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• W2044334576 abstract "SummaryBackground: A number of variables have been evaluated for risk stratification in patients with acute pulmonary embolism (PE). Whereas increased D‐dimer levels have been associated with mortality at 3 months, its role in predicting short‐term outcome (the period of time during which any therapeutic decision has to be taken) remains unclear. Methods: RIETE is an ongoing, prospective registry of consecutive patients with acute venous thromboembolism. We assessed the prognostic value of D‐dimer levels at baseline, measured with an automated latex agglutination test (IL Test D‐dimer®), on the 15‐day outcome in patients with acute PE. Overall mortality, fatal PE and major bleeding rates were compared by quartile. Results: As of February 2008, 1707 patients with acute PE underwent D‐dimer testing. Of these, 72 patients (4.2%) died during the first 15 days, 11 (0.6%) had recurrent PE, and 29 (1.7%) had major bleeding. Overall mortality increased with increasing D‐dimer levels, from 2.7% in the first quartile (< 1050 ng mL−1) to 7.0% in the fourth quartile (≥ 4200 ng mL−1). The rates of fatal PE and major bleeding also increased. On multivariate analysis, patients with D‐dimer levels in the fourth quartile had an increased risk for overall death (odds ratio, 1.8; 95% CI, 1.1–3.2), fatal PE (odds ratio, 2.0; 95% CI, 1.0–3.8) or major bleeding (odds ratio, 3.2; 95% CI, 1.5–7.0). Conclusions: PE patients with D‐dimer levels in the fourth quartile had an increased incidence of overall death, fatal PE and major bleeding within 15 days both before and after multivariate adjustment. Background: A number of variables have been evaluated for risk stratification in patients with acute pulmonary embolism (PE). Whereas increased D‐dimer levels have been associated with mortality at 3 months, its role in predicting short‐term outcome (the period of time during which any therapeutic decision has to be taken) remains unclear. Methods: RIETE is an ongoing, prospective registry of consecutive patients with acute venous thromboembolism. We assessed the prognostic value of D‐dimer levels at baseline, measured with an automated latex agglutination test (IL Test D‐dimer®), on the 15‐day outcome in patients with acute PE. Overall mortality, fatal PE and major bleeding rates were compared by quartile. Results: As of February 2008, 1707 patients with acute PE underwent D‐dimer testing. Of these, 72 patients (4.2%) died during the first 15 days, 11 (0.6%) had recurrent PE, and 29 (1.7%) had major bleeding. Overall mortality increased with increasing D‐dimer levels, from 2.7% in the first quartile (< 1050 ng mL−1) to 7.0% in the fourth quartile (≥ 4200 ng mL−1). The rates of fatal PE and major bleeding also increased. On multivariate analysis, patients with D‐dimer levels in the fourth quartile had an increased risk for overall death (odds ratio, 1.8; 95% CI, 1.1–3.2), fatal PE (odds ratio, 2.0; 95% CI, 1.0–3.8) or major bleeding (odds ratio, 3.2; 95% CI, 1.5–7.0). Conclusions: PE patients with D‐dimer levels in the fourth quartile had an increased incidence of overall death, fatal PE and major bleeding within 15 days both before and after multivariate adjustment. The use of thrombolysis and the selection of acute pulmonary embolism (PE) patients for outpatient therapy are controversial issues. There is growing evidence that outpatient therapy with low‐molecular‐weight heparin (LMWH) is effective and safe for many patients with PE [1Wells P.S. Kovacs M.J. Bormanis J. Forgie M.A. Goudie D. Morrow B. Kovacs J. Expanding eligibility