In Figure 5, the words 'PESI class III-IV or sPESI ≥ 1' should read 'PESI Class III-V or sPESI ≥ 1'.The figure, with the incorrect wording circled for clarity, is shown below.
Letters and Corrections15 February 1990Deep Vein Thrombosis and Duplex UltrasoundJ. S. Ginsberg, MD, P. Brill-Edwards, MD, G. Agnelli, MDJ. S. Ginsberg, MDSearch for more papers by this author, P. Brill-Edwards, MDSearch for more papers by this author, G. Agnelli, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-112-4-307 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:The article by White and colleagues (1) addresses the clinical utility of duplex ultrasound for the diagnosis of venous thrombosis. Duplex ultrasound appears to be sensitive and specific for the diagnosis of proximal but not calf vein thrombosis in symptomatic outpatients. It is highly likely that the test will need to be repeated at least once (and possibly on several occasions) in such patients to exclude extending calf vein thrombosis. Thus, we agree with the authors' statement that one test may be cheaper than contrast venography; however, with the need for serial testing, the cost of the...References1. WhiteMcGahanDaschbachHartling RJMR. Diagnosis of deep vein thrombosis using duplex ultrasound. Ann Intern Med. 1989;111:297-304. LinkGoogle Scholar2. HuismanBullerten CateVreeken MHJJ. Serial impedance plethysmography for suspected deep venous thrombosis in out-patients. N Engl J Med. 1986;314:823-8. CrossrefMedlineGoogle Scholar3. HullHirshCarter RJC. Diagnostic efficacy of impedance plethysmography for clinically suspected deep-vein thrombosis. A randomized trial. Ann Intern Med. 1985;102:21-8. LinkGoogle Scholar4. HuismanBullerten CateHeijermansvan der Laanvan Maanen MHJHJD. Management of clinically suspected acute venous thrombosis in outpatients with serial impedance plethysmography in a community hospital setting. Arch Intern Med. 1989;149:511-3. CrossrefMedlineGoogle Scholar5. BorrisChristiansenLassenOlsenSchott LHMAP. Comparison of real-time B-mode ultrasonography and bilateral ascending phlebography for detection of postoperative deep vein thrombosis following elective hip surgery. Thromb Haemost. 1989;61:363-5. CrossrefMedlineGoogle Scholar1. WhiteMcGahanDaschbachHartling RJMR. Diagnosis of deep-vein thrombosis using duplex ultrasound. Ann Intern Med. 1989;111:297-304. LinkGoogle Scholar2. RosnerDoris NP. Diagnosis of femoropopliteal venous thrombosis: comparison of duplex sonography and plethysmography. AJR. 1988;150:623-7. CrossrefMedlineGoogle Scholar3. PattersonFowlKellerSchomakerKempczinski RRJWR. The limitations of impedance plethysmography in the diagnosis of acute deep vein thrombosis. J Vase Surg. 1989;9:725-30. CrossrefMedlineGoogle Scholar4. HuismanBullerten CateVreeken MHJJ. Serial impedance plethysmography for suspected deep venous thrombosis in outpatients. N Engl J Med. 1986;314:823-8. CrossrefMedlineGoogle Scholar5. PolakCulterO'Leary JBD. Deep veins of the calf: assessment with color Doppler flow imaging. Radiology. 1989;171:481-5. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 February 1990Volume 112, Issue 4Page: 307-308KeywordsDeep vein thrombosisOutpatientsUltrasound imagingVeins Issue Published: 15 February 1990 PDF DownloadLoading ...
Whether elevated serum troponin levels identify patients with acute pulmonary embolism at high risk of short-term mortality or adverse outcome is undefined.We performed a meta-analysis of studies in patients with acute pulmonary embolism to assess the prognostic value of elevated troponin levels for short-term death and adverse outcome events (composite of death and any of the following: shock, need for thrombolysis, endotracheal intubation, catecholamine infusion, cardiopulmonary resuscitation, or recurrent pulmonary embolism). Unrestricted searches of MEDLINE and EMBASE bibliographic databases from January 1998 to November 2006 were performed using the terms "troponin" and "pulmonary embolism." Additionally, review articles and bibliographies were manually searched. Cohort studies were included if they had used cardiac-specific troponin assays and had reported on short-term death or adverse outcome events. A random-effects model was used to pool study results; funnel-plot inspection was done to evaluate publication bias; and I2 testing was used to test for heterogeneity. Data from 20 studies (1985 patients) were included in the analysis. Overall, 122 of 618 patients with elevated troponin levels died (19.7%; 95% confidence interval [CI], 16.6 to 22.8) compared with 51 of 1367 with normal troponin levels (3.7%; 95% CI, 2.7 to 4.7). Elevated troponin levels were significantly associated with short-term mortality (odds ratio [OR], 5.24; 95% CI, 3.28 to 8.38), with death resulting from pulmonary embolism (OR, 9.44; 95% CI, 4.14 to 21.49), and with adverse outcome events (OR, 7.03; 95% CI, 2.42 to 20.43). Elevated troponin levels were associated with a high mortality in the subgroup of hemodynamically stable patients (OR, 5.90; 95% CI, 2.68 to 12.95). Results were consistent for troponin I or T and prospective or retrospective studies.Elevated troponin levels identify patients with acute pulmonary embolism at high risk of short-term death and adverse outcome events.
