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Table 1. 
Incidence of Venous Thromboembolism (Days 1-14) by Reason of Illness
Incidence of Venous Thromboembolism (Days 1-14) by Reason of Illness
Table 2. 
Frequency of Risk Factors and Venous Thromboembolism (VTE) in All 866 Patients (Days 1-14)
Frequency of Risk Factors and Venous Thromboembolism (VTE) in All 866 Patients (Days 1-14)
Table 3. 
Univariate Logistic Analysis of Potential Risk Factors for Definite Venous Thromboembolism (VTE) in the MEDENOX5 Study Population
Univariate Logistic Analysis of Potential Risk Factors for Definite Venous Thromboembolism (VTE) in the MEDENOX5 Study Population
Table 4. 
Univariate Logistic Analysis of the Relationship Between Acute Medical Illness and Risk of Venous Thromboembolism in All 866 Patients
Univariate Logistic Analysis of the Relationship Between Acute Medical Illness and Risk of Venous Thromboembolism in All 866 Patients
Table 5. 
Univariate Logistic Analysis of Potential Risk Factors for Definite Venous Thromboembolism (VTE) Among the 575 Patients Receiving Placebo or Ineffective Antithrombotic Therapy
Univariate Logistic Analysis of Potential Risk Factors for Definite Venous Thromboembolism (VTE) Among the 575 Patients Receiving Placebo or Ineffective Antithrombotic Therapy
Table 6. 
Univariate Logistic Analysis of the Relationship Between Acute Medical Illness and Definite Venous Thromboembolism Among the 575 Patients Receiving Placebo or Ineffective Antithrombotic Therapy
Univariate Logistic Analysis of the Relationship Between Acute Medical Illness and Definite Venous Thromboembolism Among the 575 Patients Receiving Placebo or Ineffective Antithrombotic Therapy
Table 7. 
Multivariate Logistic Regression Model for Definite Venous Thromboembolism (VTE)
Multivariate Logistic Regression Model for Definite Venous Thromboembolism (VTE)
Table 8. 
Venous Thromboembolic (VTE) Events During the Treatment Period by Number of Risk Factors
Venous Thromboembolic (VTE) Events During the Treatment Period by Number of Risk Factors
1.
Geerts  WHHeit  JAClagett  GP  et al.  Prevention of venous thromboembolism. Chest. 2001;119(suppl)132S- 175S
PubMedArticle
2.
Goldhaber  SZ Venous thromboembolism prophylaxis in medical patients. Thromb Haemost. 1999;82899- 901
PubMed
3.
Sandler  DAMartin  JF Autopsy proven pulmonary embolism in hospital patients: are we detecting enough deep vein thrombosis? J R Soc Med. 1989;82203- 205
PubMed
4.
Hampton  KK Thromboprophylaxis in medical patients. Hosp Med. 2000;61656- 659
PubMedArticle
5.
Samama  MMCohen  ATDarmon  JY  et al.  A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients: Prophylaxis in Medical Patients With Enoxaparin Study Group. N Engl J Med. 1999;341793- 800
PubMedArticle
6.
Kleber  FXWitt  CVogel  GKoppenhagen  KFlosbach  CWfor THE-PRINCE Study Group, Randomized comparison of enoxaparin with unfractionated heparin for the prevention of venous thromboembolism in medical patients with heart failure or severe respiratory disease. Am Heart J. 2003;145614- 621
PubMedArticle
7.
Nicolaides  ANBreddin  HKFareed  J  et al.  Prevention of venous thromboembolism: International Consensus Statement: guidelines compiled in accordance with the scientific evidence. Int Angiol. 2001;201- 37
