Incidence of Venous Thromboembolism in Patients Hospitalized with Cancer

Stein, Paul D.; Beemath, Afzal; Meyers, Frederick A.; Skaf, Elias; Sanchez, Julia; Olson, R. E.

doi:10.1016/j.amjmed.2005.06.058

Cited by 507 publications

(379 citation statements)

References 26 publications

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“…Although 20‐year incident malignancy in patients with new‐onset AF has been reportedly low at 10%,4 incident AF may occur in up to 30% of patients with certain types of malignancy (eg, thoracic) 6. Cancer‐associated thrombosis has been well described,7, 8 and AF in patients with malignancy may independently double the risk of venous or arterial thromboembolism compared with either condition alone 9. Some malignancies may also inherently increase the risk for major bleeding in patients with AF (eg, hematologic cancer),6 which is potentiated further with anticoagulant therapy 10, 11…”

Section: Introductionmentioning

confidence: 99%

Efficacy and Safety of Edoxaban in Patients With Active Malignancy and Atrial Fibrillation: Analysis of the ENGAGE AF‐TIMI 48 Trial

Fanola

Ruff

Murphy

et al. 2018

JAHA

128

113

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BackgroundAnticoagulation in patients with malignancy and atrial fibrillation is challenging because of enhanced risks for thrombosis and bleeding and the frequent need for invasive procedures. Data on direct oral antagonists in such patients are sparse.Methods and ResultsThe ENGAGE AF‐TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation–Thrombolysis in Myocardial Infarction Study 48) trial randomized 21 105 patients with atrial fibrillation to edoxaban or warfarin. Patients with malignancy, defined as a postrandomization new diagnosis or recurrence of remote cancer, were followed up over a median of 2.8 years. Adjusted Cox proportional hazard models were used to evaluate the safety and efficacy of edoxaban versus warfarin. Over a median of 495 days (interquartile range, 230–771 days), 1153 patients (5.5%) were diagnosed with new or recurrent malignancy, most commonly involving the gastrointestinal tract (20.6%), prostate (13.6%), and lung (11.1%). Malignancy was associated with increased risk of death (adjusted hazard ratio [HR], 3.12; 95% confidence interval [CI], 2.78–3.50) and major bleeding (adjusted HR, 2.45; 95% CI, 2.07–2.89), but not stroke/systemic embolism (adjusted HR, 1.08; 95% CI, 0.83–1.42). Relative outcomes with higher‐dose edoxaban versus warfarin were consistent regardless of malignancy status for stroke/systemic embolism (HR, 0.60 [95% CI, 0.31–1.15] for malignancy versus HR, 0.89 [95% CI, 0.76–1.05] for no malignancy; interaction P=0.25) and major bleeding (HR, 0.98 [95% CI, 0.69–1.40] for malignancy versus HR, 0.79 [95% CI, 0.69–1.05] for no malignancy; interaction P=0.31). There was, however, a significant treatment interaction for the composite ischemic end point (ischemic stroke/systemic embolism/myocardial infarction), with greater efficacy of higher‐dose edoxaban versus warfarin in patients with malignancy (HR, 0.54; 95% CI, 0.31–0.93) compared with no malignancy (HR, 1.02; 95% CI, 0.88–1.18; interaction P=0.026).ConclusionsIn patients with atrial fibrillation who develop malignancy, the efficacy and safety profile of edoxaban relative to warfarin is preserved, and it may represent a more practical alternative.

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Section: Introductionmentioning

confidence: 99%

Efficacy and Safety of Edoxaban in Patients With Active Malignancy and Atrial Fibrillation: Analysis of the ENGAGE AF‐TIMI 48 Trial

Fanola

Ruff

Murphy

et al. 2018

JAHA

128

113

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“…Although the association of cancer with increased risk of thrombosis is well documented, [82][83][84] clinical studies have not consistently demonstrated benefit with thrombosis prophylaxis, likely secondary to low overall VTE event rates. 85 It is important, therefore, to identify subgroups of ambulatory cancer patients for whom the risk of VTE and the benefits of thrombosis prophylaxis (improved morbidity, reduced mortality, more consistent delivery of cancer therapy, enhanced quality of life, and decreased use of health care resources) justify the risk, cost, and inconvenience of primary prophylaxis.…”

