546 publications from this institution
In-hospital mortality in patients with acute pulmonary embolism ranges between about 1% and over 30%. Due to a particularly high mortality, hemodynamically unstable patients with pulmonary embolism should receive thrombolytic treatment. The role of thrombolytic treatment in hemodynamically stable patients with pulmonary embolism is controversial and should be restricted to those at high risk for in-hospital mortality. Prognostic stratification is crucial in hemodynamically stable patients as mortality in this group ranges between 1 and 10%. Serum troponin levels have been shown to be associated with in-hospital mortality and clinical deterioration. Studies on the prognostic value of serum troponin in patients with acute pulmonary embolism have been included in a meta-analysis that shows a 5-fold in hospital mortality in patients with high troponin compared to those with normal troponin levels. The prognostic value of elevated serum troponin levels have also been shown in studies including only hemodynamically stable patients with pulmonary embolism. Future studies will evaluate the clinical benefit of thrombolytic treatment in hemodynamically stable patients with acute pulmonary embolism at high risk for adverse outcome.
The correspondence by S. Ozsu concerns several issues. The first issue is the identification of low-risk patients with acute pulmonary embolism. According to the 2014 European Society of Cardiology (ESC) guidelines, a Simplified Pulmonary Embolism Severity Index (sPESI) score of zero efficiently identifies patients at low risk for death; assessment of right ventricle dysfunction by imaging or biomarkers is optional in patients with sPESI 0 [1]. Our study reports a simulation of what would happen in clinical practice by adopting the risk stratification model proposed by the 2014 ESC guidelines (see table 2 of our article) [2]. Patients at low risk (sPESI 0) would not undergo assessment of right ventricle dysfunction by imaging or biomarkers. The warning here is that ∼40% of these patients have right ventricle dysfunction at imaging and ∼30% of them have increased troponin levels [2]. Are these abnormalities of clinical value? It depends on the clinical relevance of the 0.5% observed 30-day mortality. In our opinion, 0.5% mortality at 30 days does not justify the mandatory assessment of right ventricle dysfunction and biomarkers in all patients with sPESI 0. However, we believe that right to left ventricle dimension ratio should be evaluated and reported for all patients who have computed tomography angiography for the diagnosis of pulmonary embolism [3]. This assessment will help clinicians to properly select low-risk patients (sPESI 0 and no right ventricle dilation) without performing any additional test. Further studies are needed to improve risk stratification in acute pulmonary embolism at intermediate risk for death <http://ow.ly/BYZo304vmUy>
The aim of this study was to compare the ability of standard heparin and recombinant (r-)hirudin, a specific inhibitor of thrombin, to inhibit thrombus growth in a rabbit jugular vein model. Doses of standard heparin and r-hirudin equivalent in prolonging the aPTT were first identified. The ability of these doses to inhibit 125I-fibrin accretion onto preexisting thrombi was then evaluated. 0.5 and 0.75 mg/kg of standard heparin and 0.8 and 1.25 mg/kg of r-hirudin infused over 3 h produced a mean prolongation of the aPTT of 1.5 and 2 times, respectively. In saline treated rabbits 62 +/- 7 micrograms of 125I-fibrin were accreted on the pre-formed thrombi. The lower doses of standard heparin and r-hirudin produced a 125I-fibrin accretion of 44 +/- 5 and 25 +/- 4 micrograms, respectively (p less than 0.01). The two higher doses of standard heparin and r-hirudin produced a 125I-fibrin accretion of 34 +/- 4 and 17 +/- 3 micrograms, respectively (p less than 0.01). The increase in the dose of standard heparin up to 2.5 mg/kg produced a 125I-fibrin accretion of 26 +/- 3 micrograms a 58% reduction when compared with saline. The increase in the dose of r-hirudin up to 5 mg/kg produced a 125I-fibrin accretion of 12 +/- 2 micrograms, an 81% reduction when compared with saline. No further inhibition was observed when the doses of both agents were further increased. We conclude that doses of standard heparin and r-hirudin equivalent in prolonging the aPTT have a different effect on thrombus growth inhibition, r-hirudin being twice as effective as standard heparin. Exclusive inhibition of thrombin without any other inhibiting effect on blood coagulation appears to be sufficient to inhibit thrombus growth. Our results seem to be promising in view of a clinical evaluation of r-hirudin.