for outpatient treatment of deep venous thrombosis and pulmonary embolism with low‐molecular‐weight heparin: a comparison of patient self‐injection with homecare injection.Arch Intern Med. 1998; 158: 1809-12Crossref PubMed Scopus (302) Google Scholar, 2Wells P.S. Anderson D.R. Rodger M.A. Florack P. Touchie D. Morrow B. Gray L. O'Rourke K. Wells G. Kovacs J. Kovacs M.J. A randomized trial comparing 2 low‐molecular‐weight heparins for the outpatient treatment of deep vein thrombosis and pulmonary embolism.Arch Intern Med. 2005; 165: 733-8Crossref PubMed Scopus (160) Google Scholar]. Conversely, the benefit of early thrombolysis or other aggressive therapies over heparin appears to only be clear in those patients with a high risk of death during hospital stay [3Konstantinides S. Geibel A. Heusel G. Heinrich F. Kasper W. for the Management Strategies and Prognosis of Pulmonary Embolism‐3 Trial InvestigatorsHeparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism.N Engl J Med. 2002; 347: 1143-50Crossref PubMed Scopus (886) Google Scholar, 4Dalen J.E. The uncertain role of thrombolytic therapy in the treatment of pulmonary embolism.Arch Intern Med. 2002; 162: 2521-3Crossref PubMed Scopus (26) Google Scholar, 5Agnelli G. Becattini C. Kirschtein T. Thrombolysis vs heparin in the treatment of pulmonary embolism. A clinical outcome‐based meta‐analysis.Arch Intern Med. 2002; 162: 2537-41Crossref PubMed Scopus (133) Google Scholar, 6Goldhaber S.Z. Elliott G. Acute pulmonary embolism: Part II. Risk stratification, treatment, and prevention.Circulation. 2003; 108: 2834-8Crossref PubMed Scopus (114) Google Scholar, 7Wan S. Quinlan D.J. Agnelli G. Eikelboom J.W. Thrombolysis compared with heparin for the initial treatment of pulmonary embolism. A meta‐analysis of the randomized controlled trials.Circulation. 2004; 110: 744-9Crossref PubMed Scopus (517) Google Scholar, 8Kearon C. Kahn S.R. Agnelli G. Goldhaber S. Raskob G.E. Comerota A.J. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians evidence‐based clinical practice guidelines (8th edition).Chest. 2008; 133: 454S-545SAbstract Full Text Full Text PDF PubMed Scopus (1872) Google Scholar, 9Torbicki A. Perrier A. Konstantinides S. Agnelli G. Galiè N. Pruszczyk P. Bengal F. Brady A.J. Ferreira D. Janssens U. Klepetko W. Mayer E. Remy‐Jardin M. Bassand J.P. Vahanian A. Camm J. De Caterina R. Dean V. Dickstein K. Filippatos G. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).Eur Heart J. 2008; 29: 2276-315Crossref PubMed Scopus (8) Google Scholar]. However, because thrombolytic therapy doubles the risk of major bleeding [7Wan S. Quinlan D.J. Agnelli G. Eikelboom J.W. Thrombolysis compared with heparin for the initial treatment of pulmonary embolism. A meta‐analysis of the randomized controlled trials.Circulation. 2004; 110: 744-9Crossref PubMed Scopus (517) Google Scholar], careful and simple risk assessment is paramount in the selection of the appropriate treatment strategy for high‐risk patients. A number of clinical models, including serum cardiac biomarkers, echocardiography and chest computed tomography (CT) have been evaluated for risk stratification, but have given conflicting results [10Kucher N. Printzen G. Doernhoefer T. Windecker S. Meier B. Kess O.M. Low pro‐brain natriuretic peptide levels predict benign clinical outcome in acute pulmonary embolism.Circulation. 2003; 107: 1576-8Crossref PubMed Scopus (235) Google Scholar, 11Aujesky D. Obrosky D.S. Stone R.A. Auble T.E. Perrier A. Cornuz J. Roy P.M. Fine M.J. Derivation and validation of a prognostic model for pulmonary embolism.Am J Respir Crit Care Med. 2005; 172: 1041-6Crossref PubMed Scopus (820) Google Scholar, 12Kucher N. Rossi E. De Rosa M. Goldhaber S.Z. Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher.Arch Intern Med. 2005; 165: 1777-81Crossref PubMed Scopus (346) Google Scholar, 13Schoepf U.J. Kucher N. Kipfmueller F. Quiroz R. Costello P. Goldhaber S.Z. Right ventricular enlargement on chest computed tomography. A predictor of early death in acute pulmonary embolism.Circulation. 2004; 110: 3276-80Crossref PubMed Scopus (457) Google Scholar, 14Lobo J.L. Zorrilla V. Aizpuru F. Uresandi F. García‐Bragado F. Conget F. Monreal M. Clinical syndromes and clinical outcome in patients with pulmonary embolism. Findings of the RIETE registry.Chest. 2006; 130: 1817-22Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar, 15Otero R. Trujillo‐Santos J. Cayuela A. Rodríguez C. Barron M. Martín J.J. Monreal M. Haemodinamically unstable pulmonary embolism in the RIETE Registry: systolic blood pressure or shock index?.Eur Respir J. 2007; 30: 1111-6Crossref PubMed Scopus (53) Google Scholar, 16Greco F. Porto I. Clinical usefulness of cardiac biomarkers in hemodinamically stable pulmonary embolism.J Thromb Haemost. 2006; 4: 550-1Crossref PubMed Scopus (2) Google Scholar, 17Stein P.D. Beemath A. Matta F. Goodman L.R. Weg J.G. Hales C.A. Hull R.D. Leeper K.V. Sostman H.D. Woodard P.K. Enlarged right ventricle without shock in acute pulmonary embolism: prognosis.Am J Med. 2008; 121: 34-42Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar, 18Kline J.A. Zeitouni R. Marchick M.R. Hernandez‐Nino J. Rose G.A. Comparison of 8 biomarkers for prediction of right ventricular hypokinesis 6 months after submassive pulmonary embolism.Am Heart J. 2008; 156: 308-14Crossref PubMed Scopus (45) Google Scholar, 19Sanchez O. Trinquart L. Colombet I. Durieux P. Huisman M.V. Chatelier G. Meyer G. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism : a systematic review.Eur Heart J. 2008; 29: 1569-77Crossref PubMed Scopus (410) Google Scholar]. Increased D‐dimer levels at baseline in patients with PE have been associated with thrombus extension and increased mortality at 3 months [20Aujesky D. Roy P.M. Meyer G. Cornuz J. Sanchez O. Perrier A. Prognostic value of D‐dimer in patients with pulmonary embolism.Thromb Haemost. 2006; 96: 478-82Crossref PubMed Scopus (87) Google Scholar, 21Grau E. Tenías J.M. Soto M.J. Gutierrez M.R. Lecumberri R. Pérez J.L. Tiberio G. for the RIETE InvestigatorsD‐Dimer levels correlate with mortality in patients with acute pulmonary embolism. Findings from the RIETE Registry.Crit Care Med. 2007; 35: 1937-41Crossref PubMed Scopus (56) Google Scholar, 22Klok F.A. Djurabi R.K. Nijkeuter M. Eikenboom H.C. Leebeek F.W. Kramer M.H. Kaasjager K. Kamphuisen P.W. Büller H.R. Huisman M.V. High D‐dimer level is associated with increased 15‐d and 3 months mortality through a more central localization of pulmonary emboli and serious comorbidity.Br J Hematol. 2008; 140: 218-22PubMed Google Scholar, 23De Monye W. Sanson B.J. Mac Gillavry M.R. Pattynama P.M.T. Büller H.R. Van Den Berg‐Huysmans A.A. Huisman M.V. on behalf of the ANTELOPE‐Study groupEmbolus location affects the sensitivity of a rapid quantitative D‐dimer assay in the diagnosis of pulmonary embolism.Am J Respir Crit Care Med. 2002; 165: 345-8Crossref PubMed Scopus (98) Google Scholar, 24Galle C. Papazyan J.P. Miron M.J. Solsman D. Bounameaux H. Perrier A. Prediction of pulmonary embolism extent by clinical findings, D‐dimer level and deep vein thrombosis shown by ultrasound.Thromb Haemost. 