Mark A Crowther

McMaster University, Hamilton, Ontario, Canada

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Publications (291)1869.1 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Non–vitamin K oral anticoagulants (NOACs) do not require routine laboratory monitoring. However, laboratory measurement may be desirable in special situations and populations. Objectives This study’s objective was to systematically review and summarize current evidence regarding laboratory measurement of the anticoagulant activity of dabigatran, rivaroxaban, and apixaban. Methods We searched PubMed and Web of Science for studies that reported a relationship between drug levels of dabigatran, rivaroxaban, and apixaban and coagulation assay results. Study quality was evaluated using QUADAS-2 (Quality Assessment of Diagnostic Accuracy Studies 2). Results We identified 17 eligible studies for dabigatran, 15 for rivaroxaban, and 4 for apixaban. For dabigatran, a normal thrombin time excludes clinically relevant drug concentrations. The activated partial thromboplastin time (APTT) and prothrombin time (PT) are less sensitive and may be normal at trough drug levels. The dilute thrombin time (R2 = 0.92 to 0.99) and ecarin-based assays (R2 = 0.92 to 1.00) show excellent linearity across on-therapy drug concentrations and may be used for drug quantification. For rivaroxaban and apixaban, anti-Xa activity is linear (R2 = 0.89 to 1.00) over a wide range of drug levels and may be used for drug quantification. Undetectable anti-Xa activity likely excludes clinically relevant drug concentrations. The PT is less sensitive (especially for apixaban); a normal PT may not exclude clinically relevant levels. The APTT demonstrates insufficient sensitivity and linearity for quantification. Conclusions Dabigatran, rivaroxaban, and apixaban exhibit variable effects on coagulation assays. Understanding these effects facilitates interpretation of test results in NOAC-treated patients. More information on the relationship between drug levels and clinical outcomes is needed.
    Journal of the American College of Cardiology 09/2014; 64(11):1128–1139. · 14.09 Impact Factor
  • James D Douketis, Marc Carrier, Mark A Crowther
    06/2014; 186(9):697-8.
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    ABSTRACT: The prevalence of deep vein thrombosis as demonstrated by routine venography in patients with distal lower-extremity injury requiring cast immobilization or surgery is 10% to 40%. These deep vein thromboses are usually asymptomatic and distal, and the need for thromboprophylaxis in these patients is not known.
    The Journal of bone and joint surgery. American volume. 05/2014; 96(10):e83.
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    ABSTRACT: Background Dabigatran etexilate (DE) is an oral direct thrombin inhibitor used to prevent strokes in patients with atrial fibrillation. No licensed DE antidote is currently available. We hypothesized that active site-mutated S195A thrombin (S195A-IIa) and/or its trypsinized derivative (γT-S195A-IIa) would sequester dabigatran, the active form of DE, and reduce its anticoagulant effects.Objective To assess active site-mutated S195A or γT-S195A-IIa as dabigatran reversal agents in vitro and in vivo. Methods Diluted Thrombin Time (dTT) assays were performed using human or murine plasma containing dabigatran, combined with S195A-IIa, γT-S195A-IIa, or FPR-chloromethyl ketone-treated thrombin (FPR-IIa). Bleeding times were determined in anaesthetized DE-treated mice also receiving γT-S195A-IIa or vehicle 15 minutes prior to tail transection. The time to occlusion of carotid arteries of DE-treated mice also receiving S195A-IIa, γT-S195A-IIa, prothrombin complex concentrate (PCC) or vehicle, 15 minutes prior to topical FeCl3, was determined using Doppler ultrasound.ResultsγT-S195A-IIa reduced dTT values of dabigatran-containing human and murine plasma more effectively than S195-IIa; FPR-IIa had no effect. 13 mg/kg DE abrogated occlusive thrombus formation in the carotid arteries of FeCl3-treated mice; γT-S195A-IIa (6 mg/kg) or PCC (14.3 IU/kg), but not saline vehicle or S195A-IIa (6 mg/kg), was equally effective in restoring thrombus formation. Bleeding times of mice treated with 60 mg/kg DE and γT-S195A-IIa (6 mg/kg) or saline vehicle did not differ.Conclusions Our data suggest that γT-S195A-IIa decreases the anticoagulant effects of dabigatran in vitro and is partially effective at restoring hemostasis-related thrombus formation in DE-treated mice in vivo.This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 05/2014; · 6.08 Impact Factor
  • Thrombosis and Haemostasis 02/2014; 111(4). · 5.76 Impact Factor
