for a mean duration of 21 ± 11.5 months (range, 6 to 36 months).

Results of Initial Data

Forty-six patients (39.3%) in the population studied were treated with anticoagulation therapy at discharge, 24 patients (52%) for a cardiac disease and 22 patients (48%) for thrombosis of the veins of the legs. Anticoagulation therapy was stopped after 3 months or 6 months among patients with venous thrombosis. At the time of follow-up, only 26% of the patients were receiving anticoagulant therapy. The duration of anticoagulation was 16.5 ± 10.6 months. No complications from anticoagulation were reported. Results of d-dimer and Doppler ultrasound are shown in Table 2 and displayed following the presence or not of a cardiorespiratory disease (Table 2).

Results of Follow-up

In 112 of the 117 patients (95.7%), a follow-up was obtained. Five patients (4.3%) were unavailable for follow-up. Twenty-two patients died during follow-up (19.6%). In 15 patients, the cause of death was determined with clinical and radiologic considerations: lung malignancy,7 GI malignancy,3 urinary tract malignancy,1 lymphoma/myeloma,3 and mesenteric ischemia1 (Table 3 ). None of them were receiving anticoagulant therapy. Medical charts did not report any suspicion of recurrence of PE. In seven patients, the cause of death could not be determined; four patients died 18 months after the initial suspicion of PE, and four patients were receiving anticoagulation. The three other patients died within 1 month of the initial event. Two patients > 90 years old died at home: one patient had a previous cancer and was not treated with anticoagulation, and other patient had a severe cardiac insufficiency and was treated with anticoagulation. In both patients, SCT and Doppler ultrasound results were negative. The third patient had COPD and was hospitalized 1 month after the initial event for ARDS, but died a few hours later before any imaging test could be performed. He was not receiving anticoagulation (Table 3).

Critical Events During Follow-up

Twelve patients, 3 of whom were treated with anticoagulation, presented with a new suspicion of PE during follow-up. For nine of these patients, new SCT, Doppler ultrasound, and d-dimer test results were negative for PE (Table 3). The final diagnosis was heart failure for three patients, atrial fibrillation for one patient, and infectious pulmonary or pleural disease for five patients. For the three other patients, the diagnosis of PE was established on the basis of imaging studies (Table 3). These events occurred 2 months after the initial event for two of these patients, and 13 months after for the last patient. None of them were receiving anticoagulant therapy. The latter occurred far too late to be considered as a recurrence of the initial event, so was considered as a new PE. For the two former patients, the first event was considered as highly suspicious of PE in the context of bronchopulmonary cancer. Both SCT and ultrasound findings were negative, and symptoms were related to the cancer. No further examination was performed.

If these two cases and the three deaths that occurred during the first 3 months after follow-up are considered as new PE, a recurrence rate of 4.5% is obtained after a negative SCT finding (5 of 112 patients; 95% confidence interval [CI], 0 to 8.8%). If the three deaths are not considered as being due to a recurrence of PE, the recurrence rate is 1.8% (2 of 112 patients; 95% CI, 0 to 4.5%).

If we excluded patients receiving anticoagulation at the follow-up, the recurrence rate was 4.9% (4 of 81 patients; 95% CI, 1.1 to 8.5%) and 2.5% (2 of 81 patients; 95% CI, 0 to 5.2%), respectively (Table 3). Moreover, when patients were classified according to their cardiopulmonary reserve, patients having the poorer underlying reserve presented less critical events and did not exhibit any recurrent thromboembolism during the follow-up period. (Table 3). When patients were classified following the initial clinical probability of PE, intermediate- and high-risk patients presented more critical events and recurrent thromboembolism during the follow-up period than low-risk patients.

Our goal in this study was to evaluate the clinical outcome following negative SCT findings in a population of patients of whom 70% have a known cardiorespiratory disease and 36% have an inadequate cardiorespiratory reserve. This population is specific since their symptoms may be particularly misleading and the risk factors for PE are frequent. To our knowledge, the role of SCT to rule out PE has not yet been specifically studied in this type of population. Carlson et al6 showed that patients with COPD and PE have an increased rate of mortality compared to patients with PE and without COPD. Our study population was broader since it included all patients hospitalized in pneumology and cardiology wards of our institution, with 70% having a known chronic cardiac or pulmonary disease. Therefore, it is of primary importance to rule out or to confirm the diagnosis of PE in this particular population and to evaluate the safety of withholding anticoagulation after a negative SCT finding.