2001; 86: 1156-60Crossref PubMed Scopus (75) Google Scholar, 25Ghanima W. Abdelnoor M. Holmen L.O. Nielssen B.E. Ross S. Sandset P.M. D‐dimer level is associated with the extent of pulmonary embolism.Thromb Res. 2007; 120: 281-8Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar, 26Hochuli M. Duewell S. Frauchiger B. Quantitative d‐dimer levels and the extent of venous thromboembolism in CT angiography and lower limb ultrasonography.Vasa. 2007; 36: 267-74Crossref PubMed Scopus (29) Google Scholar], but its ability to predict short‐term outcome remains unclear. The RIETE (Registro Informatizado de Enfermedad TromboEmbólica) initiative is an ongoing, multicenter, international (Spain, France, Italy, Israel and Brazil) observational registry, designed to gather data on the clinical characteristics, treatment patterns and outcome in consecutive patients with symptomatic, objectively confirmed, acute venous thromboembolism [14Lobo J.L. Zorrilla V. Aizpuru F. Uresandi F. García‐Bragado F. Conget F. Monreal M. Clinical syndromes and clinical outcome in patients with pulmonary embolism. Findings of the RIETE registry.Chest. 2006; 130: 1817-22Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar, 15Otero R. Trujillo‐Santos J. Cayuela A. Rodríguez C. Barron M. Martín J.J. Monreal M. Haemodinamically unstable pulmonary embolism in the RIETE Registry: systolic blood pressure or shock index?.Eur Respir J. 2007; 30: 1111-6Crossref PubMed Scopus (53) Google Scholar]. The aim of the present study was to assess the predictive value of D‐dimer levels measured at baseline for the 15‐day outcome in a series of consecutive patients with acute PE. The study population includes consecutive patients with symptomatic PE, confirmed by objective tests (pulmonary angiography, lung scintigraphy or helical CT), that underwent testing with a turbidimetric immunoassay test (IL Test D‐dimer®, Instrumental Laboratory SpA, Milano, Italy) at baseline [27Hlavac M. Cook J. Ojala R. Town I. Beckert L. Latex‐enhanced immunoassay d‐dimer and blood gases can exclude pulmonary embolism in low‐risk patients presenting to an acute care setting.Chest. 2005; 128: 2183-9Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar]. Blood specimens were obtained by phlebotomy prior to starting treatment with anticoagulants or thrombolytic agents. Patients with no D‐dimer testing and those with D‐dimer performed by other assays were excluded. Patients were also excluded if they were currently participating in a therapeutic clinical trial. All patients provided oral consent to their participation in the registry, according to the requirements of the Ethics Committee within each hospital. The therapeutic approach was the decision of the attending physician. Patients were divided into quartiles according to their D‐dimer levels at baseline, and their event rates within 15 days of PE diagnosis were compared by quartile (Table S1). The major outcome was overall mortality; secondary outcomes were fatal PE and major bleeding. Causes of death were determined by the attending physicians. In case of doubt, they addressed the case‐report to the Adjudication Committee of the RIETE Registry. Fatal PE, in the absence of autopsy, was defined as any death appearing shortly after PE diagnosis, in the absence of any alternative cause of death. Bleeding complications were classified as ‘major’ if they were overt and required a transfusion of two or more units of blood, or were retroperitoneal, spinal or intracranial, or were fatal. The following parameters were recorded: patient’s baseline characteristics; clinical status, including any coexisting or underlying conditions such as chronic heart or lung disease; risk factors for PE; the