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    ABSTRACT: Rivaroxaban is an ideal potential candidate for treatment of heparin-induced thrombocytopenia (HIT) because it is administered orally by fixed dosing, requires no laboratory monitoring and is effective in the treatment of venous and arterial thromboembolism in other settings. The Rivaroxaban for HIT study is a prospective, multicentre, single-arm, cohort study evaluating the incidence of new symptomatic venous and arterial thromboembolism in patients with suspected or confirmed HIT who are treated with rivaroxaban. Methodological challenges faced in the design of this study include heterogeneity of the patient population, differences in the baseline risk of thrombosis and bleeding dependent on whether HIT is confirmed or just suspected, and heterogeneity in laboratory confirmation of HIT. The rationale for how these challenges were addressed and the final design of the Rivaroxaban for HIT study is reviewed.
    Journal of Thrombosis and Thrombolysis 02/2014; · 1.99 Impact Factor
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    ABSTRACT: While the incidence of venous thromboembolism increases with age, little is known about its contemporary management or outcomes in older patients. Our goal was to compare the characteristics, treatment, and outcomes associated with venous thromboembolism, in patients aged 65-69 years, 70-74 years, 75-79 years, and 80+ years. Methods/Participants: We prospectively followed 542 subjects age ≥65 years with venous thromboembolism from January 2008 till August 2011 at 6 sites. In addition, a retrospective study of 681 additional subjects age ≥65 years with venous thromboembolism diagnosed in 2007 and 2009 was conducted at the same six sites. With advancing age, patients were more likely to suffer provoked venous thromboembolism but less likely to present with pulmonary embolism. Patients with unprovoked, provoked, or malignancy associated venous thromboembolism received warfarin for a median of 401 days, 203 days, and 529 days, respectively. Age ≥ 80 years was not associated with an increased risk of recurrent venous thromboembolism but there was an increased risk of all-cause mortality. With advancing age, patients are more likely to suffer hospital-associated and provoked venous thromboembolism. Many elderly patients with provoked or unprovoked venous thromboembolism were treated for >3 months or >12 months, respectively. Given that advanced age was not associated with increased risk of recurrent venous thromboembolism but elderly patients in general have a higher risk of bleeding from continued anticoagulant therapy, such practice is potentially harmful. At the same time such argument could be used to more vigorously offer prophylaxis in the first place.
    The American journal of medicine 02/2014; · 5.30 Impact Factor
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    ABSTRACT: IMPORTANCE The effect of antibiotic coadministration on the international normalized ratio (INR) in a relatively stable, real-world warfarin population has not been adequately described. Case reports and studies of healthy volunteers do not account for the potential contribution of acute illness to INR variability. OBJECTIVE To compare the risk of excessive anticoagulation among patients with stable warfarin therapy purchasing an antibiotic (antibiotic group) with the risk in patients purchasing a warfarin refill (stable controls) and patients with upper respiratory tract infection but not receiving an antibiotic (sick controls). DESIGN, SETTING, AND PARTICIPANTS A retrospective, longitudinal cohort study evaluated patients receiving warfarin between January 1, 2005, and March 31, 2011, at Kaiser Permanente Colorado, an integrated health care delivery system. Continuous data were expressed as mean (SD) or median (interquartile range). Multivariable logistic regression analysis was used to identify factors independently associated with a follow-up INR of 5.0 or more. A total of 5857 (48.8%), 5579 (46.5%), and 570 (4.7%) patients were included in the antibiotic, stable control, and sick control groups, respectively. Mean age was 68.3 years, and atrial fibrillation was the most common (44.4%) indication for anticoagulation. EXPOSURES Warfarin therapy with a medical visit for upper respiratory tract infection or coadministration of antibiotics. MAIN OUTCOMES AND MEASURES Primary outcomes were the proportion of patients experiencing a follow-up INR of 5.0 or more and change between the last INR measured before the index date and the follow-up INR. RESULTS The proportion of patients experiencing an INR of 5.0 or more was 3.2%, 2.6%, and 1.2% for the antibiotic, sick, and stable groups, respectively (P < .001, antibiotic vs stable control group; P < .017, sick vs stable control group; P = .44, antibiotic vs sick control group). Cancer diagnosis, elevated baseline INR, and female sex predicted a follow-up INR of 5.0 or more. Among antibiotics, those interfering with warfarin metabolism posed the greatest risk for an INR of 5.0 or more. CONCLUSIONS AND RELEVANCE Acute upper respiratory tract infection increases the risk of excessive anticoagulation independent of antibiotic use. Antibiotics also increase the risk; however, most patients with previously stable warfarin therapy will not experience clinically relevant increases in INR following antibiotic exposure or acute upper respiratory tract infection.