PubMedArticle
8.
Samama  MM An epidemiologic study of risk factors for deep vein thrombosis in medical outpatients: the Sirius study. Arch Intern Med. 2000;1603415- 3420
PubMedArticle
9.
Cogo  ABernardi  EPrandoni  P  et al.  Acquired risk factors for deep-vein thrombosis in symptomatic outpatients. Arch Intern Med. 1994;154164- 168
PubMedArticle
10.
Cohen  AT Prevention of deep vein thrombosis after hip replacement [letter]. Thromb Haemost. 2000;83- 171
PubMed
11.
Eikelboom  JWQuinlan  DJDouketis  JD Extended-duration prophylaxis against venous thromboembolism after total hip or knee replacement: a meta-analysis of the randomised trials. Lancet. 2001;3589- 15
PubMedArticle
12.
Bonifacj  CQuere  IDupuy  CJanbon  CDaures  JP Case control studies of the risk factors for deep-vein thrombosis in an adult population hospitalized in internal medicine [in French]. Rev Epidemiol Sante Publique. 1997;45465- 473
PubMed
13.
Falanga  ARickles  FR Pathophysiology of the thrombophilic state in the cancer patient. Semin Thromb Hemost. 1999;25173- 182
PubMedArticle
14.
Grady  DWenger  NKHerrington  D  et al.  Postmenopausal hormone therapy increases risk for venous thromboembolic disease: the Heart and Estrogen/progestin Replacement Study. Ann Intern Med. 2000;132689- 696
PubMedArticle
15.
Belch  JJLowe  GDWard  AGForbes  CDPrentice  CR Prevention of deep vein thrombosis in medical patients by low-dose heparin. Scott Med J. 1981;26115- 117
PubMed
16.
Anderson  FA  JrWheeler  HBGoldberg  RJ  et al.  A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism: the Worcester DVT Study. Arch Intern Med. 1991;151933- 938
PubMedArticle
17.
Rosendaal  FR Venous thrombosis: a multicausal disease. Lancet. 1999;3531167- 1173
PubMedArticle
18.
Heit  JASilverstein  MDMohr  DNPetterson  TMO'Fallon  WMMelton III  LJ Predictors of survival after deep vein thrombosis and pulmonary embolism: a population-based, cohort study. Arch Intern Med. 1999;159445- 453
PubMedArticle
19.
Oger  E Incidence of venous thromboembolism: a community-based study in Western France: EPI-GETBP Study Group: Groupe d'Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost. 2000;83657- 660
PubMed
20.
Alikhan  RCohen  ATCombe  S  et al.  Prevention of venous thromboembolism in medical patients with enoxaparin: a subgroup analysis of the MEDENOX study. Blood Coagul Fibrinolysis. 2003;14341- 346
PubMedArticle
21.
Goldhaber  SZGrodstein  FStampfer  MJ  et al.  A prospective study of risk factors for pulmonary embolism in women. JAMA. 1997;277642- 645
PubMedArticle
22.
Hansson  POEriksson  HWelin  LSvardsudd  KWilhelmsen  L Smoking and abdominal obesity: risk factors for venous thromboembolism among middle-aged men: "the study of men born in 1913." Arch Intern Med. 1999;1591886- 1890
PubMedArticle
23.
Goldhaber  SZSavage  DDGarrison  RJ  et al.  Risk factors for pulmonary embolism: the Framingham Study. Am J Med. 1983;741023- 1028
PubMedArticle
24.
Clagett  GPAnderson  FA  JrHeit  JLevine  MNWheeler  HB Prevention of venous thromboembolism. Chest. 1995;108(suppl)312S- 334S
PubMedArticle
Original Investigation
May 10, 2004

