Search

Your search keyword '"van der Laarse, Arnoud"' showing total 573 results
Start Over Author "van der Laarse, Arnoud"
573 results on '"van der Laarse, Arnoud"'

9. Peak and Fixed-Time High-Sensitive Troponin for Prediction of Infarct Size, Impaired Left Ventricular Function, and Adverse Outcomes in Patients With First ST-Segment Elevation Myocardial Infarction Receiving Percutaneous Coronary Intervention

Author

Boden, Helèn, Ahmed, Tarek A.N., Velders, Matthijs A., van der Hoeven, Bas L., Hoogslag, Georgette E., Bootsma, Marianne, le Cessie, Saskia, Cobbaert, Christa M., Delgado, Victoria, van der Laarse, Arnoud, and Schalij, Martin J.

Published
2013
Full Text
View/download PDF

10. Value of admission electrocardiogram in predicting outcome of thrombolytic therapy in acute myocardial infarction : A randomized trial conducted by The Netherlands Interuniversity Cardiology Institute

Author

Bär, Fritz W., Vermeer, Frank, De Zwaan, Chris, Ramentol, Mercedes, Braat, Simon, Simoons, Maarten L., Hermens, Wim T., Van Der Laarse, Arnoud, Verheugt, Freek W. A., Krauss, X. Hanno, Wellens, Hein J. J., Smeets, J. L. R. M., editor, Doevendans, P. A., editor, Josephson, M. E., editor, Kirchhof, Ch., editor, and Vos, M. A., editor

Published
2000
Full Text
View/download PDF

21. Allogenic stem cell therapy improves right ventricular function by improving lung pathology in rats with pulmonary hypertension

Author

Umar, Soban, de Visser, Yvonne P., Steendijk, Paul, Schutte, Cindy I., Laghmani, El Houari, Wagenaar, Gerry T.M., Bax, Wilhelmina H., Mantikou, Eleni, Pijnappels, Daniel A., Atsma, Douwe E., Schalij, Martin J., van der Wall, Ernst E., and van der Laarse, Arnoud

Subjects
Heart ventricle, Right -- Properties, Physiology, Pathological -- Research, Pulmonary hypertension -- Development and progression, Pulmonary hypertension -- Care and treatment, Stem cells -- Transplantation, Stem cells -- Methods, Biological sciences
Abstract

Pulmonary arterial hypertension (PAH) is a chronic lung disease that leads to right ventricular (RV) hypertrophy (RVH), remodeling, and failure. We tested treatment with bone marrow-derived mesenchymal stem cells (MSCs) obtained from donor rats with monocrotaline (MCT)-induced PAH to recipient rats with MCT-induced PAH on pulmonary artery pressure, lung pathology, and RV function. This model was chosen to mimic autologous MSC therapy. On day 1, PAH was induced by MCT (60 mg/kg) in 20 female Wistar rats. On day 14, rats were treated with [10.sup.6] MSCs intravenously (MCT + MSC) or with saline (MCT60). MSCs were obtained from donor rats with PAH at 28 days after MCT. A control group received saline on days 1 and 14. On day 28, the RV function of recipient rats was assessed, followed by isolation of the lungs and heart. RVH was quantified by the weight ratio of the RV/(left ventricle + interventricular septum). MCT induced an increase of RV peak pressure (from 27 [+ or -] 5 to 42 [+ or -] 17 mmHg) and RVH (from 0.25 [+ or -] 0.04 to 0.47 [+ or -] 0.12), depressed the RV ejection fraction (from 56 [+ or -] 11 to 43 [+ or -] 6%), and increased lung weight (from 0.96 [+ or -] 0.15 to 1.66 [+ or -] 0.32 g), including thickening of the arteriolar walls and alveolar septa. MSC treatment attenuated PAH (31 [+ or -] 4 mmHg) and RVH (0.32 [+ or -] 0.07), normalized the RV ejection fraction (52 [+ or -] 5%), reduced lung weight (1.16 [+ or -] 0.24 g), and inhibited the thickening of the arterioles and alveolar septa. We conclude that the application of MSCs from donor rats with PAH reduces RV pressure overload, RV dysfunction, and lung pathology in recipient rats with PAH. These results suggest that autologous MSC therapy may alleviate cardiac and pulmonary symptoms in PAH patients. pulmonary arterial hypertension; heart failure; hypertrophy; remodeling; monocrotaline doi: 10.1152/ajpheart.00590.2009.