type and dose of treatment received upon PE diagnosis; and the outcome during the first 15 days. Immobilized patients were defined in this analysis as non‐surgical patients who had been immobilized (i.e. total bed rest with bathroom privileges) for ≥ 4 days in the 2‐month period prior to PE diagnosis. Surgical patients were defined as those who had undergone an operation in the 2 months prior to VTE diagnosis. The attending physicians ensured that eligible patients were consecutively enrolled. Data were recorded on to a computer‐based case report form at each participating hospital and submitted to a centralized coordinating centre through a secure website. Encryption of data was used to enhance confidentiality and security. Data quality was regularly monitored and documented electronically to detect inconsistencies or errors, which were resolved by the local coordinators. Data quality was also monitored by periodic visits to participating hospitals, by contract research organizations that compare the medical records with the data in the web. A data audit was performed at periodic intervals. Patient identities remain confidential as they are identified by a unique number assigned by the study coordinating centre responsible for all data management. Odds ratios and corresponding 95% confidence intervals (CI) were calculated for categorical variables. First, the influence of a number of variables on the risk of overall death, fatal PE or major bleeding was tested by a chi‐square test for categorical variables, and Student’s t‐test for continuous variables. A P‐value < 0.05 was considered statistically significant. Candidate variables were selected from clinical variables based on published literature. To measure predictors of outcome, a multivariate analysis was carried out using a forward stepwise logistic regression analysis. Significance level of P < 0.10 was considered to include variables and P > 0.15 to exclude variables in the final multivariate model. D‐dimer levels entered in the model dichotomized as quartile 4 vs. quartile 1–3. Finally, to assess the accuracy of predicting mortality, we assessed the sensitivity, specificity, positive and negative predictive values. All analyses were completed with the Statistical Package for Social Sciences (spss) program (version 16.0 for Windows, 2008; SPSS Inc., Chicago, Illinois, USA). As of February 2008, 10293 consecutive patients with symptomatic PE had been enrolled in RIETE. Of these, 1707 (17%) underwent D‐dimer testing using the IL Test D‐dimer® (and were included in the study), 5876 (57%) underwent testing with other reagents, and 2710 (26%) were not tested. Fewer patients that underwent D‐dimer testing had chronic lung disease, recent immobility, cancer, atrial fibrillation, fatal bleeding, fatal PE or overall death than those patients that were not tested (Table 1). There were no significant differences in baseline characteristics or outcomes between patients tested with the IL Test D‐dimer® or with other reagents.Table 1Clinical characteristics, therapeutic strategies and outcome in all patients with acute PE, according to D‐dimer testing at baselineD‐dimer IL‐testD‐dimer, other reagentsNo D‐dimer testingPatients, n170758762710Clinical characteristics Gender (male) 765 (45%)2664 (45%)1274 (47%) Mean age (years ± SD) 70 ± 15 68 ± 17‡ 68 ± 16PE characteristics Systolic BP < 100 mmHg 138 (8.1%) 420 (7.1%) 212 (7.8%) Arterial PO2 < 60 mmHg 547 (42%)1913 (41%) 830 (43%)15‐day outcome Major bleeding 29 (1.7%) 105 (1.8%) 54 (2.0%) Recurrent PE 9 (0.5%) 37 (0.6%) 28 (1.0%)* Fatal, initial PE 36 (2.1%) 131 (2.2%) 79 (2.9%)* Fatal, recurrent