Risk Factors for Venous Thromboembolism in Hospitalized Patients With Acute Medical IllnessAnalysis of the MEDENOX Study

Author Affiliations

From the Academic Department of Surgery, Guy's, King's, and St Thomas' School of Medicine, London, England (Drs Alikhan and Cohen); Département Cardiovasculaire, Laboratoires Rhône-Poulenc Rorer, Montrouge, France (Dr Combe); Département d'Hématologie Biologique, Hôtel Dieu, Paris, France (Dr Samama); Service d'Hématologie, Centre Hospitalier Université Laval, St Foy, Quebec (Dr Desjardins); Institute of Hematology, Sourasky Medical Center, Ichilov Hospital, Tel-Aviv, Israel (Dr Eldor); Service de Médecine Interne, Centre Hospitalier Université Hôpital Saint-Eloi, Montpellier, France (Dr Janbon); Service de Pharmacologie Clinique, University of Lyon, Lyon, France (Dr Leizorovicz); Internal Medicine Department, University Hospital of Lund, Lund, Sweden (Dr Olsson); and the Department of Medicine, McMaster University, Hamilton, Ontario (Dr Turpie). The authors have no relevant financial interest in this article. Dr Eldor is deceased.

Arch Intern Med. 2004;164(9):963-968. doi:10.1001/archinte.164.9.963
Abstract

Background  There is limited information about risk factors for venous thromboembolism (VTE) in acutely ill hospitalized general medical patients.

Methods  An international, randomized, double-masked, placebo-controlled trial (MEDENOX) has previously been conducted in 1102 acutely ill, immobilized general medical patients and has shown the efficacy of using a low-molecular-weight heparin, enoxaparin sodium, in preventing thrombosis. We performed logistic regression analysis to evaluate the independent nature of different types of acute medical illness (heart failure, respiratory failure, infection, rheumatic disorder, and inflammatory bowel disease) and predefined factors (chronic heart and respiratory failure, age, previous VTE, and cancer) as risk factors for VTE.

Results  The primary univariate analysis showed that the presence of an acute infectious disease, age older than 75 years, cancer, and a history of VTE were statistically significantly associated with an increased VTE risk. Multiple logistic regression analysis indicated that these factors were independently associated with VTE.

Conclusions  Several independent risk factors for VTE were identified. These findings allow recognition of individuals at increased risk of VTE and will contribute to the formulation of an evidence-based risk assessment model for thromboprophylaxis in hospitalized general medical patients.

Venous thromboembolism (VTE) remains an important cause of morbidity and mortality in a wide range of patients and conditions.1 The rationale for providing thromboprophylaxis is that prevention is clinically and financially beneficial compared with treatment of a thromboembolic event once it has occurred. Extensive data have been collected to support this position for surgical patients. Until recently, there was a paucity of data on the benefits of thromboprophylaxis in general medical patients,2 despite evidence showing that VTE is a substantial problem in medical populations.3 Although thromboprophylaxis studies had been performed, they tended to focus on the use of thromboprophylaxis in high-risk patients, such as those with myocardial infarction or stroke.1 In contrast, the limited data in general medical patients were based on small, open-label studies, some of which used diagnostic methods now considered obsolete to detect VTE.4

Recent randomized trials5,6 have helped define the level of thromboembolic risk in well-characterized acutely ill medical patients, particularly those with cardiorespiratory disease. The MEDENOX (prophylaxis in MEDical patients with ENOXaparin) trial5 was a randomized, double-masked, placebo-controlled study designed to clarify the actual thromboembolic risk in clearly defined populations of medical patients and to evaluate the benefit-risk ratio of 2-dose regimens of a low-molecular-weight heparin. The study showed that these patients were at moderate risk of VTE according to accepted criteria (a 15% incidence in the placebo arm), and these findings are now reflected in the American College of Chest Physicians and International Consensus Statements that recommend thromboprophylaxis.1,7 However, there remains limited data on the independent nature of either disease- or patient-related VTE risk factors in medical patients.8 This uncertainty, we suggest, has resulted in certain empiricism in the selection of patients who require thromboprophylaxis. We aim to identify independent risk factors for VTE using logistic regression analyses in the well-defined, hospitalized, general medical patients in the MEDENOX study.

METHODS

The MEDENOX study was a multicenter, randomized, double-masked trial that compared low-molecular-weight heparin (20 or 40 mg of enoxaparin sodium subcutaneously once daily) with placebo, as previously described elsewhere.5 The primary outcome event was the occurrence of documented VTE between day 1 and day 14. Venous thromboembolism was defined as deep vein thrombosis identified by either mandatory lower limb contrast venography or (1) compression ultrasound (mean ± SD day 10 ± 4), (2) clinical suspicion of deep vein thrombosis, (3) pulmonary embolism confirmed by pulmonary angiography or high-probability lung scan, or (4) fatal pulmonary embolism.