Background and Purpose— The role of anticoagulant treatment for acute cardioembolic stroke is uncertain. We performed an updated meta-analysis of all randomized trials to obtain the best estimates of the efficacy and safety of anticoagulants for the initial treatment of acute cardioembolic stroke. Methods— Using electronic and manual searches of the literature, we identified randomized trials comparing anticoagulants (unfractionated heparin or low-molecular-weight heparin or heparinoids), started within 48 hours, with other treatments (aspirin or placebo) in patients with acute ischemic cardioembolic stroke. Two reviewers independently selected studies and extracted data on study design, quality, and clinical outcomes, including death or disability, all strokes, recurrent ischemic stroke, and cerebral symptomatic bleeding. Odds ratios for individual outcomes were calculated for each trial and data from all the trials were pooled using the Mantel-Haenszel method. Results— Seven trials, involving 4624 patients with acute cardioembolic stroke, met the criteria for inclusion. Compared with other treatments, anticoagulants were associated with a nonsignificant reduction in recurrent ischemic stroke within 7 to 14 days (3.0% versus 4.9%, odds ratio 0.68, 95% CI: 0.44 to 1.06, P =0.09, number needed to treat=53), a significant increase in symptomatic intracranial bleeding (2.5% versus 0.7%, odds ratio 2.89; 95% CI: 1.19 to 7.01, P =0.02, number needed to harm=55), and a similar rate of death or disability at final follow up (73.5% versus 73.8%, odds ratio 1.01; 95% CI: 0.82 to 1.24, P =0.9). Conclusions— Our findings indicate that in patients with acute cardioembolic stroke, early anticoagulation is associated with a nonsignificant reduction in recurrence of ischemic stroke, no substantial reduction in death and disability, and an increased intracranial bleeding.
<h3>Background</h3> In patients with acute pulmonary embolism, thrombolysis results in a more rapid resolution of pulmonary emboli than heparin treatment. Whether this advantage results in an improved clinical outcome is unclear. We sought to perform a clinical outcome–based meta-analysis of studies comparing thrombolytic and heparin treatment in patients with pulmonary embolism. <h3>Methods</h3> Data concerning adverse outcome events (death, recurrent pulmonary embolism, and major bleeding events) were extracted from the identified randomized studies. <h3>Results</h3> A total of 56 (23.2%) of 241 patients treated with thrombolytic agents in 9 randomized trials experienced an adverse outcome event compared with 57 (25.9%) of 220 patients treated with heparin (relative risk [RR], 0.9; 95% confidence interval [CI], 0.57-1.32). In the thrombolysis group, 11 patients (4.6%) died compared with 17 (7.7%) in the heparin group (RR, 0.59; 95% CI, 0.27-1.25). Thirty-one patients (12.9%) undergoing thrombolysis had a major bleeding episode compared with 19 patients (8.6%) treated with heparin (RR, 1.49; 95% CI, 0.85-2.81). Five fatal bleeding episodes (2.1%) occurred in the thrombolysis group and none in the heparin group. Six studies provided data on recurrent pulmonary embolism. A recurrence occurred in 14 (6.6%) of 214 patients treated with thrombolytic agents and in 22 (10.9%) of 201 patients treated with heparin (RR, 0.60; 95% CI, 0.29-1.15). Recurrence and/or death occurred in 25 (10.4%) of 241 and in 38 (17.3%) of 220 patients treated with thrombolytic agents and heparin, respectively (RR, 0.55; 95% CI, 0.33-0.96;<i>P</i>= .03). <h3>Conclusions</h3> In patients with pulmonary embolism, thrombolysis had a lower composite end point of death/recurrence than heparin treatment. Excessive bleeding is the trade-off for improved efficacy. A comparative clinical outcome trial of thrombolysis and heparin treatment is warranted in patients with pulmonary embolism and selected for high risk of death and/or recurrence and low risk of bleeding.
Two hybrid plasminogen activators (K2tu-PA and FK2tu-PA), linking the kringle 2 domain or the finger plus the kringle 2 domains of tissue-type plasminogen activator (t-PA) to the catalytic domain of single-chain urokinase-type plasminogen activator (scu-PA) were studied. At variance with similar constructs previously reported, they were obtained by fusion of the t-PA and scu-PA derived portions at their plasmin cleavage site (between Arg275 of t-PA and Ile159 of scu-PA), thus eliminating from scu-PA the two peptide bonds (Glu143-Leu144 and Arg156-Phe157) that lead to low molecular weight scu-PA and to thrombin-inactivated tcu-PA. The specific activities of K2tu-PA and FK2tu-PA, as measured by fibrin plate were 2.5 x 10(6) and 1.0 x 10(6) t-PA equivalent units/mg, respectively. Activation of plasminogen by hybrid PAs was stimulated by both CNBr-digested fibrinogen (40- and 80-fold) and Des-A-fibrin monomers (6- and 12-fold). The relatively weak stimulation of chimeric PAs by minimally degraded fibrin monomers was consistent with their reduced fibrin binding capacity. Like scu-PA, the chimeric PAs, in the single-chain form, were insensitive to inhibition, as they retained full activity after prolonged incubation in plasma and did not interact with SDS-reactivated recombinant PAI-1. The concentration producing 50% lysis of blood clots in 3 h was 0.5 microgram/ml for K2tu-PA and 1 microgram/ml for FK2tu-PA, as compared to 0.5 microgram/ml and > 2 micrograms/ml for t-PA and scu-PA, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