    JAMA Internal Medicine 01/2014; · 10.58 Impact Factor
  • Deborah M Siegal, David A Garcia, Mark A Crowther
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    ABSTRACT: Target specific oral anticoagulants (TSOACs) that directly inhibit thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban) are effective and safe alternatives to vitamin K antagonists (VKA) and low molecular weight heparin (LMWH). While these agents have practical advantages compared to VKAs and LMWH, there are no antidotes that reverse their anticoagulant effect. Clinical evidence for the efficacy of non-specific therapies that promote formation of fibrin (prothrombin complex concentrate [PCC], activated prothrombin complex concentrate [aPCC], recombinant factor VIIa) in the setting of TSOAC-associated bleeding is lacking and these pro-hemostatic products are associated with a risk of thrombosis. In the absence of specific antidotes, addition of PCC or aPCC to maximum supportive therapy may be reasonable for patients with severe or life-threatening TSOAC-associated bleeding. Targeted antidotes for these agents are in development.
    Blood 01/2014; · 9.78 Impact Factor
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    ABSTRACT: Choosing Wisely(®) is a medical stewardship and quality improvement initiative led by the American Board of Internal Medicine Foundation in collaboration with leading medical societies in the United States. The ASH is an active participant in the Choosing Wisely(®) project. Using an iterative process and an evidence-based method, ASH has identified 5 tests and treatments that in some circumstances are not well supported by evidence and which in certain cases involve a risk of adverse events and financial costs with low likelihood of benefit. The ASH Choosing Wisely(®) recommendations focus on avoiding liberal RBC transfusion, avoiding thrombophilia testing in adults in the setting of transient major thrombosis risk factors, avoiding inferior vena cava filter usage except in specified circumstances, avoiding the use of plasma or prothrombin complex concentrate in the nonemergent reversal of vitamin K antagonists, and limiting routine computed tomography surveillance after curative-intent treatment of non-Hodgkin lymphoma. We recommend that clinicians carefully consider anticipated benefits of the identified tests and treatments before performing them.
    Blood 12/2013; 122(24):3879-83. · 9.78 Impact Factor
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    ABSTRACT: The role of ABO blood type as a risk factor for recurrent venous thromboembolism (VTE) in patients with a first unprovoked VTE who complete oral anticoagulation therapy is unknown. The aim of this study was to determine if non-OO blood type is a risk factor for recurrent VTE in patients with a first unprovoked VTE who completed 5-7 months of anticoagulant therapy. In an ongoing cohort study of patients with unprovoked VTE who discontinued oral anticoagulation after 5-7 months of therapy, six single nucleotide polymorphisms sites were tested to determine ABO blood type using banked DNA. The main outcome was objectively proven recurrent VTE. Mean follow-up for the cohort was 4.19 years (SD 2.16). During 1,553 patient-years of follow-up, 101 events occurred in 380 non-OO patients (6.5 events per 100 patient years; 95% CI 5.3-7.7) compared to 14 events during 560 patient years of follow-up in 129 OO patients (2.5 per 100 patient years; 95% CI 1.2-3.7), the adjusted hazard ratio was 1.98 (1.2-3.8). In conclusion, non-OO blood type is associated with a statistically significant and clinically relevant increased risk of recurrent VTE following discontinuation of anticoagulant therapy for a first episode of unprovoked VTE.