Section: D-dimer Testing For Venous Thromboembolism Risk Stratificatimentioning

confidence: 99%

D-Dimer Assays in Diagnosis and Management of Thrombotic and Bleeding Disorders

Bates

2012

Semin Thromb Hemost

101

103

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).D-dimer is a global indicator of coagulation activation and fibrinolysis and, therefore, an indirect marker of thrombotic activity. This specific cross-linked fibrin degradation product is formed through the sequential action thrombin, activated factor XIII (FXIIIa), and plasmin (►Fig. 1). 1-3 First, thrombin, generated when coagulation is activated, converts fibrinogen to fibrin and activates FXIII. Second, FXIIIa covalently crosslinks D-domains in adjacent fibrin monomers. Third, plasmin (formed on the fibrin surface by plasminogen activation) cleaves substrate fibrin at specific sites, and when it cleaves fibrin cross-linked by FXIIIa, it generates D-dimer. D-dimer is cleared through the kidneys and the reticuloendothelial system and has a plasma half-life of approximately 8 hours. 4 Low levels of D-dimer can be found circulating under normal physiologic conditions, while pathologically elevated levels can be found in any condition associated with enhanced fibrin formation and fibrinolysis (►Table 1). 1-3 The utility of D-dimer measurement has been evaluated in several clinical situations; however, the D-dimer assays have been best validated for the exclusion of venous thromboembolism (VTE) and the diagnosis and monitoring of disseminated intravascular coagulation (DIC). This article will review the available evidence for the utilization of D-dimer antigen measurement in the management of thrombotic and bleeding disorders. Measurement of D-DimerThe presence of D-dimer in plasma can be detected using monoclonal antibodies that recognize an epitope present in FXIIIa-cross-linked fragment D-domain of fibrin but not in fibrinogen degradation products or noncross-linked fibrin degradation products. Many different D-dimer assays have been developed and marketed. All of these tests rely on the use of monoclonal antibodies to detect D-dimer molecules. In general, three techniques are available to assay D-dimer (►Fig. 2). 1-3 These are (1) enzyme-linked immunosorbent assays (ELISAs) that rely on antibody capture and labeling of D-dimer; (2) a whole-blood agglutination assay (SimpliRED, Siemens Healthcare Diagnostics, Newcastle, DE), that uses a bispecific antibody conjugate with binding sites for both D-dimer and a red cell antigen and is performed on whole blood; (3) latex agglutination assays that also use bispecific antibodies with specificity for the latex particle and D-dimer antigen. Earlier latex agglutination assays for D-dimer were qualitative or semiquantitative; however, newer automated, quantitative D-dimer assays (which are immunoturbidometric assays) are performed on routine, automated coagulation instruments. It is important to recognize that results are not comparable between different assays, even between those of similar formats. Potential reasons for the lack of comparable results are listed in ►Table 2. Numeric results of D-dimerAbstract D-dimer is a global indicator of coagulation activation and fibrinolysis and, therefore, an indirect marker of thrombotic activity. The utility of D-dimer measur...

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“…This is consistent with reports of an increase in risk of cancer-associated VTE over time in this and in other populations, a trend which may be the result of either more aggressive cancer treatments or ascertainment resulting from greater knowledge of the link between cancer and thrombosis. 1,[20][21][22] This report contained both absolute risks (unadjusted) and adjusted HRs. Absolute risks and associated unadjusted HRs may be more useful in terms of clinical decision making if they are interpreted on the basis of a single factor.…”

Section: 2mentioning

confidence: 99%

When are breast cancer patients at highest risk of venous thromboembolism? A cohort study using English health care data

Walker

West

Card

et al. 2016

Blood

100

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Key Points• Patients with breast cancer have a risk of VTE equivalent to 6% a year while undergoing chemotherapy and in the month after treatment.• Tamoxifen is associated with a risk of VTE equivalent to 2% a year, which is 4 times higher than the risk before starting therapy.Patients with breast cancer are at increased risk of venous thromboembolism (VTE), particularly in the peridiagnosis period. However, no previous epidemiologic studies have investigated the relative impact of breast cancer treatments in a time-dependent manner. We aimed to determine the impact of breast cancer stage, biology, and treatment on the absolute and relative risks of VTE by using several recently linked data sources from England. .6 per 1000 person-years) than that in women who did not receive chemotherapy. After surgery, the risk was significantly increased in the first month (hazard ratio [HR], 2.2; 95% CI, 1.4-3.4; AR, 23.5; reference group, no surgery), but the risk was not increased after the first month. Risk of VTE was noticeably higher in the 3 months after initiation of tamoxifen compared with the risk before therapy (HR, 5.5; 95% CI, 2.3-12.7; AR, 24.1); however, initiating therapy with aromatase inhibitors was not associated with VTE (HR, 0.8; 95% CI, 0.5-1.4; AR, 28.3). In conclusion, women receiving chemotherapy for breast cancer have a clinically important risk of VTE, whereas an increased risk of VTE immediately after endocrine therapy is restricted to tamoxifen. (Blood. 2016;127(7):849-857) Medscape Continuing Medical Education onlineThis activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint providership of Medscape, LLC and the American Society of Hematology. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians. Medscape, LLC designates this Journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. All other clinicians completing this activity will be issued a certificate of participation. To participate in this journal CME activity: (1) review the learning objectives and author disclosures; (2) study the education content; (3) take the post-test with a 75% minimum passing score and complete the evaluation at http://www.medscape.org/journal/blood; and (4) view/print certificate. For CME questions, see page 953. Disclosures Thomas L. Ortel, Associate Editor, served as an advisor or consultant for Instrumentation Laboratory and received grants for clinical research from Instrumentation Laboratory; Eisai; Pfizer; and GlaxoSmithKline. The authors and CME questions author Laurie Barclay, freelance writer and reviewer, Medscape, LLC, declare no competing financial interests. Learning objectives1. Identify the effect of chemotherapy for breast cancer on the risk for venous thromboembolism, based on an English cohort study.2. Determi...

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Incidence of Venous Thromboembolism in Patients Hospitalized with Cancer

Cited by 507 publications

References 26 publications

Efficacy and Safety of Edoxaban in Patients With Active Malignancy and Atrial Fibrillation: Analysis of the ENGAGE AF‐TIMI 48 Trial

Efficacy and Safety of Edoxaban in Patients With Active Malignancy and Atrial Fibrillation: Analysis of the ENGAGE AF‐TIMI 48 Trial

D-Dimer Assays in Diagnosis and Management of Thrombotic and Bleeding Disorders

When are breast cancer patients at highest risk of venous thromboembolism? A cohort study using English health care data

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