Korte W.,Center for Laboratory Medicine |
Cattaneo M.,University of Milan |
Chassot P.-G.,University of Lausanne |
Eichinger S.,Medical University of Vienna |
And 4 more authors.
Thrombosis and Haemostasis | Year: 2011
An increasing number of patients suffering from cardiovascular disease, especially coronary artery disease (CAD), are treated with aspirin and/or clopidogrel for the prevention of major adverse events. Unfortunately, there are no specific, widely accepted recommendations for the perioperative management of patients receiving antiplatelet therapy. Therefore, members of the Perioperative Haemostasis Group of the Society on Thrombosis and Haemostasis Research (GTH), the Perioperative Coagulation Group of the Austrian Society for Anesthesiology, Reanimation and Intensive Care (ÖGARI) and the Working Group Thrombosis of the European Society of Cardiology (ESC) have created this consensus position paper to provide clear recommendations on the perioperative use of anti-platelet agents (specifically with semi-urgent and urgent surgery), strongly supporting a multidisciplinary approach to optimize the treatment of individual patients with coronary artery disease who need major cardiac and non-cardiac surgery. With planned surgery, drug eluting stents (DES) should not be used unless surgery can be delayed for ≥12 months after DES implantation. If surgery cannot be delayed, surgical revascularisation, bare-metal stents or pure balloon angioplasty should be considered. During ongoing antiplatelet therapy, elective surgery should be delayed for the recommended duration of treatment. In patients with semi-urgent surgery, the decision to prematurely stop one or both antiplatelet agents (at least 5 days pre-operatively) has to be taken after multidisciplinary consultation, evaluating the individual thrombotic and bleeding risk. Urgently needed surgery has to take place under full antiplatelet therapy despite the increased bleeding risk. A multidisciplinary approach for optimal antithrombotic and haemostatic patient management is thus mandatory. © Schattauer 2011.
Katsaros K.M.,Medical University of Vienna |
Katsaros K.M.,Ludwig Boltzmann Cluster for Cardiovascular Research |
Kastl S.P.,Medical University of Vienna |
Kastl S.P.,Ludwig Boltzmann Cluster for Cardiovascular Research |
And 10 more authors.
EuroIntervention | Year: 2014
Aims: Drug-eluting stents (DES) reduce late lumen loss compared to bare metal stents but were not able to eradicate in-stent restenosis (ISR) fully. Vascular endothelial growth factor (VEGF) may inhibit late lumen loss through accelerated reendothelialisation, but may also promote neointima formation by proinflammatory effects. The aim of this study was to evaluate whether endogenous plasma levels of VEGF are associated with development of ISR after implantation of DES. Methods and results: We studied 85 patients who were treated with 159 DES. VEGF plasma levels were determined before and 24 hours after PCI. During the eight-month follow-up period, two patients (2.4%) died of cardiovascular causes and 12 patients (14.5% of patients, 7.6% of stents) developed angiographic ISR. Basal VEGF plasma levels were not different in patients with and without ISR at follow-up. In contrast to patients without ISR, VEGF increased significantly upon PCI in patients with ISR (p<0.005). Patients with a decrease of VEGF after PCI had a restenosis rate of 2.4% compared to a restenosis rate of 26.2% in patients with an increase of VEGF after the procedure (p<0.05). This was independent from clinical and angiographic risk factors. Conclusions: Basal plasma levels of VEGF are not associated with the development of ISR. However, an increase of VEGF after PCI is associated with a dramatically increased ISR rate after implantation of DES. © Europa Digital & Publishing 2014. All rights reserved.
Verschure D.O.,University of Amsterdam |
Verschure D.O.,Medical Center Alkmaar |
De Wit T.C.,University of Amsterdam |
Bongers V.,Diakonessenhuis |
And 6 more authors.