    Thrombosis and Haemostasis 09/2013; 110(6). · 5.76 Impact Factor
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    ABSTRACT: B-cell depletion therapy may impair vaccine responses and increase infection risk in patients with immune thrombocytopenia (ITP). Capitalizing on a multicenter randomized placebo-controlled trial, we investigated the effects of rituximab on the antibody and cellular responses to Streptococcus pneumoniae polysaccharide vaccine and Haemophilus influenzae type b (Hib) conjugate vaccine in ITP patients. Of 60 patients in the main trial, 24 patients received both vaccines 6 months after rituximab (n=17) or placebo (n=7). Among 20 evaluable patients, 3/14 (21%) in the rituximab group and 4/6 (67%) in the placebo group achieved a 4-fold increase in anti-pneumococcal antibodies (p=0.12). For anti-Hib antibodies, 4/14 (29%) and 5/6 (83%), respectively, achieved a 4-fold increase (p<0.05). Fewer patients in the rituximab group demonstrated functional Hib killing (2/14 [14%] versus 5/6 [83%], p<0.05). Three of 14 rituximab-treated patients failed to respond to vaccines by any criteria. After vaccinations, pre-plasma cell blasts and interferon-γ secreting T-cells were reduced in rituximab-treated patients. We found that antibody responses were impaired for at least 6 months after rituximab. Cellular immunity was reduced in parallel with the depleted B-cell pool. These findings have implications for the timing of vaccinations and the mechanism of infection after rituximab in patients with ITP.
    Blood 07/2013; · 9.78 Impact Factor
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    ABSTRACT: This study tests the hypothesis that nonadherence with INR monitoring is associated with an increased risk for warfarin-related bleeding and thrombosis and describes patient characteristics associated with INR monitoring nonadherence. This was a retrospective, longitudinal, matched cohort study wherein patients were categorized into adherent and nonadherent cohorts; adherent patients were matched 2:1 to nonadherent patients. The primary study endpoint was the first occurrence of bleeding or thromboembolism. Multivariate logistic regression modeling identified patient characteristics associated with INR monitoring adherence or nonadherence. A total of 4995 and 2544 patients contributed 10729 and 5385 patient-years of warfarin therapy in the adherent and nonadherent groups, respectively. The rate of thromboembolic events during follow up was higher in the nonadherent group than in the adherent group (0.95% vs. 0.62% per patient-year, respectively; p=0.019) and nonadherence to INR monitoring was associated with a moderately higher risk of thromboembolism (adjusted Hazard Ratio=1.51; 95% confidence interval=1.04 - 2.20). The difference in bleeding between the two groups was not statistically significant. Repeatedly missing INR tests is an easily identified clinical parameter that is associated with moderately increased risk for thromboembolism in patients taking chronic warfarin therapy. Clinicians should carefully consider the underlying thromboembolic risk and extent of nonadherence when weighing the benefits of continued warfarin therapy for a given patient.