Patients were older than 40 years with a planned hospital stay of at least 6 days and had been recently immobilized for 3 days or less. Patients were hospitalized for acute heart failure, New York Heart Association class III or IV, or acute respiratory failure that did not require immediate ventilatory support. Other patients included had 1 of 3 medical conditions (acute infectious disease without septic shock, an acute rheumatic disorder, or an active episode of inflammatory bowel disease) and at least 1 predefined VTE risk factor (age >75 years, cancer, previous history of VTE, obesity, varicose veins, hormone therapy, and chronic heart or respiratory failure). Chronic respiratory disease and chronic heart failure were not assessed as risk factors if the patient was hospitalized with the corresponding acute medical illness.

Aventis Pharmaceuticals (Bridgewater, NJ) made the complete MEDENOX database available. A total of 1102 patients were enrolled in 60 medical centers in 9 countries. All analyses were performed on this database using the intention-to-treat population, defined as all patients with an evaluable primary end point assessment (n = 866). Evaluable patients were divided equally among the 3 treatment groups: placebo (n = 288), 20 mg of enoxaparin (n = 287), and 40 mg of enoxaparin (n = 291).

In the initial step of building a regression model, 8 explanatory variables (age >75 years, cancer, history of VTE, obesity, varicose veins, hormone therapy, chronic heart failure, and chronic respiratory failure) were given binary values (ie, present or not present), and their effect on the response variable (the presence or not of VTE) was considered individually (univariate analysis). In addition, the disease groupings defined in the MEDENOX trial were examined in an identical manner.

Univariate analyses were performed on 2 populations: (1) the complete MEDENOX patient population for whom primary outcome data were available (n = 866) and (2) patients who had not received active or effective antithrombotic treatment (patients who received placebo or 20 mg of enoxaparin) (n = 575). Relative risks were calculated as the risk of events in patients with the characteristic divided by the risk of events in patients without the characteristic. Evidence of association was calculated using the Fisher exact test. Characteristics identified by the univariate analyses as potential risk factors were considered for inclusion in a multivariate logistic regression analysis. To ensure selection of the best combination of explanatory variables, only those with a P<.20 were included in the model, and they remained in the model only if they were significantly related to the response variable (P<.10).

A multiple logistic regression analysis was conducted to determine the independent nature of the risk factors while adjusting for other characteristics. A stepwise selection model was used to look for other characteristics, and a stepwise selection procedure was used that started with all covariates in the model.

The software package used for the analyses was SAS version 6.12 (SAS Institute Inc, Cary, NC).

RESULTS
OVERALL MEDENOX STUDY FINDINGS

The incidence of VTE by day 14 (the primary outcome event) was significantly lower in the group assigned to receive 40 mg of enoxaparin (16 [5.5%] of 291 patients) than in the placebo group (43 [14.9%] of 288 patients), a risk reduction of 63% (relative risk, 0.37; 97.6% confidence interval [CI], 0.22-0.63; P<.001). There was no significant difference in the incidence of VTE between the group that received 20 mg of enoxaparin (43 [15.0%] of 287 patients) and the placebo group (P = .90).5 Considering the disease groups separately, the highest incidence of VTE occurred in patients with New York Heart Association class IV heart failure (Table 1). Patients who had experienced a previous thromboembolic episode or cancer where found to have experienced the highest incidence of VTE (Table 2).

UNIVARIATE ANALYSIS
Complete MEDENOX Population

Among the predefined risk factors, age older than 75 years, cancer, and previous VTE were significantly associated with an increased risk of VTE (Table 3). The only acute medical illness significantly associated with an increased risk of VTE was an acute infectious disease (Table 4). Acute respiratory failure and chronic respiratory disease had the lowest risk of VTE (9.2% and 9.0%, respectively) compared with other acute medical illnesses and risk factors (Table 3 and Table 4).

Placebo and 20-mg Treatment Groups

Comparing the complete patient population with the patients who did not receive effective antithrombotic prophylaxis, there was no difference in the risk factors (Table 5) or type of acute medical illness (Table 6) associated with an increased risk of VTE (age >75 years, cancer, previous VTE, and the presence of an acute infectious disease).

MULTIPLE LOGISTIC REGRESSION ANALYSIS

The multiple regression model showed that age older than 75 years, cancer, previous VTE, acute infectious disease, and chronic respiratory disease were all independently related to risk of VTE (Table 7). Previous VTE had the highest odds ratio (OR, 2.06; 95% CI, 1.10-3.69).