PE 3 (0.2%) 25 (0.4%) 8 (0.3%) Overall death 72 (4.2%) 244 (4.2%) 182 (6.7%)‡Comparisons between patients: *P < 0.05; †P < 0.01; ‡P < 0.001.Patients with D‐dimer tested with IL‐test were compared with those tested with other reagents. Patients not tested were compared with those tested.SD, standard deviation; VTE, venous thromboembolism; BP, blood pressure; PE, pulmonary embolism. Open table in a new tab Comparisons between patients: *P < 0.05; †P < 0.01; ‡P < 0.001. Patients with D‐dimer tested with IL‐test were compared with those tested with other reagents. Patients not tested were compared with those tested. SD, standard deviation; VTE, venous thromboembolism; BP, blood pressure; PE, pulmonary embolism. The study population included 765 males and 942 females, aged 14–99 years (mean, 70 years). PE diagnosis was confirmed in 1294 patients (75.8%) with a positive CT scan, in 369 (21.6%) with a high‐probability ventilation‐perfusion lung scan, and in 44 (2.6%) with intermediate‐probability lung scan plus evidence of deep vein thrombosis in the lower limbs. Seventy‐two patients (4.2%) died during the first 15 days. Of these, 36 (50%) died of the initial PE, three (4.2%) died of recurrent PE, and one patient died of bleeding. Twenty‐nine patients (1.7%) had major bleeding (six had fatal bleeding) but only one of these died during the 15‐day study period. Overall mortality increased with increasing D‐dimer levels, from 2.7% in the first quartile (< 1050 ng mL−1) to 7.0% in the fourth quartile (≥ 4200 ng mL−1). The rates of fatal PE and major bleeding also increased with increasing D‐dimer levels (Table 2). Patient age, heart rate, hypoxemia, abnormal creatinine levels, and the use of thrombolytic therapy also increased with increasing D‐dimer levels (Table 2).Table 2Clinical characteristics, therapeutic strategies and outcome in 1707 patients with acute PE, according to their D‐dimer levels at baseline1st quartile2nd quartile3rd quartile4rth quartileP trendPatients, n 413 440 428426 D‐dimer levels (ng mL−1)< 1050 1050–2150 2151–4199≥ 4200Clinical characteristics Gender (males) 204 (49%) 197 (45%) 186 (44%) 178 (42%)0.027 Mean age (years ± SD) 66 ± 16 70 ± 15 70 ± 15 74 ± 12< 0.001 Body weight (kg ± SD) 74 ± 14 75 ± 14 74 ± 16 73 ± 12N.S.Underlying conditions Chronic lung disease 47 (12%) 64 (15%) 45 (11%) 38 (9.2%)N.S. Chronic heart failure 31 (7.9%) 31 (7.4%) 25 (6.1%) 26 (6.3%)N.S. Creatinine levels > 1.2 mg dL−1 65 (16%) 91 (21%) 81 (19%) 113 (27%)0.001Risk factors Postoperative 59 (14%) 52 (12%) 64 (15%) 42 (9.9%)N.S. Immobility ≥ 4 days 94 (23%) 116 (26%) 105 (25%) 125 (29%)N.S. Cancer 72 (17%) 84 (19%) 79 (18%) 96 (23%)N.S. Idiopathic (none of the above) 174 (42%) 180 (41%) 173 (40%) 163 (38%)N.S. Prior VTE 56 (14%) 74 (17%) 59 (14%) 56 (13%)N.S.PE characteristics Systolic BP < 100 mmHg 22 (5.3%) 43 (9.8%) 32 (7.5%) 41 (9.6%)N.S. Heart rate > 100 bpm 84 (21%) 144 (33%) 145 (34%) 159 (37%)< 0.001 Atrial fibrillation 33 (8.7%) 36 (8.9%) 44 (11%) 49 (12%)N.S. PO2 < 60 mmHg (n = 1292) 111 (36%) 147 (43%) 122 (38%) 167 (51%)0.002Treatment Initial therapy, LMWH 391 (95%) 399 (91%) 396 (92%) 398 (93%))N.S. Median LMWH dose (IU d−1) 142611486614324 14243N.S. Thrombolytics 5 (1.2%) 7 (1.6%) 14 (3.3%) 15 (3.5%)0.010 Inferior vena cava filter 4 (1.0%) 5 (1.1%) 3 (0.7%) 11 (2.6%)N.S.15‐day outcome Major bleeding 4 (1.0%) 2 (0.5%) 8 (1.9%) 15 (3.5%)0.001 Fatal bleeding 2 (0.5%) 0 1 (0.2%) 3 (0.7%)N.S. Recurrent PE 3 (0.7%) 0 4 (0.9%) 4 (0.9%)N.S. Fatal, initial PE 4 (1.0%) 8 (1.8%) 7 (1.6%) 17 (4.0%)0.005 Fatal, recurrent PE 1 (0.2%) 0 2 (0.5%) 0N.S. Overall death 11 (2.7%) 15 (3.4%) 16 (3.7%) 30 (7.0%)0.002SD, standard deviation; VTE, venous thromboembolism; BP, blood pressure; PE, pulmonary embolism; LMWH, low‐molecular‐weight heparin. Open table in a new tab SD, standard deviation; VTE, venous thromboembolism; BP, blood pressure; PE, pulmonary embolism; LMWH, low‐molecular‐weight heparin. On univariate analysis, female patients and those with chronic heart failure, abnormal creatinine levels, recent immobility, cancer, hypotension, tachycardia, atrial fibrillation and D‐dimer levels in the fourth quartile had an increased 15‐day mortality, while those with idiopathic PE had a lower death rate (Table 3). Female patients and those with abnormal creatinine levels, immobility, hypotension, tachycardia or D‐dimer levels in the fourth quartile also had an increased incidence of fatal PE, while those with idiopathic PE had a lower rate. Finally, female patients, or those aged > 70 years, with chronic heart failure, abnormal creatinine levels or D‐dimer levels in the fourth quartile had an increased incidence of major bleeding (Table 4). Multivariate analysis confirmed that patients with D‐dimer levels in the fourth quartile had an increased risk for overall death (odds ratio, 1.8; 95% CI, 1.1–3.2), fatal PE (odds ratio, 2.0; 95% CI, 1.0–3.8) or major bleeding (odds ratio, 3.2; 95% CI, 1.5–7.0), as shown in Table 5. After excluding those patients that received thrombolytic therapy or a vena cava filter, the odds ratios were: 1.8 (95% CI, 1.1–3.2) and 2.2 (95% CI, 1.1–4.3), respectively.Table 3Univariate analysis of the risk for overall death or fatal PEOverall deathFatal PEYesNoOdds ratio (95% CI)YesNoOdds ratio (95% CI)Patients, n 72 1635 39 1668Clinical characteristics Age > 70 years 49 (68%) 984 (60%)1.4 (0.9–2.3) 25 (64%) 1008 (60%)1.2 (0.6–2.3) Gender (males) 23 (32%) 742 (45%)0.6 (0.3–0.9) 10 (26%) 755 (45%)0.4 (0.2–0.9) Body weight < 60 kg 11 (15%) 179 (11%)1.5 (0.7–2.8) 3 (7.7%) 187 (11%)0.7 (0.2–2.2)Underlying conditions Chronic lung disease 9 (13%) 185 (12%)1.1 (0.5–2.3) 6 (17%) 188 (12%)1.5 (0.6–3.7) Chronic heart failure 9 (13%) 104 (6.6%)2.1 (1.0–4.4) 5 (14%) 108 (6.7%)2.2 (0.8–5.8) Creatinine levels > 1.2 mg dL−1 28 (39%) 322 (20%)2.6 (1.6–4.2) 13 (33%) 337 (20%)2.0 (1.0–3.9)Risk factors Postoperative 6 (8.3%) 211 (13%)0.6 (0.3–1.4) 3 (7.7%) 214 (13%)0.6 (0.2–1.8) Immobility ≥ 4 days 36 (50%) 404 (25%)3.0 (1.9–4.9) 22 (56%) 418 (25%)3.9 (2.0–7.3) Cancer 29 (40%) 302 (18%)3.0 (1.8–4.8) 12 (31%) 319 (19%)1.9 (0.9–3.7) Idiopathic 13 (18%) 677 (41%)0.3 (0.2–0.6) 6 (15%) 684 (41%)0.3 (0.1–0.6) Prior VTE 5 (7%) 240 (15%)0.4 (0.2–1.1) 4 (10%) 241 (14%)0.7 (0.2–1.9)PE characteristics SBP < 100 mmHg 13 (18%) 125 (7.6%)2.7 (1.4–5.0) 9 (23%) 129 (7.7%)3.6 (1.7–7.7) Heart rate > 100 bpm 38 (53%) 494 (30%)2.6 (1.6–4.2) 20 (51%) 512 (31%)2.3 (1.2–4.4) Atrial fibrillation 16 (25%) 146 (9.6%)3.1 (1.7–5.7) 7 (19%) 155 (10%)2.2 (0.9–5.0) PO2 < 60 mmHg (n = 1292) 26 (46%) 521 (42%)1.2 (0.7–2.0) 13 (39%) 534 (42%)0.9 (0.4–1.8)Treatment Initial therapy, LMWH 52 (74%) 1532 (94%)0.2 (0.1–0.3) 25 (67%) 1559 (93%)0.1 (0.07–0.3) Mean LMWH dose (IU/kg/d)1278213788P = 0.0051327513762P = NS Thrombolytic therapy 5 (7%) 36 (2%)3.3 (1.3–8.7) 4 (10%) 37 (2%)5.0 (1.7–14.9) Inferior vena cava filter 1 (1.4%) 22 (1.3%)1.0 (0.1–7.2) 0 23 (1.4%)0.98 (0.97–0.99)D‐dimer levels (ng mL−1) 1st quartile (< 1050) 11 (15%) 402 (25%)1.0 5 (19%) 408 (24%)1.0 2nd quartile (1050–2150) 15 (21%) 425 (26%)1.3 (0.6–2.8) 8 (20%) 432 (26%)1.5 (0.5–4.7) 3rd quartile (2151–4219) 16 (22%) 412 (25%)1.4 (0.7–3.1) 9 (23%) 419 (25%)1.8 (0.6–5.3) 4th quartile (≥ 4200) 30 (42%) 396 (24%)2.8 (1.4–5.6) 17 (44%) 