In the near future, SCT may play a central role for diagnosing PE, since it is a simple, easily performed, noninvasive investigative technique of only moderate cost; however, the sensitivity and specificity have been shown to vary widely in published series.8,1011,1920

In our series, laboratory and imaging tests other than SCT contributed little to the diagnosis of PE, emphasizing the role of SCT in this distinctive population (Table 2). d-Dimer results were positive in 64.1% of patients without PE, although only 18.8% had venous thrombosis. This high rate in this inpatient population was due to advanced age, and to the presence of infectious, inflammatory, or neoplastic diseases.4,2122 Nor was echocardiography useful in patients with a chronic cardiac disease because 50% had previous signs of right ventricular impairment. We did not perform ventilation-perfusion scintigraphy in our study. However, we know from the Prospective Investigation of Pulmonary Embolism Diagnosis study,23that the diagnosis of PE may remained undetermined in as many as 75% of patients when this test is used solely. This rate is likely to be even higher in a population of inpatients with cardiac or respiratory disease. We did not perform angiography if SCT was considered to be of sufficient quality. As underlined by several investigators, clinicians are reluctant to use angiography for reasons of invasiveness and cost, even though it remains the “gold standard.”24Although angiography is still more reliable than SCT for detecting subsegmental emboli, the interobserver agreement in the Prospective Investigation of Pulmonary Embolism Diagnosis study was only 90% for segmental arteries and only 66% for subsegmental arteries.25

The rate of recurrence of PE after negative angiographic or scintigraphic findings varies between 0.6% and 4.9% in series reporting this parameter.15,24,2628 Event-free survival without the administration of anticoagulant medication is a criterion used in patients who do not undergo pulmonary angiography. A 3-month follow-up seems adequate since most deaths related to recurrent emboli occur within 2 weeks of diagnosis.2,13,2930 Our results confirm that recurrent PE occurs within the first 3 months. In only one patient of our series did an event diagnosed as a PE occur later; this was 13 months after the initial event and was considered as a new PE rather than a recurrence.

The recurrence rate in our series varies between 1.8% and 4.9%, depending on which patients are considered as recurrent PE, and depending on exclusion of patients receiving anticoagulant therapy. The risk of recurrence after a negative SCT finding has been evaluated in several series, and varies from 0 to 2.7%.5,9,1314,3132 Rates of 0% were found in the series of 44 patients reported by Mayo et al,9 1% in the series of 198 patients reported by Goodman et al13with a 3-month follow-up, 1.2% in the series by Garg et al14 of 78 patients with a 6-month follow-up, and 2.7% in the 112 patients reported by Ferretti et al.5 Our rate of recurrence is slightly higher, between 1.8% to 4.9% depending on what is considered to constitute a recurrence of PE. Several factors may account for these differences. First, we included as recurrences those patients with an undetermined cause of death during the 3 months following the initial event. Moreover, the mortality rate is high in our series (18.8% in 21 months) due to the mean age (65 years) of our patients compared to those of Lomis et al,12(n = 55), Goodman et al13(n = 56), and Garg et al14 (n = 65). Furthermore, 70% of our patients had a known cardiac or respiratory disease and 60% of deaths were due to a neoplasia. Second, 36% of the patients have a poor cardiorespiratory reserve that could account for a higher recurrence or a higher mortality rate from PE recurrence. However, withholding anticoagulant therapy in this subgroup of patient with negative SCT finding appear to be safe since they have exhibited less events in the follow-up and no recurrence of PE. Third, the rate of patients unavailable for follow-up is low in our population (4.3%) compared to those in other studies with a similar methodology: 11.3% in 9 months follow-up for Lomis et al,12 9.3% in 6 months for Garg et al,14 and 8.4% in 3 months for Goodman et al.13

Another particularity of our population is that 39.3% of our patients received anticoagulation after the first event and 26% during the follow-up. In most, this was because of their underlying cardiac disease. The rate of recurrence of PE in patients treated with anticoagulation after a suspicion of PE varied between 2.7% and 5%.2,3334 Of the 12 patients with a new event, 3 patients received anticoagulation but a new PE had been ruled out. Excluding patients receiving anticoagulation from this study gives a recurrence rate between 2.5% and 4.9% (n = 81), which is comparable to that of previous studies.

The rate of recurrence of PE after negative SCT findings in patients with known cardiorespiratory disease ranged from 1.8% to 4.9%, a rate similar to that in previous studies. Therefore, our study confirms the usefulness of SCT to rule out PE in patients with cardiac and pulmonary disease and to withhold anticoagulant therapy when not necessary for the underlying pathology. In addition, although results based on a larger study group are suitable, a negative CT finding can exclude PE in patients with altered cardiopulmonary reserve

Abbreviations: CI = confidence interval; HU = Hounsfield units; PE = pulmonary embolism; SCT = spiral CT

Table Graphic Jump Location
Table 1. Causes of Previously Known Cardiac and Respiratory Diseases in the Population Studied and Evaluation of the Cardiopulmonary Reserve
Table Graphic Jump Location
Table 2. Results of Tests in the Population Studied*
* 

Data are presented as No. (%).