RISK FACTORS AND VTE EVENTS

The number of VTE events was categorized by the number of risk factors present in each patient (Table 8). The proportion of patients experiencing a thromboembolic event increased with the number of risk factors. The increase in the number of VTE events as the number of risk factors increased from zero to more than 2 was not statistically significant (χ2 test for linear trend: OR, 1.47; P = .47).

COMMENT

The MEDENOX study offered a unique opportunity to examine the independent nature of specific patient- and disease-related risk factors in acutely ill, hospitalized medical patients. The MEDENOX study comprised 3 treatment populations—those who received effective antithrombotic therapy (40 mg of enoxaparin once daily), those who received ineffective therapy (20 mg of enoxaparin once daily), and those who received placebo.5 We considered that effective antithrombotic therapy may exert a confounding effect on the risk findings and therefore performed univariate analyses on 2 populations: the complete MEDENOX population and the subset of patients treated with placebo or ineffective thromboprophylaxis. Our findings were similar in each group and in the choice of factors to enter into the multivariate logistic regression analyses made from the complete MEDENOX population.

Our analysis shows that the presence of an acute infectious disease or cancer and a previous history of VTE or age older than 75 years are independent risk factors for objectively confirmed VTE. The MEDENOX study, in keeping with most thromboprophylaxis trials, used accurate objective testing by ascending contrast venography to detect deep vein thrombosis as the main efficacy finding. The thrombi detected were largely asymptomatic, an important point to consider when reviewing the independent risk factors found in this study as, in risk studies previously described,9 clinically apparent VTE frequently was the variable analyzed. A relationship between venographically detected deep vein thrombosis and symptomatic VTE has been shown in surgical patients,10,11 but there is a paucity of data in medical patients.

The risk of VTE was highest among patients who had previously experienced a thromboembolic event and was independently associated with confirmed VTE (OR, 2.06; 95% CI, 1.10-3.69). In a French study12 of hospital inpatients admitted to a medical ward for deep vein thrombosis, multivariate analysis showed that a personal history of VTE was an independent risk factor (OR, 4.7; 95% CI, 2.4-8.9). In addition, the study also showed that a family history of VTE was independently related (OR, 3.3). In an analysis of medical outpatients, the Sirius study8 showed a very strong association with previous VTE, showing that it was independently associated with symptomatic VTE (OR, 15.6; 95% CI, 6.77-35.89).

Patients with cancer are at increased risk of VTE, which is related to factors associated with the cancer, the interventions used (such as central venous catheters, chemotherapy, and radiotherapy), and surgery.13 Our analysis shows that in general medical patients, a history of or the presence of an active cancer is statistically significantly related to high risk of VTE (OR, 1.62; 95% CI, 0.93-2.75). These findings closely mirror those of other studies. Cancer has been shown to be an independent risk factor in a population case-control series of outpatients with symptomatic VTE,9 and in the HERS (Heart and Estrogen/progestin Replacement Study),14 cancer was independently associated with first-episode VTE.

This analysis shows that acute infection was an independent risk factor in the generation of venous thrombosis. An early study of VTE in medical patients revealed a benefit of heparin use in immobilized patients with heart failure or chest infection. Low-dose unfractionated heparin therapy statistically significantly reduced deep vein thrombosis from 26% to 4%.15 This study and the MEDENOX study confirm that elderly immobilized medical patients frequently have multiple comorbidities, including infection. In the MEDENOX study, a substantial proportion of patients had infection concomitant with cardiorespiratory disease. This is the first time that infection has been reported as an independent risk factor in hospitalized medical patients. The SIRIUS study8 found infectious disease to be a risk factor for VTE in medical outpatients (OR, 1.95; 95% CI, 1.31-2.92). The importance of identifying infection as an independent risk factor for VTE in medical patients has also been demonstrated by an association recently described between fatal pulmonary embolism and infection (R. Alikhan, MBBS, F. Peters, MBBS, R. Wilmott, A.T. Cohen, MD, unpublished data, 2002).