409 (24%)3.4 (1.2–9.3)SD, standard deviation; VTE, venous thromboembolism; SBP, systolic blood pressure; bpm, beats per minute; LMWH, low‐molecular‐weight heparin; PE, pulmonary embolism; CI, confidence intervals. Open table in a new tab Table 4Multivariate analysis of the risk for overall death, fatal PE or major bleeding in the 1707 patients with acute PEOdds ratio (95% CI)P valueOverall death Gender (females)2.0 (1.1–3.3)0.026 Creatinine levels > 1.2 mg dL−12.7 (1.5–4.9)0.001 Immobility ≥ 4 days2.9 (1.7–5.1)< 0.001 Cancer3.8 (2.1–6.8)< 0.001 Systolic blood pressure < 100 mmHg2.2 (1.1–4.5)0.035 Heart rate > 100 beats per minute2.1 (1.2–3.7)0.008 Atrial fibrillation2.5 (1.3–4.8)0.007 D‐dimer, 4th quartile (≥ 4200 ng mL−1)1.8 (1.1–3.2)0.032Fatal PE Gender (females)2.0 (1.0–4.8)0.043 Immobility ≥ 4 days3.2 (1.7–6.2)< 0.001 Systolic blood pressure < 100 mmHg2.5 (1.1–5.6)0.025 D‐dimer, 4th quartile (≥ 4200 ng mL−1)2.0 (1.0–3.8)0.044Major bleeding Gender (females)2.5 (1.0–5.0)0.061 Creatinine levels > 1.2 mg dL−12.0 (0.9–4.3)0.095 Thrombolytic therapy6.7 (2.2–20)0.001 D‐dimer, 4th quartile (≥ 4200 ng mL−1)3.2 (1.5–7.0)0.002PE, pulmonary embolism; SBP, systolic blood pressure; CI, confidence intervals. Open table in a new tab Table 5Univariate analysis of the risk for developing major bleeding in 1707 patients with acute PEYesNoOdds ratio (95% CI)Patients, n 29 1678Clinical characteristics Age > 70 years 23 (79%) 1010 (60%)2.5 (1.0–6.2) Gender (males) 9 (31%) 756 (45%)0.5 (0.2–1.2) Body weight < 60 kg 6 (21%) 184 (11%)2.1 (0.8–5.3)Underlying conditions Chronic lung disease 1 (3.4%) 193 (12%)0.3 (0.04–2.0) Chronic heart failure 6 (21%) 107 (6.6%)3.8 (1.5–9.6) Creatinine levels > 1.2 mg dL−1 11 (38%) 339 (20%)2.4 (1.1–5.1)Risk factors Postoperative 4 (14%) 213 (13%)1.1 (0.4–3.2) Immobility ≥ 4 days 11 (38%) 429 (26%)1.8 (0.8–3.8) Cancer 7 (24%) 324 (19%)1.3 (0.6–3.1) Prior VTE 3 (10%) 242 (14%)0.7 (0.2–2.3) None of the above 9 (31%) 681 (41%)0.6 (0.3–1.4)PE characteristics SBP < 100 mmHg 3 (10%) 135 (8.0%)1.3 (0.4–4.4) Heart rate > 100 bpm 10 (34%) 522 (31%)1.1 (0.5–2.5) Atrial fibrillation 2 (6.9%) 160 (10%)0.7 (0.2–3.0) PO2 < 60 mmHg (n = 1292) 13 (52%) 534 (42%)1.5 (0.7–3.3)Treatment Thrombolytic 4 (14%) 37 (2.2%)7.1 (2.3–21.4) Initial therapy, LMWH 23 (79%) 1561 (93%)0.3 (0.1–0.7) Mean LMWH dose (IU/kg/d)1331813767P = N.S. Inferior vena cava filter 5 (17%) 18 (1.1%)19 (6.6–56)D‐dimer levels (ng mL−1) 1st quartile (< 1050) 4 (14%) 409 (24%)1 2nd quartile (1050–2150) 2 (6.9%) 438 (26%)0.5 (0.1–2.6) 3rd quartile (2151–4200) 8 (28%) 420 (25%)1.9 (0.6–6.5) 4th quartile (≥ 4200) 15 (52%) 411 (24%)3.7 (1.2–11)VTE, venous thromboembolism; SBP, systolic blood pressure; bpm, beats per minute; LMWH, low‐molecular‐weight heparin; CI, confidence intervals. Open table in a new tab SD, standard deviation; VTE, venous thromboembolism; SBP, systolic blood pressure; bpm, beats per minute; LMWH, low‐molecular‐weight heparin; PE, pulmonary embolism; CI, confidence intervals. PE, pulmonary embolism; SBP, systolic blood pressure; CI, confidence intervals. VTE, venous thromboembolism; SBP, systolic blood pressure; bpm, beats per minute; LMWH, low‐molecular‐weight heparin; CI, confidence intervals. The sensitivity, specificity, positive predictive value and negative predictive value for predicting overall death in patients with D‐dimer levels in the fourth quar" @default.
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• W2044334576 title "D‐dimer levels and 15‐day outcome in acute pulmonary embolism. Findings from the RIETE Registry" @default.
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