Schuster A.,King's College London |
Morton G.,King's College London |
Chiribiri A.,King's College London |
Perera D.,King's College London |
And 2 more authors.
Journal of the American College of Cardiology | Year: 2012
Heart failure of ischemic origin has become increasingly common over the last decade because of the improved survival of patients with acute myocardial infarction. Revascularization with coronary bypass grafting or percutaneous coronary intervention plays a pivotal role in patients with ischemic cardiomyopathy, although these interventions are often associated with relatively high peri-procedural risk. The pathophysiological substrate of ischemic cardiomyopathy is heterogeneous, varying from predominantly hibernating myocardium to irreversible scarring. There is evidence to suggest that patients with hibernating myocardium benefit most from revascularization, whereas medical therapy is associated with an adverse prognosis. Therefore, noninvasive testing is recommended by relevant guidelines to guide optimal management in these patients. However, the role of noninvasive testing has recently been challenged. There are various imaging modalities available that provide information on different aspects of the disease, and therefore, they differ significantly in sensitivity and specificity. In clinical practice, choosing among the different imaging modalities can be difficult. Cardiac magnetic resonance has evolved into a comprehensive modality that can accurately determine the amount of hibernating myocardium as well as the presence and degree of myocardial ischemia and the extent of the scar. This paper reviews the indications, accuracy, and clinical utility of the available imaging techniques, with a special focus on cardiac magnetic resonance in ischemic cardiomyopathy, and provides an outlook on how this field might evolve in the future. © 2012 American College of Cardiology Foundation.
Grigoriadis N.,Aristotle University of Thessaloniki |
van Pesch V.,Cliniques Universitaires St Luc
European Journal of Neurology | Year: 2015
Multiple sclerosis (MS) is a multi-component disease characterized by inflammation, neurodegeneration and failure of central nervous system (CNS) repair mechanisms. Immune dysregulation appears to originate with dendritic cells (antigen-presenting cells) which have an activated phenotype in individuals with MS. Dendritic cells migrate across the blood-brain barrier and induce differentiation of memory T cells into pro-inflammatory T helper 1 (Th1) and Th17 lymphocytes. In turn, induction of macrophage and microglial activation produces other pro-inflammatory cytokines and oxygen and nitric oxide radicals responsible for the demyelination and axonal loss. Other known mediators of MS pathology include CD8+ T cells and memory B cells within the CNS. Some pathological hallmarks of MS are early axonal degeneration and progressive decline of brain volume in patients with clinically isolated syndromes who progress to clinically definite MS. Many new options to interfere with the course of MS have become available in recent years. To limit inflammatory demyelinating processes and delay disease progression, intervention to control inflammation must begin as early as possible. Each distinct type of immunotherapy (immunomodulation, immunosuppression and immune-selective intervention - blockade type, sequestering type or depleting type) corresponds to a specific underlying immunopathology of MS. © 2015 European Academy of Neurology.
Pirson Y.,Cliniques Universitaires St Luc
Advances in Chronic Kidney Disease | Year: 2010
Although asymptomatic in most patients, extrarenal manifestations of ADPKD may become more clinically relevant with the increasing life expectancy of affected patients. They mainly encompass cysts in other organs than the kidney (liver: 94%, seminal vesicle: 40%, pancreas: 9%, arachnoid membrane: 8%, and spinal meningeal, 2%) and connective tissue abnormalities (mitral valve prolapse: 25%, intracranial aneurysms: 8%, and abdominal hernia: 10%). Their recognition may spare the patient from other, useless investigations (eg, when an arachnoid cyst is incidentally found) or lead to the implementation of prophylactic or therapeutic measures (eg, screening, sometimes followed by the treatment of an asymptomatic intracranial aneurysm in at-risk patients, or, in the presence of a severe polycystic liver disease, avoidance from estrogens and treatment aimed to slow cyst growth). © 2010 National Kidney Foundation, Inc.
Vancraeynest D.,Catholic University of Louvain |
Pasquet A.,Catholic University of Louvain |
Roelants V.,Catholic University of Louvain |
Gerber B.L.,Catholic University of Louvain |
And 2 more authors.
Journal of the American College of Cardiology | Year: 2011
Cardiovascular diseases are still the primary causes of mortality in the United States and in Western Europe. Arterial thrombosis is triggered by a ruptured atherosclerotic plaque and precipitates an acute vascular event, which is responsible for the high mortality rate. These rupture-prone plaques are called "vulnerable plaques." During the past decades, much effort has been put toward accurately detecting the presence of vulnerable plaques with different imaging techniques. In this review, we provide an overview of the currently available invasive and noninvasive imaging modalities used to detect vulnerable plaques. We will discuss the upcoming challenges in translating these techniques into clinical practice and in assigning them their exact place in the decision-making process. © 2011 American College of Cardiology Foundation.
Marot J.C.,Cliniques Universitaires St Luc
Acta clinica Belgica | Year: 2012
Tigecycline (formerly CAR-936, Tygacyl) is the first glycylcycline antibiotic available for clinical use. It has an expanded broad-spectrum antibiotic activity. Phase III studies have identified gastrointestinal side-effects, especially nausea and vomiting, as the most common adverse events. Few cases of acute pancreatitis (AP) have been described in the literature. We report two new cases of mild tigecycline-induced pancreatitis. Tigecycline was given for soft-tissue infection in both cases. Symptoms such as nausea, vomiting and mostly abdominal pain occurred within 5 days after starting Tigecycline. Pancreatic enzymes elevation occurred five to six days after initiation of treatment, and resolved within a week after drug-discontinuation. Diagnosis of mild pancreatitis was confirmed after performing CT-Scan of the abdomen in both cases. We take this opportunity to review the literature about this potentially serious side-effect induced by tigecycline.