The risk of thrombosis increases sharply with age, from approximately 1 in 10 000 people per year for those younger than 40 years to 1 in 100 people per year for those 75 years and older,16 and is an independent risk factor for VTE.1 Although it is not certain why risk is dependent on age, it has been suggested that it is related to a combination of decreased mobility and muscle tone with increased morbidity and degenerative vascular changes.17 In a population-based cohort study18 that examined independent predictors of death within 7 days after a VTE and during a 25-year period in 2218 patients, the OR of death was 1.3 times higher in the 75-year-old patients compared with the 60-year-olds. A further study19 showed that the incidence of VTE is markedly raised with age, with patients older than 75 years experiencing an annual incidence of 1% and VTE rates twice those for 60- to 74-year-olds. A previous analysis20 of the MEDENOX study identified individuals older than 75 years as gaining marked benefit from taking 40 mg of enoxaparin in reducing the incidence of VTE (78% relative risk reduction).

Obesity was not found to be a risk factor for VTE in the present study, in keeping with the findings from HERS, which showed that, in 2763 postmenopausal women with no previous history of VTE, there was no association between obesity and symptomatic VTE (relative risk, 1.0).14 However, the results of 3 other studies—the SIRIUS study,8 a prospective nurses health study,21 and a prospective Swedish cohort study22—suggested that obesity was linked to VTE.

The link between varicose veins and VTE is a contentious one with somewhat conflicting findings. In our analysis, varicose veins were not an independent risk factor for VTE. This is in keeping with findings from the Framingham Study,23 which did not identify varicose veins as an independent predictor of pulmonary embolism.

In a group of medical outpatients, but not patients with chronic respiratory disease, the SIRIUS study8 showed that chronic heart failure was independently associated with VTE (OR, 2.93; 95% CI, 1.55-5.56). In our analysis of acutely ill immobilized medical patients, chronic heart failure was not independently related to VTE, and patients with chronic respiratory disease had statistically significantly less VTE relative to the other higher-risk disease groups and risk factors in the model.

In 1995, the American College of Chest Physicians added a "grade A" recommendation for "general medical patients with clinical risk factors for venous thromboembolism, particularly those with congestive heart failure and/or chest infections" and recommended low-dose unfractionated heparin or low-molecular-weight heparin therapy.24 In 2001, the American College of Chest Physicians extended the recommendations to include medical patients with the following risk factors: severe lung disease, cancer, and bed rest.1 Our analysis extends the findings of the MEDENOX study, revealing that certain disease and patient factors are independently related to the genesis of VTE in acutely ill medical patients. This analysis shows that a previous history of VTE in medical patients seems to be the most important predictor of future events. Currently, there is no precise patient risk profile for medical illness that would precipitate a mandatory recommendation for thromboprophylaxis, and we believe that these findings will facilitate the formulation of a risk assessment model based on clinical evidence.

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Article Information

Corresponding author and reprints: Alexander T. Cohen, MBBS, MSc, MD, FRACP, Academic Department of Surgery, Guy's, King's, and St Thomas' School of Medicine, Bessemer Road, London SE5 9PJ, England (e-mail: alexander.cohen@kcl.ac.uk).

Accepted for publication June 24, 2003.

This analysis was supported by a grant from Aventis Pharmaceuticals.