Nuclear Medicine Communications | Year: 2015
AIM: The I-metaiodobenzylguanidine (I-MIBG) late heart-to-mediastinum ratio (H/M) is a well-established prognostic parameter in patients with chronic heart failure (CHF). However, I presents imaging problems owing to high-energy photon emission leading to penetration of collimator septa and subsequent reduction in image quality. Most likely this affects the H/M ratio and may subsequently lead to incorrect patient risk classification. In this prospective study we assessed the intrapatient variation in late H/M ratio between low-energy high-resolution (LEHR) and medium-energy (ME) collimators in patients with CHF. MATERIALS AND METHODS: Fifty-three patients with CHF (87% male, age 63±8.3 years, left ventricular ejection fraction 29±7.8) referred for I-MIBG scintigraphy were enrolled in the study. In each patient, after the administration of 185MBq I-MIBG, early (15min after injection) and late (4h after injection) planar anterior thoracic images were acquired with both LEHR and ME collimators. Early and late H/M ratios were calculated on the basis of the mean count densities from the manually drawn regions of interest (ROIs) over the left ventricle and a predefined fixed ROI placed in the upper mediastinum. Additional ROIs were drawn over the liver and lungs. Liver/lung to myocardium and liver/lung to mediastinal ratios were calculated to estimate the effect of collimator septa penetration from liver and lung activity on the myocardial and mediastinal ROIs. RESULTS: The mean LEHR collimator-derived parameters were lower compared with those from the ME collimator (late H/M 1.41±0.18 vs. 1.80±0.41, P<0.001). Moreover, Bland-Altman analysis showed that with increasing late H/M ratios the difference between the ratios from the two collimator types increased (R=0.73, P=0.001). Multivariate regression analysis showed that almost 90% of the variation in the difference between ME and LEHR late H/M ratios could be explained by scatter from the liver in both the mediastinal and myocardial ROIs (R=0.90, P=0.001). Independent predictors for the difference in the late H/M between ME and LEHR were the liver-to-heart ratio and the liver-to-mediastinum ratio assessed by ME (standardized coefficient of-1.69 and 1.16, respectively) and LEHR (standardized coefficient of 1.24 and-0.90, respectively) (P<0.001 for all). CONCLUSION: Intrapatient comparison in H/M between the ME and LEHR collimators in patients with CHF showed that with increasing H/M the difference between the ratios increased in favour of the ME collimator. These differences could be explained by septal penetration of high-energy photons from both the liver and the lung in the mediastinum and myocardium, being lowest when using the ME collimator. These results strengthen the importance of the recommendation to use ME collimators in semiquantitative I-MIBG studies.. Copyright © 2015 Wolters Kluwer Health, Inc.
Zeymer U.,Klinikum Ludwigshafen |
Zeymer U.,University of Heidelberg |
Arntz H.-R.,Medizinische Klinik II |
Mark B.,Klinikum Ludwigshafen |
And 8 more authors.
Clinical Research in Cardiology | Year: 2012
Objectives: To compare a loading dose of 600 mg clopidogrel given in the prehospital phase versus clopidogrel administered only after the diagnostic angiogram in patients with STEMI scheduled for primary PCI. Background The optimal time and dose for the initiation of clopidogrel therapy in patients with STEMI scheduled for primary PCI has not been studied in prospective randomized trials. Methods: The primary efficacy endpoint was the TIMI 2/3 patency of the infarct-related artery in the diagnostic angiography immediately prior to PCI. Results: We randomized 337 patients to prehospital (n = 166) loading dose versus standard therapy (n = 171). The time interval between initiation of clopidogrel therapy and diagnostic angiography was 47 min. TIMI 2/3 patency before PCI was not different between the groups (49.3 vs. 45.1%, P = 0.5). We observed a trend towards a reduction of the combined endpoint death, re-infarction, and urgent target vessel revascularization in the prehospital-treated patients (3.0 vs. 7.0%, P = 0.09), this difference was significant if patients were classified as treated (4/161 vs. 13/174; 2.5 vs. 7.5%, P<0.05). There was no difference in TIMI major bleeding complications (9.1 vs. 8.2%, P = 0.8). Conclusions: Early inhibition of the platelet ADP-receptor with a high loading dose of 600 mg clopidogrel given in the prehospital phase in patients with STEMI scheduled for primary PCI is safe, did not increase pre-PCI patency of the infarct vessel, but was associated with a trend towards a reduction in clinical events. © Springer-Verlag 2011.
Goliasch G.,Medical University of Vienna |
Wiesbauer F.,Medical University of Vienna |
Kastl S.P.,Medical University of Vienna |
Kastl S.P.,Ludwig Boltzmann Foundation for Cardiovascular Research |
And 9 more authors.
Atherosclerosis | Year: 2012
Objective: Besides its effects on glucose and lipid metabolism, the Wnt pathway has been increasingly implicated in the regulation of proliferation, migration and survival of vascular cells. In addition, defective Wnt signaling has been identified in a family with autosomal dominant early coronary artery disease. The aim of this study was to investigate whether premature coronary artery disease is associated with features of decreased Wnt signaling. Methods and results: We prospectively enrolled 100 consecutive young survivors of myocardial infarction (MI ≤ 40. years of age) from two high-volume cardiac catheterization centers and 100 sex and age matched hospital controls. We determined serum levels of Wnt-1 and its antagonist Dkk-1 by ELISA. MI patients showed significantly lower Wnt-1 levels as compared to controls (151. ng/mL, IQR 38-473. ng/mL vs. 233. ng/mL, IQR 62-1756; p< 0.005) whereas Dkk-1 was not different at baseline. Wnt-1 levels remained stable over time, whereas Dkk-1 significantly increased at one-year follow-up from 3557, IQR 2306-5810. pg/mL to 4973, IQR 3293-7093. pg/mL (p< 0.001). In the stable phase of the disease, Wnt-1 levels were lower (p< 0.005) and Dkk-1 levels were significantly higher (p< 0.001) as compared to controls. Wnt-1 at follow-up was associated with glucose, HbA1c, non-HDL-, HDL-cholesterol and triglyceride levels but no other features of the metabolic syndrome. Conclusion: This study establishes an association between low Wnt-1 and high Dkk-1 serum levels and premature myocardial infarction. Wnt-1 is associated with markers of glucose and lipid metabolism. Further research elucidating the role of Wnt pathways in premature coronary artery disease and metabolic syndrome is warranted. © 2012 Elsevier Ireland Ltd.