    Thrombosis Research 06/2013; · 3.13 Impact Factor
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    ABSTRACT: ABSTRACT BACKGROUND: In a recent multicenter randomized trial comparing unfractionated heparin (UFH) with low-molecular-weight heparin (dalteparin) for thromboprophylaxis in 3746 critically-ill patients, 17 (0.5%) patients developed heparin-induced thrombocytopenia (HIT) based on serotonin-release assay-positive (SRA+) status. A trend to lower frequency of HIT with dalteparin vs UFH was observed in the intention-to-treat analysis (5 vs 12 patients; P=0.14), which was statistically significant (3 vs 12 patients; P=0.046) in a prespecified per-protocol analysis which excluded patients with deep-vein thrombosis (DVT) at study entry. We sought to characterize HIT outcomes and to determine how dalteparin thromboprophylaxis might reduce HIT frequency in ICU patients. METHODS: In 17 patients with HIT, we analyzed platelet counts and thrombotic events in relation to study drug and other open-label heparin, to determine whether study drug plausibly explained seroconversion to SRA+ status and/or breakthrough of thrombocytopenia/thrombosis. We also compared antibody frequencies (dalteparin vs UFH) in 409 patients serologically investigated for HIT. RESULTS: HIT-associated thrombosis occurred in 10/17 (58.8%) patients (8:1:1 venous:arterial:both). Dalteparin was associated with fewer study drug-attributable HIT-related events (P=0.020), including less seroconversion (P=0.058) and less breakthrough of thrombocytopenia/thrombosis (P=0.032). Anti-PF4/heparin IgG antibodies by ELISA were less frequent among patients receiving dalteparin vs UFH (13.5% vs 27.3%; P<0.001). One patient with HIT-associated DVT died post-UFH bolus, whereas platelet counts recovered in two others with HIT-associated VTE despite continuation of therapeutic-dose UFH. CONCLUSIONS: The lower risk of HIT in ICU patients receiving dalteparin appears related to both decreased antibody formation and decreased clinical breakthrough of HIT among patients forming antibodies.
    Chest 05/2013; · 5.85 Impact Factor
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    ABSTRACT: BACKGROUND:Coagulopathy leading to excessive blood loss and large volume red cell transfusion is a frequent complication of cardiac surgery with cardiopulmonary bypass (CPB) that may be caused by low perioperative fibrinogen levels. We explored the relationship between post-CPB fibrinogen levels and large volume red cell transfusion.METHODS:Patients who underwent cardiac surgery with CPB from 2005 to 2011 at a single institution and had a fibrinogen level measured after CPB were included in this retrospective observational study. The relationship between post-CPB fibrinogen levels and large volume red cell transfusion (defined as ≥5 units transfused on the day of or the day after surgery) was assessed by cubic spline function and receiver operating characteristic analyses. The independent relationship between fibrinogen levels and large volume transfusion was assessed by multivariable logistic regression and propensity score analyses.RESULTS:In the 4606 patients included, the probability of large volume transfusion increased when fibrinogen levels decreased below approximately 2.0 g/L. Using <2.0 g/L as the threshold for low fibrinogen, 1918 (42%) were categorized into the low fibrinogen group, of whom 363 (18.9%) had large volume transfusion compared with 164 (13.5%) of the 2688 patients whose fibrinogen level was ≥2.0 g/L (P < 0.0001). In the low fibrinogen group, the unadjusted odds ratio (95% confidence interval) for large volume transfusion was 1.5 (1.3-1.7). The risk-adjusted odds ratio obtained by logistic regression was 1.8 (1.4-2.2) and by propensity score methods was 1.5 (1.2-2.0).CONCLUSIONS:While this study was not equipped to detect the critical fibrinogen level in bleeding patients, its results suggest that current recommendations that fibrinogen replacement not be initiated in bleeding patients unless fibrinogen levels decrease below 0.8 to 1.0 g/L may be too conservative. Randomized trials are needed to determine whether maintaining higher fibrinogen levels in bleeding patients can reduce blood loss and transfusions and by that means improve clinical outcomes in cardiac surgery.