References
1.
Geerts  WHHeit  JAClagett  GP  et al.  Prevention of venous thromboembolism. Chest. 2001;119(suppl)132S- 175S
PubMedArticle
2.
Goldhaber  SZ Venous thromboembolism prophylaxis in medical patients. Thromb Haemost. 1999;82899- 901
PubMed
3.
Sandler  DAMartin  JF Autopsy proven pulmonary embolism in hospital patients: are we detecting enough deep vein thrombosis? J R Soc Med. 1989;82203- 205
PubMed
4.
Hampton  KK Thromboprophylaxis in medical patients. Hosp Med. 2000;61656- 659
PubMedArticle
5.
Samama  MMCohen  ATDarmon  JY  et al.  A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients: Prophylaxis in Medical Patients With Enoxaparin Study Group. N Engl J Med. 1999;341793- 800
PubMedArticle
6.
Kleber  FXWitt  CVogel  GKoppenhagen  KFlosbach  CWfor THE-PRINCE Study Group, Randomized comparison of enoxaparin with unfractionated heparin for the prevention of venous thromboembolism in medical patients with heart failure or severe respiratory disease. Am Heart J. 2003;145614- 621
PubMedArticle
7.
Nicolaides  ANBreddin  HKFareed  J  et al.  Prevention of venous thromboembolism: International Consensus Statement: guidelines compiled in accordance with the scientific evidence. Int Angiol. 2001;201- 37
PubMedArticle
8.
Samama  MM An epidemiologic study of risk factors for deep vein thrombosis in medical outpatients: the Sirius study. Arch Intern Med. 2000;1603415- 3420
PubMedArticle
9.
Cogo  ABernardi  EPrandoni  P  et al.  Acquired risk factors for deep-vein thrombosis in symptomatic outpatients. Arch Intern Med. 1994;154164- 168
PubMedArticle
10.
Cohen  AT Prevention of deep vein thrombosis after hip replacement [letter]. Thromb Haemost. 2000;83- 171
PubMed
11.
Eikelboom  JWQuinlan  DJDouketis  JD Extended-duration prophylaxis against venous thromboembolism after total hip or knee replacement: a meta-analysis of the randomised trials. Lancet. 2001;3589- 15
PubMedArticle
12.
Bonifacj  CQuere  IDupuy  CJanbon  CDaures  JP Case control studies of the risk factors for deep-vein thrombosis in an adult population hospitalized in internal medicine [in French]. Rev Epidemiol Sante Publique. 1997;45465- 473
PubMed
13.
Falanga  ARickles  FR Pathophysiology of the thrombophilic state in the cancer patient. Semin Thromb Hemost. 1999;25173- 182
PubMedArticle
14.
Grady  DWenger  NKHerrington  D  et al.  Postmenopausal hormone therapy increases risk for venous thromboembolic disease: the Heart and Estrogen/progestin Replacement Study. Ann Intern Med. 2000;132689- 696
PubMedArticle
15.
Belch  JJLowe  GDWard  AGForbes  CDPrentice  CR Prevention of deep vein thrombosis in medical patients by low-dose heparin. Scott Med J. 1981;26115- 117
PubMed
16.
Anderson  FA  JrWheeler  HBGoldberg  RJ  et al.  A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism: the Worcester DVT Study. Arch Intern Med. 1991;151933- 938
PubMedArticle
17.
Rosendaal  FR Venous thrombosis: a multicausal disease. Lancet. 1999;3531167- 1173
PubMedArticle
18.
Heit  JASilverstein  MDMohr  DNPetterson  TMO'Fallon  WMMelton III  LJ Predictors of survival after deep vein thrombosis and pulmonary embolism: a population-based, cohort study. Arch Intern Med. 1999;159445- 453
PubMedArticle
19.
Oger  E Incidence of venous thromboembolism: a community-based study in Western France: EPI-GETBP Study Group: Groupe d'Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost. 2000;83657- 660
PubMed
20.
Alikhan  RCohen  ATCombe  S  et al.  Prevention of venous thromboembolism in medical patients with enoxaparin: a subgroup analysis of the MEDENOX study. Blood Coagul Fibrinolysis. 2003;14341- 346
PubMedArticle
21.
Goldhaber  SZGrodstein  FStampfer  MJ  et al.  A prospective study of risk factors for pulmonary embolism in women. JAMA. 1997;277642- 645
PubMedArticle
22.
Hansson  POEriksson  HWelin  LSvardsudd  KWilhelmsen  L Smoking and abdominal obesity: risk factors for venous thromboembolism among middle-aged men: "the study of men born in 1913." Arch Intern Med. 1999;1591886- 1890
PubMedArticle
23.
Goldhaber  SZSavage  DDGarrison  RJ  et al.  Risk factors for pulmonary embolism: the Framingham Study. Am J Med. 1983;741023- 1028
PubMedArticle
24.
Clagett  GPAnderson  FA  JrHeit  JLevine  MNWheeler  HB Prevention of venous thromboembolism. Chest. 1995;108(suppl)312S- 334S
PubMedArticle
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