 

d-Dimer test results were positive when > 500 ng/mL.

Table Graphic Jump Location
Table 3. Results of Death and Critical Events During Follow-up in the Whole Population*
* 

Data are presented as No. (%).

Quinn, DA, Thompson, BT, Terrin, ML, et al (1992) A prospective investigation of pulmonary embolism in women and men.JAMA268,1689-1696. [PubMed] [CrossRef]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Goldhaber, SZ Pulmonary embolism.N Engl J Med1998;339,93-104. [PubMed]
 
Perrier, A, Bounameaux, H, Morabia, A, et al Diagnosis of pulmonary embolism by a decision analysis-based strategy including clinical probability, D-dimer levels, and ultrasonography: a management study.Arch Intern Med1996;156,531-536. [PubMed]
 
Ferretti, GR, Bosson, JL, Bullaz, PD Acute pulmonary embolism: role of helical HCT in 164 patients with intermediate probability at ventilation-perfusion scintigraphy and normal results at duplex US of the legs.Radiology1997;205,453-458. [PubMed]
 
Carson, JL, Terrin, ML, Duff, A, et al Pulmonary embolism and mortality in patients with COPD.Chest1996;110,1212-1219. [PubMed]
 
Rémy-Jardin, M, Remy, J, Wattinne, L, et al Central pulmonary thromboembolism: diagnosis with helical volumetric CT with the single-breath-hold technique; comparison with pulmonary angiography.Radiology1992;185,381-387. [PubMed]
 
Garg, K, Welsh, CH, Feyerabend, AJ, et al Pulmonary embolism: diagnosis with spiral CT and ventilation-perfusion scanning; correlation with pulmonary angiographic results or clinical outcome.Radiology1998;208,201-208. [PubMed]
 
Mayo, JR, Rémy-Jardin, M, Muller, NL Pulmonary embolism: prospective comparison of spiral helical CT with ventilation-perfusion scintigraphy.Radiology1997;205,445-452
 
Rémy-Jardin, M, Remy, J, Deschildre, F, et al Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography.Radiology1996;200,699-706. [PubMed]
 
Rathbun, SW, Raskob, GE, Whitsett, TL Sensitivity and specificity of helical computed tomography in the diagnosis of pulmonary embolism: a systematic review.Ann Intern Med2000;132,227-232. [PubMed]
 
Lomis, NN, Yoon, HC, Moran, AG, et al Clinical outcomes of patients after a negative spiral CT pulmonary arteriogram in the evaluation of acute pulmonary embolism.J Vasc Interv Radiol1999;10,707-712. [PubMed]
 
Goodman, LR, Lipchik, RJ, Kuzo, RS, et al Subsequent pulmonary embolism: risk after a negative helical CT pulmonary angiogram: prospective comparison with scintigraphy.Radiology2000;215,535-542
 
Garg, K, Sieler, H, Welsh, CH, et al Clinical validity of helical CT being interpreted as negative for pulmonary embolism: implications for patient treatment.AJR Am J Roentgenol1999;172,1627-1631. [PubMed]
 
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Blachere, H, Latrabe, V, Montaudon, M, et al Pulmonary embolism revealed on helical CT angiography: comparison with ventilation-perfusion radionuclide lung scanning.AJR Am J Roentgenol2000;174,1041-1047. [PubMed]
 
Hull, RD, Raskob, GE, Ginsberg, JS, et al A noninvasive strategy for the treatment of patients with suspected pulmonary embolism.Arch Intern Med1994;154,289-297. [PubMed]
 
Ribeiro, A, Lindmarker, P, Juhlin-Dannfelt, A, et al Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate.Am Heart J1997;134,479-487. [PubMed]
 
Bankier, AA, Janata, K, Fleischmann, D, et al Severity assessment of acute pulmonary embolism with spiral CT: evaluation of two modified angiographic scores and comparison with clinical data.J Thorac Imaging1997;12,150-158. [PubMed]
 
van Erkel, AR, van Rossum, AB, Bloem, JL, et al Spiral CT angiography for suspected pulmonary embolism: a cost effectiveness analysis.Radiology1996;201,29-36. [PubMed]
 