    Anesthesia and analgesia 05/2013; · 3.08 Impact Factor
  • Daniel M Witt, Thomas Delate, Mark A Crowther
    JAMA Internal Medicine 05/2013; 173(9):833-834. · 10.58 Impact Factor
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    ABSTRACT: BACKGROUND: A significant challenge in the management of heparin-induced thrombocytopenia (HIT) patients is making a timely and accurate diagnosis. The readily available enzyme immunoassays (EIAs) have low specificities. In contrast, platelet activation assays have higher specificities, but they are technically demanding and not widely available. In addition, about 10% of samples referred for HIT testing are initially classified as indeterminate by the serotonin release assay (SRA), which further delays an accurate diagnosis. HIT is characterized by platelet activation, which leads to FcγRIIa proteolysis. This raises the possibility that identification of the proteolytic fragment of FcγRIIa could serve as a surrogate marker for HIT. OBJECTIVES: To determine the specificity of platelet FcγRIIa proteolysis induced by sera from patients with HIT and to correlate results with the SRA. METHODS/PATIENTS: Sera from HIT patients and control patients with other thrombocytopenic/prothrombotic disorders were tested for their ability to proteolyse FcγRIIa. The results were correlated to anti-PF4/heparin antibodies (EIA), and heparin-dependent platelet activation (SRA). RESULTS: Only HIT patient samples (20/20) caused heparin-dependent FcγRIIa proteolysis, similar to the SRA. None of the samples from the other patient groups or hospital controls caused FcγRIIa proteolysis. Of 9 additional samples that tested indeterminate in the SRA, FcγRIIa proteolysis resolved five samples that had a positive anti-PF4/heparin EIA; three had no FcγRIIa proteolysis and two were shown to have heparin-dependent FcγRIIa proteolysis CONCLUSIONS: This study suggests that heparin-dependent FcγRIIa proteolysis is at least as specific as the SRA for the diagnosis of HIT. © 2013 International Society on Thrombosis and Haemostasis.
    Journal of Thrombosis and Haemostasis 04/2013; · 6.08 Impact Factor
  • Mark A Crowther
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    ABSTRACT: Medical thromboprophylaxis reduces venous thromboembolism (VTE), while causing bleeding. Routine application of pharmacological VTE prophylaxis to low risk medical patients is likely to cause net harm; as a result only moderate or high risk patients should be exposed to VTE prophylaxis. To avoid unneeded exposure to VTE prophylaxis health care providers should use an "opt-in" policy which does not default to the use of VTE prophylaxis in inappropriate patients.
    Journal of Thrombosis and Thrombolysis 02/2013; · 1.99 Impact Factor
  • Pankaj Handa, Mark Crowther, James D Douketis
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    ABSTRACT: With advances in modern imaging techniques, portal vein thrombosis (PVT) is being increasingly diagnosed. It has a wide ranging clinical spectrum from being an asymptomatic state to a potentially life-threatening situation. It is not unusual to find it as an incidental finding in the abdominal imagings done for other reasons. It is commonly associated with cirrhosis and abdominal malignancies and also has a strong association with prothrombotic disorders. It is often difficult for the clinicians to decide whether PVT is acute or chronic. This poses great challenges to its management strategies that include anticoagulants, thrombolysis, and surgical options. Timely diagnosis and appropriate management have great bearings on its outcomes of morbidity and mortality. In this clinician-oriented review, we have provided a concise review of clinical aspects of PVT and discussed various management strategies while addressing the common questions that come to a physician's mind dealing with such a patient.
    Clinical and Applied Thrombosis/Hemostasis 01/2013; · 1.02 Impact Factor
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    ABSTRACT: Chinese translation d-Dimer testing is sensitive but not specific for diagnosing deep venous thrombosis (DVT). Changing the use of testing and the threshold level for a positive test result on the basis of risk for DVT might improve the tradeoff between sensitivity and specificity and reduce the need for testing. To determine whether using a selective d-dimer testing strategy based on clinical pretest probability (C-PTP) for DVT is safe and reduces diagnostic testing compared with using a single d-dimer threshold for all patients. Randomized, multicenter, controlled trial. Patients were allocated using a central automated system. Ultrasonographers and study adjudicators but not other study personnel were blinded to trial allocation. (ClinicalTrials.gov: NCT00157677) 5 Canadian hospitals. Consecutive symptomatic patients with a first episode of suspected DVT. Selective testing (n = 860), defined as d-dimer testing for outpatients with low or moderate C-PTP (DVT excluded at d-dimer levels <1.0 µg/mL [low C-PTP] or <0.5 µg/mL [moderate C-PTP]) and venous ultrasonography without d-dimer testing for outpatients with high C-PTP and inpatients, or uniform testing (n = 863), defined as d-dimer testing for all participants (DVT excluded at d-dimer levels <0.5 µg/mL). The proportion of patients not diagnosed with DVT during initial testing who had symptomatic venous thromboembolism during 3-month follow-up and the proportion of patients undergoing d-dimer testing and ultrasonography. The incidence of symptomatic venous thromboembolism at 3 months was 0.5% in both study groups (difference, 0.0 percentage point [95% CI, -0.8 to 0.8 percentage points]). Selective testing reduced the proportion of patients who required d-dimer testing by 21.8 percentage points (CI, 19.1 to 24.8 percentage points). It reduced the proportion who required ultrasonography by 7.6 percentage points (CI, 2.9 to 12.2 percentage points) overall and by 21.0 percentage points (CI, 14.2 to 27.6 percentage points) in outpatients with low C-PTP. Results may not be generalizable to all d-dimer assays or patients with previous DVT, study personnel were not blinded, and the trial was stopped prematurely. A selective d-dimer testing strategy seems as safe as and more efficient than having everyone undergo d-dimer testing when diagnosing a first episode of suspected DVT. Heart and Stroke Foundation of Ontario.