Published
2009

24. Mesenchymal stem cells from ischemic heart disease patients improve left ventricular function after acute myocardial infarction

Author

Grauss, Robert W., Winter, Elizabeth M., van Tuyn, John, Pijnappels, Daniel A., Steijn, Rebecca Vicente, Hogers, Bianca, van der Geest, Rob J., de Vries, Antoine A.F., Steendijk, Paul, van der Laarse, Arnoud, Gittenberger-de Groot, Adriana C., Schalij, Martin J., and Atsma, Douwe E.

Subjects
Stem cells -- Properties, Myocardial ischemia -- Physiological aspects, Heart ventricle, Left -- Properties, Heart attack -- Physiological aspects, Magnetic resonance imaging -- Methods, Biological sciences
Abstract

Mesenchymal stem cells (MSCs) from healthy donors improve cardiac function in experimental acute myocardial infarction (AMI) models. However, little is known about the therapeutic capacity of human MSCs (hMSCs) from patients with ischemic heart disease (IHD). Therefore, the behavior of hMSCs from IHD patients in an immunecompromised mouse AMI model was studied. Enhanced green fluorescent protein-labeled hMSCs from IHD patients (hMSC group: 2 x [10.sup.5] cells in 20 [micro]l, n = 12) or vehicle only (medium group: n = 14) were injected into infarcted myocardium of NOD/scid mice. Sham-operated mice were used as the control (n = 10). Cardiac anatomy and function were serially assessed using 9.4-T magnetic resonance imaging (MRI); 2 wk after cell transplantation, immunohistological analysis was performed. At day 2, delayed-enhancement MRI showed no difference in myocardial infarction (MI) size between the hMSC and medium groups (33 [+ or -] 2% vs. 36 [+ or -] 2%: P = not significant). A comparable increase in left ventricular (LV) volume and decrease in ejection fraction (EF) was observed in both MI groups. However, at day 14, EF was higher in the hMSC than in the medium group (24 [+ or -] 3% vs. 16 [+ or -] 2%; P < 0.05). This was accompanied by increased vascularity and reduced thinning of the infarct scar. Engrafted hMSCs (4.1 [+ or -] 0.3% of injected cells) expressed von Willebrand factor (16.9 [+ or -] 2.7%) but no stringent cardiac or smooth muscle markers. hMSCs from patients with IHD engraft in infarcted mouse myocardium and preserve LV function 2 wk after AMI, potentially through an enhancement of scar vascularity and a reduction of wall thinning. magnetic resonance imaging; cell therapy; animal model

Published
2007

26. Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat

Author

Hessel, Marleen H.M., Steendijk, Paul, den Adel, Brigit, Schutte, Cindy I., and van der Laarse, Arnoud

Subjects
Pulmonary hypertension -- Physiological aspects, Pulmonary hypertension -- Research, Heart enlargement -- Physiological aspects, Biological sciences
Abstract

We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with MCT at 30 mg/kg body wt (MCT30, n = 15) and 80 mg/kg body wt (MCT80, n = 16) to induce compensated RV hypertrophy and RV failure, respectively. Saline-treated rats served as control (Cont, n = 13). After 4 wk, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were killed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV), and interventricular septum (IVS) were weighed and analyzed histochemically. RV-to-(LV + IVS) weight ratio was 0.29 [+ or -] 0.05 in Cont, 0.35 [+ or -] 0.05 in MCF30, and 0.49 [+ or -] 0.10 in MCT80 (P < 0.001 vs. Cont and MCT30) rats, confirming MCT-induced RV hypertrophy. RV ejection fraction was 49 [+ or -] 6% in Cont, 40 [+ or -] 12% in MCT30 (P < 0.05 vs. Cont), and 26 [+ or -] 6% in MCT80 (P < 0.05 vs. Cont and MCT30) rats. In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared with Cont (all P < 0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes, and peak wall stress were further increased, and cardiac output was significantly decreased (all P < 0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under nonfailing conditions. right ventricular hypertrophy; right ventricular failure; pressure-volume relations