No Abstract
Venous thromboembolism (VTE) is often asymptomatic, mis-diagnosed, and unrecognized at death, and there is a lack of routine postmortem examinations. These factors are thought to result in marked underestimates ofVTE incidence. The objective of our study was to estimate the total burden of VTE within the European Union (EU) per annum. An epidemiological model was constructed to estimate the number of community- and hospital-acquired incidents and recurrent cases (attack rate) of nonfatal VTE and VTE-related deaths, as well as incident and prevalent cases of post-thrombotic syndrome (PTS) and chronic thromboembolic pulmonary hypertension (PH) occurring in the EU per annum. Individual models were developed for six EU countries. The models were populated with data from published literature and, where necessary, expert opinions. The findings were tested using probabilistic sensitivity analyses. The estimated total number of symptomaticVTE events (range based on probabilistic sensitivity analysis) per annum within the six EU countries was 465,715 (404,664-538,189) cases of deep-vein thrombosis, 295,982 (242,450-360,363) cases of pulmonary embolism (PE), and 370,012 (300,193-483,108) VTE-related deaths. Of these deaths, an estimated 27,473 (7%) were diagnosed as being antemortem; 126,145 (34%) were sudden fatal PE, and 217,394 (59%) followed undiagnosed PE. Almost three-quarters of all VTE-related deaths were from hospital-acquired VTE. VTE is a major health problem in the EU, with over one million VTE events or deaths per annum in the six countries examined. Given the availability of effective VTE prophylaxis, many of these events and deaths could have been prevented. These results have important implications for the allocation of healthcare resources.
Despite the recent advancements, oral anticoagulation is still challenging in some patients and this is the case for old and frail patients. The large majority of frail patients with atrial fibrillation should receive anticoagulation since the associated benefits outweigh the risk of bleeding. A multidisciplinary consensus document on the use and prescription of direct oral anticoagulants (DOACs) in older and frail patients with atrial fibrillation has been recently published. In this manuscript we provide a comment on this document and add insights into the management of these patients. The new DOAC age had imposed a paradigm shift in the management of patients with the need for clinically-oriented services rather than laboratory-oriented services. In this paper we provide tools for a structured patient-oriented DOACs treatment service supported by a multidisciplinary approach.
Summary Intracranial haemorrhage (ICH), which affects up to 1% of patients on oral anticoagulation per year, is the most feared and devastating complication of this treatment. After such an event, it is unclear whether anticoagulant therapy should be resumed. Such a decision hinges upon the assessment of the competing risks of haematoma growth or recurrent ICH and thromboembolic events. ICH location and the risk for ischaemic cerebrovascular event seem to be the key factors that lead to risk/benefit balance of restarting anticoagulation after ICH. Patients with lobar haemorrhage or cerebral amyloid angiopathy remain at higher risk for anticoagulant-related ICH recurrence than thromboembolic events and, therefore would be best managed without anticoagulants. Patients with deep hemispheric ICH and a baseline risk of ischemic stroke >6.5% per year, that corresponds to CHADS2 ≥ 4 or CHA2DS2-VASc ≥ 5, may receive net benefit from restarting anticoagulation. To date, a reasonable recommendation regarding time to resumption of anticoagulation therapy would be after 10 weeks. Available data regarding the role of magnetic resonance imaging in assessing the risks of both ICH and warfarin-related ICH do not support the use of this test for excluding anticoagulation in patients with atrial fibrillation.
This supplement represents the first publication of Thrombosis Quorum (TQ), a recently established international consortium of multidisciplinary thrombosis-related specialists dedicated to raising the priority of thrombosis. TQ aims to address the unmet clinical needs in the prevention and treatment of thromboembolic conditions, and promote the optimum management of patients with or at risk of these disorders by providing a cross-disciplinary forum for information exchange and debate. This publication incorporates a collection of state-of-the-art articles written by the TQ Steering Group and co-authors, and in this instance, focuses on the management and treatment of patients with atrial fibrillation (AF). AF is the strongest independent predictor for stroke, the leading cause of disability, and the second leading cause of death worldwide. As such, AF has become accepted as a common and rapidly growing clinical problem and disease entity, as highlighted in the first article of this series by Bernard Gersh and coworkers who describe AF as a ‘growing epidemic’ and ‘an enormous public-health burden’. Although AF is primarily a disease of the elderly, the authors suggest that in most patients, the development of AF may …