Veyckemans F.,Cliniques Universitaires St Luc
Paediatric Anaesthesia | Year: 2012
The 'new' challenging pediatric patients are those who could be called 'the survivors' and neonates undergoing birth under materno-fetal circulation. Their anesthetic management is complex because their initial pathology was previously lethal: the physiologic, pharmacologic, and or technical aspect of their management is presently unknown or hypothetical. Some examples are described. Communication with the pediatrician in charge of the child is the key to safe and effective anesthetic care of these cases. © 2012 Blackwell Publishing Ltd.
Coche E.,Cliniques Universitaires St Luc
JBR-BTR | Year: 2013
Perfusion CT permits evaluation of lung cancer angiogenesis and response to therapy by demonstrating alterations in lung tumor vascularity. It is advocated that perfusion CT performed shortly after initiating therapy may provide a better evaluation of physiological changes rather than the conventional size assessment obtained with RECIST. The radiation dose,the volume of contrast medium delivered to the patient and the reproducibility of blood flow parameters remain an issue for this type of investigation.
Leclercq S.,Catholic University of Louvain |
De Saeger C.,Catholic University of Louvain |
Delzenne N.,Catholic University of Louvain |
De Timary P.,Catholic University of Louvain |
And 2 more authors.
Biological Psychiatry | Year: 2014
Background: Inflammation might play a role in the development of several psychiatric diseases. However, the origins of processes that mediate inflammation are unknown. We previously reported increased intestinal permeability, elevated blood lipopolysaccharide levels, and low-grade systemic inflammation associated with psychological symptoms of alcohol dependence in alcohol-dependent subjects. In this study, we tested inflammatory responses of peripheral blood mononuclear cells (PBMCs) to gut-derived bacterial products during detoxification and the relationship to alcohol craving. Methods: In 63 actively drinking noncirrhotic alcohol-dependent subjects, testing was performed at the beginning (day 2) and end (day 18) of alcohol detoxification and compared with testing in 14 healthy subjects. Activation of various intracellular signaling pathways by gut-derived bacterial products was analyzed by quantitative polymerase chain reaction, Western blotting, and DNA binding assays (for transcription factors). Toll-like receptor activation was assessed by cell cultures. Results: In addition to lipopolysaccharides, we showed that peptidoglycans may also cross the gut barrier to reach the systemic circulation. Both activate their respective Toll-like receptors in peripheral blood mononuclear cells. Chronic alcohol consumption inhibited the nuclear factor kappa B proinflammatory cytokine pathway but activated the mitogen-activated protein kinase/activator protein 1 pathway, together with the inflammasome complex. This activity resulted in increased messenger RNA and plasma levels of interleukin (IL)-8, IL-1β, and IL-18. Activated proinflammatory pathways, in particular, IL-8 and IL-1β, were positively correlated with alcohol consumption and alcohol-craving scores. Short-term alcohol withdrawal was associated with the recovery of lipopolysaccharidedependent receptors but not peptidoglycan-dependent receptors. Conclusions: Lipopolysaccharides and peptidoglycans from the gut microbiota stimulate specific inflammatory pathways in peripheral blood mononuclear cells that are correlated with alcohol craving. © 2014 Society of Biological Psychiatry.
Hermida N.,Catholic University of Louvain |
Balligand J.-L.,Catholic University of Louvain |
Balligand J.-L.,Cliniques Universitaires St Luc
Antioxidants and Redox Signaling | Year: 2014
Significance: Cardiovascular diseases (CVD) represent a major public health burden. High low-density lipoprotein (LDL)-cholesterol is a recognized pathogenic factor for atherosclerosis, and its complications and statins represent the most potent and widely used therapeutic approach to prevent and control these disorders. Recent Advances: A number of clinical and experimental studies concur to identify endothelial dysfunction as a primary step in the development of atherosclerosis, as well as a risk factor for subsequent clinical events. Oxidant stress resulting from chronic elevation of plasma LDL-cholesterol (LDL-chol) is a major contributor to both endothelial dysfunction and its complications, for example, through alterations of endothelial nitric oxide signaling. Critical Issues: Statin treatment reduces morbidity and mortality of CVD, but increasing evidence questions that this is exclusively through reduction of plasma LDL-chol. The identification of ancillary effects on (cardio)vascular biology, for example, through their modulation of oxidative stress, will not only increase our understanding of their mechanisms of action, with a potential broadening of their indication(s), but also lead to the identification of new molecular targets for future therapeutic developments in CVD. Future Directions: Further characterization of molecular pathways targeted by statins, for example, not directly mediated by changes in plasma lipid concentrations, should enable a more comprehensive approach to the pathogenesis of (cardio)vascular disease, including, for example, epigenetic regulation and fine tuning of cell metabolism. Antioxid. Redox Signal. 20, 1216-1237. © 2014, Mary Ann Liebert, Inc.
Coche E.,Cliniques Universitaires St Luc
JBR-BTR | Year: 2013
The role of imaging in the evaluation of tumor response is expanding rapidly. The current response evaluation criteria in solid tumors (RECIST) based on anatomical changes suffers from many limitations related mainly to the interand intra-observer variability to delineate the tumoral edges. Consequently, there is a need to update and integrate the RECIST criteria beyond the classical anatomical changes with other more sophisticated methods using three-dimensional and functional criteria. The goal of this paper is to review the current criteria of RECIST measurements (RECIST 1.1) with their limitations and to evaluate the emerging solutions available with the new imaging techniques like PET-CT.