Published
2006

28. Vascular smooth muscle cells and calcification in atherosclerosis

Author

Trion, Astrid and van der Laarse, Arnoud

Subjects
Vascular smooth muscle -- Physiological aspects, Vascular smooth muscle -- Diseases, Calcification -- Causes of, Atherosclerosis -- Diseases, Atherosclerosis -- Causes of, Apoptosis -- Physiological aspects, Bones -- Growth, Bones -- Physiological aspects, Health
Published
2004

33. Cardiomyogenic differentiation-independent improvement of cardiac function by human cardiomyocyte progenitor cell injection in ischaemic mouse hearts

Author

den Haan, Melina C., Grauss, Robert W., Smits, Anke M., Winter, Elizabeth M., van Tuyn, John, Pijnappels, Daniël A., Steendijk, Paul, Gittenberger-De Groot, Adriana C., van der Laarse, Arnoud, Fibbe, Willem E., de Vries, Antoine A. F., Schalij, Martin J., Doevendans, Pieter A., Goumans, Marie-José, and Atsma, Douwe E.

Published
2012
Full Text
View/download PDF

43. In-ambulance abciximab administration in STEMI patients prior to primary PCI is associated with smaller infarct size, improved LV function and lower incidence of heart failure: Results from the Leiden MISSION! acute myocardial infarction treatment optimization program

Author

Hassan, Ayman K. M., Liem, Su San, van der Kley, Frank, Bergheanu, Sandrin C., Wolterbeek, Ron, Bosch, Jan, Bootsma, Marianne, Zeppenfeld, Katja, van der Laarse, Arnoud, Atsma, Douwe E., Jukema, Wouter J., and Schalij, Martin J.

Published
2009
Full Text
View/download PDF

47. Association of apolipoproteins C-I, C-II, C-III and E with coagulation markers and venous thromboembolism risk

Author

Orsi, Fernanda A, Lijfering, Willem M, Van der Laarse, Arnoud, Ruhaak, L Renee, Rosendaal, Frits R, Cannegieter, Suzanne C, and Cobbaert, Christa

Subjects
lipids, proteomics, risk factors, cholesterol, Clinical Epidemiology, cardiovascular diseases, coagulation, thrombosis, Original Research
Abstract

Fernanda A Orsi,1,2Willem M Lijfering,2,3Arnoud Van der Laarse,4,5L Renee Ruhaak,4 Frits R Rosendaal,2 Suzanne C Cannegieter,2–3,6 Christa Cobbaert41Department of Clinical Pathology, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, Brazil; 2Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands; 3Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands; 4Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, The Netherlands; 5Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands; 6Department of Internal Medicine, Section of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The NetherlandsPurpose: Apolipoproteins C-I, C-II, C-III and E have been associated with risk of arterial thrombotic diseases. We investigated whether these apolipoproteins have prothrombotic properties and are associated with risk of venous thromboembolism (VTE).Patients and methods: A total of 127 VTE patients and 299 controls were randomly selected from the Multiple Environmental and Genetic Assessment of Risk Factors for Venous Thrombosis study (1999–2004), in the Netherlands. The apolipoproteins were quantified using mass spectrometry (LC/MS/MS), and their levels were analyzed as continuous variable (per SD increase).Results: In controls, increases in levels of apolipoproteins were associated with increases in levels of vitamin K-dependent factors, factor XI, antithrombin and clot lysis time. Additionally, increasing apolipoproteins C-III and E levels were associated with higher factor VIII and von Willebrand factor levels. Levels of C-reactive protein were not associated with any apolipoprotein. The age- and sex-adjusted odds ratios of apolipoproteins E, C-III, CII and CI to the risk of venous thrombosis were 1.21 (95% CI, 0.98–1.49), 1.19 (95% CI, 0.99–1.44), 1.24 (95% CI, 0.95–1.61) and 1.06 (95% CI, 0.87–1.30) per SD increase, respectively. These odds ratios did not attenuate after adjustments for statin use, estrogen use, BMI, alcohol use, and self-reported diabetes.Conclusions: Levels of apolipoproteins C-I, C-II, C-III and E are associated with those of several coagulation factors. However, whether these apolipoproteins are also associated with an increased risk of VTE remains to be established.Keywords: thrombosis, proteomics, lipids, cholesterol, coagulation, risk factors

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results