Goldstein P.,CHRU de Lille |
Elalamy I.,Hopital Tenon |
Huber K.,Cardiology and Emergency Medicine |
Danchin N.,Hopital Europeen Georges Pompidou |
Wiel E.,CHRU de Lille
International Journal of Emergency Medicine | Year: 2013
Pulmonary embolism (PE) is potentially fatal and often requires emergency management. Because PE associated with shock and/or hypotension carries a high risk of sudden death, emergency clinicians must rapidly make a diagnosis and initiate appropriate therapeutic strategies, usually involving anticoagulant treatment. Traditional anticoagulants, such as heparins and vitamin K antagonists, although effective and recommended by guidelines, are associated with limitations. Several targeted, orally administered anticoagulants that may overcome some of these constraints have been developed recently and undergone analysis in randomised, phase III clinical trials. Rivaroxaban, a direct factor Xa inhibitor, was non-inferior to standard therapy with enoxaparin plus a vitamin K antagonist for the prevention of recurrent, symptomatic venous thromboembolism (VTE) in patients with acute PE and led to a 50% reduction in major bleeding. Dabigatran, a direct thrombin inhibitor, was also non-inferior to standard therapy for the prevention of recurrent VTE or VTE-related death when given after a parenteral anticoagulant and had a similar incidence of major bleeding. The results of a phase III study of apixaban, another direct factor Xa inhibitor, for the acute treatment of VTE are expected in the near future. Rivaroxaban is now approved in Europe and the US for the treatment of acute PE and prevention of recurrent VTE. This article reviews the current guidance on the treatment of PE with special focus on the emergency setting, and considers data regarding rivaroxaban and the other non-vitamin K antagonist oral anticoagulants and their potential role, including patients who are and are not appropriate for treatment with these agents. Issues such as drug interactions, reversal of anticoagulant effect and coagulation monitoring are also discussed. © 2013 Goldstein et al.; licensee Springer.
Kopec G.,Jagiellonian University |
Moertl D.,Cardiology and Emergency Medicine |
Miszalski-Jamka T.,John Paul II Hospital in Cracow |
Waligora M.,Jagiellonian University |
And 3 more authors.
Heart Lung and Circulation | Year: 2014
Background: Left ventricular (LV) atrophic remodelling was described for chronic thromboembolic pulmonary hypertension (PH) but not in other forms of PH. We aimed to assess LV morphometric changes in idiopathic pulmonary arterial hypertension (IPAH) and Eisenmenger's syndrome(ES). Methods: Fifteen patients with IPAH, 15 patients with ES and 15 healthy volunteers were included. Magnetic resonance was used to measure masses of LV, interventricular septum (IVS), LV free wall (LVFW), and LV end diastolic volume (LVEDV) indexed for body surface area. Results: Between patients with IPAH, ES and controls no differences in LVmassindex (54.4[45.2-63.3] vs 58.7[41.5-106.1] vs 52.8[46.5-59.3], p=0.50), IVSmassindex (21.6[18.2-21.9)] vs 27.4[18.0-32.9] vs 20.7[18.2-23.2], p=0.18), and LVFWmassindex ([32.4[27.1-40.0] vs 36.7[30.9-62.1] vs 32.5[26.9-36.1], p=0.29) were found. LVEDVindex was lower in IPAH patients than in controls and in ES patients (54.9[46.9-58.5] vs 75.2[62.4-88.9] vs 73.5[62.1-77.5], p<0.001). In IPAH LVEDV but not LV mass correlated with pulmonary vascular resistance (r=-0.56, p=0.03) and cardiac output (r=0.59, p=0.02). Conclusions: LV mass is not reduced in patients with IPAH and with ES and is not affected by haemodynamic severity of PH. LVEDV is reduced in IPAH patients in proportion to reduced pulmonary flow but preserved in patients with ES, where reduced pulmonary flow to LV is compensated by right-to left shunt. © 2013 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ).