Publications

Real-life use of non-vitamin K antagonist oral anticoagulants in comparison with vitamin K antagonists for non-valvular atrial fibrillation: data from a prospective cohort

Thrombosis and cancer: clinical relevance of a dangerous liaison.

Treatment of venous thromboembolism in patients with cancer: What news from clinical trials?

Prognostic value of trans-thoracic echocardiography in patients with acute stroke and atrial fibrillation: findings from the RAF study

Editorial (Thematic Issue: Antithrombotic Therapy: Current and Future Clinical Use)

Keywords: Venous thromboembolism, ischemic stroke, anticoagulant treatment, antiplatelet therapy, thrombolysis.

Clinical skills or high-tech MR in TIA patients: what makes the difference?

Thrombin plays a pivotal role in vascular re-occlusion after PTCA and coronary thrombolysis

Acute coronary syndromes are the clinical presentations of complex biochemical events which in most cases culminate in intracoronary thrombosis. A central role in the process of intravascular thrombosis is played by thrombin, a glycosylated trypsin-like serine protease with multiple action in vascular biology [l]. In patients with acute coronary syndromes thrombin is generated by the exposure of tissue factor after fissuring or rupture of a coronary plaque. Tissue factor leads to thrombin generation through the activation of the coagulation factors VII and IX and the prothrombinase complex. Once generated, thrombin initiates a positive feed-back autocatalytic loop by directly activating factors V and VIII, thus amplifying its generation by about lOOO-fold. At substrate level, other than activating factors V and VIII, thrombin cleaves fibrinogen to fibrin and activates factor XIII which results in formation of stable, cross-linked fibrin clot. Thrombin binds to a specific receptor on the platelet surface initiating a number of intracellular processes, including ADP and thromboxane A, release and expression of GP IIb/IIIa receptors, which result in platelet aggregation. Thrombin receptors have been cloned from human platelets and vascular smooth muscle cells [2,3]. The activation of thrombin receptor on vascular smooth muscle cells is followed by most of the multiple cellular effects of thrombin, mainly by smooth muscle cell mitogenesis and migration. High concentrations of thrombin are present at the time and the site of mechanical injury or PTCA and persist throughout the period of vascular formation. The restenosis process appears to be triggered by the formation of a “neointima”

Stroke pharmacogenomics

Circulatory disease accounts for fifteen million deaths each year, of which stroke accounts for four and a half million- with an estimated nine million stroke survivors annually. The overall incidence rate of stroke is 2 to 2.5 per thousand adults with an approximate prevalence of 5 per thousand and an estimated 5-year risk of stroke recurrence of 15 to 40 percent. Conventional risk factors for stroke include: increasing age, hypertension, diabetes mellitus, smoking, increased body mass index, ischemic heart disease, heart failure, atrial fibrillation and lack of physical activity. Age is the strongest risk factor for both ischemic and haemorrhagic stroke with its incidence doubling for each successive decade after the age of fifty-five years. However, there is a substantial portion of patients with significant cerebrovascular disease who do not have any of these stroke risk-factors, leading to the speculation that there are other factors that have not been identified yet So as to improve diagnosis and treatment strategies, as well as to reduce the related public health burden, it could be helpful to successfully identify its extremely complex genetic determinants (polygenic, multiple genes play a role).Pharmacogenetics is the field of pharmacology that deals with the influence of genetic variation on drug response by correlating gene expression and gene variants with the efficacy or toxicity of drugs. The principle drugs in stroke medicine are antithrombotics. The aim of this paper was to review the most commonly used drugs for stroke such as rtPA in the acute phase as well as antiplatelets and wafarin for secondary prophylaxis.

Thrombolysis in hemodynamically stable patients with acute pulmonary embolism: A meta-analysis

A Clinical Outcome-Based Prospective Study on Venous Thromboembolism After Cancer Surgery

The epidemiology of venous thromboembolism (VTE) after cancer surgery is based on clinical trials on VTE prophylaxis that used venography to screen deep vein thrombosis (DVT). However, the clinical relevance of asymptomatic venography-detected DVT is unclear, and the population of these clinical trials is not necessarily representative of the overall cancer surgery population.The aim of this study was to evaluate the incidence of clinically overt VTE in a wide spectrum of consecutive patients undergoing surgery for cancer and to identify risk factors for VTE.@RISTOS was a prospective observational study in patients undergoing general, urologic, or gynecologic surgery. Patients were assessed for clinically overt VTE occurring up to 30 +/- 5 days after surgery or more if the hospital stay was longer than 35 days. All outcome events were evaluated by an independent Adjudication Committee.A total of 2373 patients were included in the study: 1238 (52%) undergoing general, 685 (29%) urologic, and 450 (19%) gynecologic surgery. In-hospital prophylaxis was given in 81.6% and postdischarge prophylaxis in 30.7% of the patients. Fifty patients (2.1%) were adjudicated as affected by clinically overt VTE (DVT, 0.42%; nonfatal pulmonary embolism, 0.88%; death 0.80%). The incidence of VTE was 2.83% in general surgery, 2.0% in gynecologic surgery, and 0.87% in urologic surgery. Forty percent of the events occurred later than 21 days from surgery. The overall death rate was 1.72%; in 46.3% of the cases, death was caused by VTE. In a multivariable analysis, 5 risk factors were identified: age above 60 years (2.63, 95% confidence interval, 1.21-5.71), previous VTE (5.98, 2.13-16.80), advanced cancer (2.68, 1.37-5.24), anesthesia lasting more than 2 hours (4.50, 1.06-19.04), and bed rest longer than 3 days (4.37, 2.45-7.78).VTE remains a common complication of cancer surgery, with a remarkable proportion of events occurring late after surgery. In patients undergoing cancer surgery, VTE is the most common cause of death at 30 days after surgery.

PROSPECTIVE ASSESSMENT OF CLINICAL ENDPOINTS OF VKA TREATMENT IN A PRIMARY CARE COMPUTER ASSISTED MANAGEMENT MODEL

A phase II study of the oral factor Xa inhibitor LY517717 for the prevention of venous thromboembolism after hip or knee replacement

P4603The burden of atrial fibrillation in the more populated European countries: perspectives from the GARFIELD-AF registry

Safety of the combination of low-molecular weight heparin and glycoprotein IIb/IIIa inhibitors: observations from the GLobal Registry of Acute Coronary Events (GRACE)

Prognostic value of respiratory index in haemodynamically stable patients with acute pulmonary embolism: The Respiratory Index model study

Background: Current strategies for prognostic stratification in haemodynamically stable patients with acute pulmonary embolism require improvement. The aims of this study in haemodynamically stable patients with acute pulmonary embolism were (a) to evaluate the prognostic value of a novel respiratory index (oxygen saturation in air to respiratory rate ratio) and (b) to derive a risk model which includes the respiratory index and evaluate its value in predicting 30-day mortality. Methods: Prospective cohorts of haemodynamically stable patients with acute pulmonary embolism were merged to a collaborative database that served to create two subsequent derivation and validation cohorts based on a temporal criterion. The study outcome was 30-day all-cause death. Results: Thirty-day all-cause death occurred in 7.5% and in 6.9% of patients in the derivation and validation cohorts (each composed of 319 patients). In the derivation cohort, the respiratory index (odds ratio 0.66, 95% confidence interval 0.48–0.90) and simplified Pulmonary Embolism Severity Index (odds ratio 9.16, 95% confidence interval 1.22–68.89) were predictors of 30-day mortality. The cut-off value of the respiratory index ⩽3.8 was identified to best predict 30-day all-cause death (15.4% vs 5.0%, odds ratio 2.94, 95% confidence interval 1.22–7.11). The respiratory index ⩽3.8 was combined with the simplified Pulmonary Embolism Severity Index to create the Respiratory Index model that showed a good discriminatory power in the derivation (c-statistic 0.703, 95% confidence interval 0.60–0.80) and in the validation cohort (c-statistic 0.838, 95% confidence interval 0.768–0.907). Conclusion: In hemodynamically stable patients with acute pulmonary embolism, the respiratory index was an independent predictor of 30-day all-cause death. The Respiratory Index model which includes the simplified Pulmonary Embolism Severity Index and the respiratory index, provides a good risk stratification of haemodynamically stable patients with acute pulmonary embolism.

Critical Issues in Peripheral Arterial Disease Detection and Management<subtitle>A Call to Action</subtitle>

Jill J. F. Belch, MD; Eric J. Topol, MD; Giancarlo Agnelli, MD; Michel Bertrand, MD; Robert M. Califf, MD; Denis L. Clement, MD; Mark A. Creager, MD; J. Donald Easton, MD; James R. Gavin III, MD, PhD; Philip Greenland, MD; Graeme Hankey, MD; Peter Hanrath, MD; Alan T. Hirsch, MD; Jurgen Meyer, MD; Sidney C. Smith, MD; Frank Sullivan, PhD; Michael A. Weber, MD; for the Prevention of Atherothrombotic Disease Network

Duration of Anticoagulant Treatment after VenousThromboembolism

The current recommended treatment of venous thromboembolism (VTE) consists of an initial treatment with heparin (either subcutaneous low-molecular-weight heparin or intravenous unfractionated heparin) relayed with a longterm treatment with oral anticoagulants (INR 2.0 3.0) given for at least three months [1]. The majority of the studies on the long-term treatment of VTE included patients with deep vein thrombosis (DVT). Based on the assumption that DVT and pulmonary embolism (PE) are two manifestations of the same disease, information available for patients with DVT are commonly translated to patients with PE. Recently, several differences regarding the risk for recurrent VTE in patients with DVT and PE have been reported. In particular, it has been shown that patients with PE are at slightly higher risk of dying from recurrent PE than are patients with DVT [2-3]. For this reason, more prolonged anticoagulation has been proposed for patients with PE, but this choice is not evidence based. Need for Shortand Long-Term Anticoagulant Treatment

ANALYSIS OF THE BLEEDING AND THROMBOEMBOLIC RISK WITH CONCOMITANT USE OF ANTIPLATELET TREATMENT IN THE AMPLIFY TRIAL