    Annals of internal medicine 01/2013; 158(2):93-100. · 13.98 Impact Factor

Publication Stats

6k Citations
1,869.10 Total Impact Points

Institutions

  • 1995–2014
    • McMaster University
      • • Department of Medicine
      • • Department of Pathology and Molecular Medicine
      • • Division of Rheumatology
      • • Department of Clinical Epidemiology and Biostatistics
      Hamilton, Ontario, Canada
  • 2013
    • St. Michael's Hospital
      Toronto, Ontario, Canada
  • 2008–2013
    • Kaiser Permanente
      Oakland, California, United States
    • Massachusetts General Hospital
      Boston, Massachusetts, United States
    • La Jolla Pharmaceutical
      San Diego, California, United States
  • 2004–2013
    • University of Toronto
      • • Faculty of Medicine
      • • Department of Anesthesia
      Toronto, Ontario, Canada
    • National Health Laboratory Service
      Johannesburg, Gauteng, South Africa
    • Oslo University Hospital
      • Department of Haematology
      Oslo, Oslo, Norway
  • 2012
    • Jewish General Hospital
      Montréal, Quebec, Canada
  • 2010–2012
    • University of Pennsylvania
      • Perelman School of Medicine
      Philadelphia, PA, United States
    • University of Florida
      • Department of Medicine
      Gainesville, FL, United States
    • University of Colorado
      Denver, Colorado, United States
    • UHN: Toronto General Hospital
      Toronto, Ontario, Canada
    • Women's College Hospital
      Toronto, Ontario, Canada
  • 2007–2012
    • St. Joseph's Hospital
      Savannah, Georgia, United States
  • 2005–2012
    • University of New Mexico
      • Department of Internal Medicine
      Albuquerque, NM, United States
    • McGill University
      Montréal, Quebec, Canada
    • CHA University
      • College of Medicine
      Seoul, Seoul, South Korea
  • 2002–2012
    • St. Joseph's Healthcare Hamilton
      Hamilton, Ontario, Canada
  • 2011
    • Duke University Medical Center
      • Duke Clinical Research Institute
      Durham, NC, United States
    • University of Texas at Dallas
      Richardson, Texas, United States
    • University Children's Hospital Basel
      Bâle, Basel-City, Switzerland
  • 2010–2011
    • Worcestershire Acute Hospitals NHS Trust
      Worcester, England, United Kingdom
  • 2006–2011
    • University of Insubria
      Varese, Lombardy, Italy
  • 2004–2011
    • Università degli Studi dell'Insubria
      • Department of Clinical and Experimental Medicine
      Varese, Lombardy, Italy
  • 2009
    • University of Massachusetts Medical School
      • Department of Medicine
      Worcester, Massachusetts, United States
    • National Health Service
      • Department of Haematology
      Radditch, England, United Kingdom
  • 2005–2006
    • Singapore General Hospital
      • • Department of Haematology
      • • Department of Medicine
      Singapore, Singapore
  • 1998
    • Hamilton Health Sciences
      Hamilton, Ontario, Canada