Reber, G, Boehlen, F, de Moerloose, P The practical value of the level of D-dimer in the exclusion diagnosis of deep vein thrombosis.Rev Med Interne1998;19,442-444. [PubMed]
 
van Beek, EJ, Schenk, BE, Michel, BC, et al The role of plasma D-dimers concentration in the exclusion of pulmonary embolism.Br J Haematol1996;92,725-732. [PubMed]
 
The diagnosis of pulmonary embolism.JAMA1990;264,2623-2625
 
Stein, PD, Athanasoulis, C, Alavi, A, et al Complications and validity of pulmonary angiography in acute pulmonary embolism.Circulation1992;85,462-468. [PubMed]
 
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Novelline, RA, Baltarowich, OH, Athanasoulis, CA, et al The clinical course of patients with suspected pulmonary embolism and a negative pulmonary arteriogram.Radiology1978;126,561-567. [PubMed]
 
van Beek, EJR, Philomen, MM, Schenk, BE, et al A normal perfusion lung scan in patients with clinically suspected pulmonary embolism.Chest1995;108,170-173. [PubMed]
 
Hull, RD, Hirsh, J, Carter, CJ Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan.Ann Intern Med1983;98,891-899. [PubMed]
 
Stein, PD, Henry, JW, Relyea, B Untreated patients with pulmonary embolism: outcome, clinical, and laboratory assessment.Chest1995;107,931-935. [PubMed]
 
van Beek, EJ, Kuijer, PM, Buller, HR, et al The clinical course of patients with suspected pulmonary embolism.Arch Intern Med1997;157,2593-2598. [PubMed]
 
Gottsater, A, Berg, A, Centergard, J, et al Clinically suspected pulmonary embolism: is it safe to withhold anticoagulation after a negative spiral CT?Eur Radiol2001;11,65-72. [PubMed]
 
Swensen, SJ, Sheedy, PF, II, Ryu, JH, et al Outcomes after withholding anticoagulation from patients with suspected acute pulmonary embolism and negative computed tomographic findings: a cohort study.Mayo Clin Proc2002;77,130-138. [PubMed]
 
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Figures

Tables

Table Graphic Jump Location
Table 1. Causes of Previously Known Cardiac and Respiratory Diseases in the Population Studied and Evaluation of the Cardiopulmonary Reserve
Table Graphic Jump Location
Table 2. Results of Tests in the Population Studied*
* 

Data are presented as No. (%).

 

d-Dimer test results were positive when > 500 ng/mL.

Table Graphic Jump Location
Table 3. Results of Death and Critical Events During Follow-up in the Whole Population*
* 

Data are presented as No. (%).

References

Quinn, DA, Thompson, BT, Terrin, ML, et al (1992) A prospective investigation of pulmonary embolism in women and men.JAMA268,1689-1696. [PubMed] [CrossRef]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Goldhaber, SZ Pulmonary embolism.N Engl J Med1998;339,93-104. [PubMed]
 
Perrier, A, Bounameaux, H, Morabia, A, et al Diagnosis of pulmonary embolism by a decision analysis-based strategy including clinical probability, D-dimer levels, and ultrasonography: a management study.Arch Intern Med1996;156,531-536. [PubMed]
 
Ferretti, GR, Bosson, JL, Bullaz, PD Acute pulmonary embolism: role of helical HCT in 164 patients with intermediate probability at ventilation-perfusion scintigraphy and normal results at duplex US of the legs.Radiology1997;205,453-458. [PubMed]
 
Carson, JL, Terrin, ML, Duff, A, et al Pulmonary embolism and mortality in patients with COPD.Chest1996;110,1212-1219. [PubMed]
 
Rémy-Jardin, M, Remy, J, Wattinne, L, et al Central pulmonary thromboembolism: diagnosis with helical volumetric CT with the single-breath-hold technique; comparison with pulmonary angiography.Radiology1992;185,381-387. [PubMed]
 
Garg, K, Welsh, CH, Feyerabend, AJ, et al Pulmonary embolism: diagnosis with spiral CT and ventilation-perfusion scanning; correlation with pulmonary angiographic results or clinical outcome.Radiology1998;208,201-208. [PubMed]
 
Mayo, JR, Rémy-Jardin, M, Muller, NL Pulmonary embolism: prospective comparison of spiral helical CT with ventilation-perfusion scintigraphy.Radiology1997;205,445-452
 
Rémy-Jardin, M, Remy, J, Deschildre, F, et al Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography.Radiology1996;200,699-706. [PubMed]
 
Rathbun, SW, Raskob, GE, Whitsett, TL Sensitivity and specificity of helical computed tomography in the diagnosis of pulmonary embolism: a systematic review.Ann Intern Med2000;132,227-232. [PubMed]
 
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