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Tag Archives: inflammation

February 2019 Br J Cardiol 2019;26:10

Cytokine removal in sepsis and endocarditis

BJC Staff

Abstract

The technology is already used to treat inflammation in critically ill and cardiac surgery patients as an early standalone (I.e. without combined renal replacement) therapy for extracorporeal cytokine removal. It is designed to reduce the ‘cytokine storm’ or ‘cytokine release syndrome’, a major contributing factor in inflammation. The controlled study of 20 patients was conducted by a team at the Department of Anesthesiology and Intensive Therapy of the University Szeged in Hungary, led by Professor Zsolt Molnar. They investigated the effects of a single treatment of extracorporeal cytokine removal with CytoSorb® therapy, in additio

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October 2017

ESC 2017: CANTOS – a focus on inflammation and atherosclerosis

Chris Allen

Abstract

Atherosclerosis has long been characterised as a chronic inflammatory condition. Elevation of the non-specific inflammatory marker high sensitivity c-reactive protein (hs-CRP) is an accepted predictor of adverse cardiovascular events and its reduction in JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) and other statin trials has been linked with improved outcomes, even with low-density lipoprotein (LDL) cholesterol levels within the normal range.1 Although a specific aetiological link has proven harder to delineate, the cytokine interleukin 1β (IL-1β), pro-inflammatory messenger of

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August 2015 Br J Cardiol 2015;22:101–4 doi:10.5837/bjc.2015.029

Inflammation is associated with myocardial ischaemia

Kushal Pujara, Ashan Gunarathne, Anthony H Gershlick

Abstract

Introduction Coronary heart disease (CHD) is the leading cause of death worldwide. Chronic subclinical inflammation is a key recognised process in the pathogenesis of CHD, and may play an important role in atherogenesis. Figure 1. Atherosclerotic plaque rupture Atherosclerosis is a complex multi-factorial disease process, which is initiated at the endothelium in response to various forms of injurious stimuli (shear stress, oxidative stress, arterial pressure changes) including inflammation. These factors appear to alter the endothelial cell’s capacity to maintain homeostasis and vascular tone and leads to the so-called endothelial ‘dysfun

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News from the 7th Annual Scientific Meeting of the Cardiorenal Forum

December 2012 Br J Cardiol 2013;20:20–1 Online First

News from the 7th Annual Scientific Meeting of the Cardiorenal Forum

Abstract

Introduction As doctors and scientists we are accustomed to breaking down problems and simplifying complex pathology in order to focus our management and identify possible targets for future therapies. The pathophysiology of cardiorenal disease is no different but, as yet, attempts to elucidate the complex interaction between heart and kidneys has failed. Although cardiac and renal disease are often diagnosed together, it is clear that a straightforward causal relationship does not exist. Disease in either serves as a risk factor for disease in the other and perpetuates the progression of that disease, but why this is so is unclear. Whilst th

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March 2010 Br J Cardiol 2009;17(Suppl 1):S5-S7

What is aspirin resistance?

Karsten Schrör

Abstract

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May 2009 Br J Cardiol 2009;16:113–15

Cardiovascular risk in rheumatoid arthritis

Ian Kelt, Neal Uren

Abstract

Atherosclerosis and inflammation It is not clearly understood why patients with rheumatoid arthritis should suffer accelerated atherosclerosis. Traditional modifiable risk factors alone are insufficient to explain the excess cardiovascular risk.3-5 Part of the answer is that rheumatoid arthritis causes chronic systemic inflammation, which may accelerate the atherosclerotic process. Atherosclerosis is essentially an inflammatory disease, with levels of different biomarkers of inflammation such as C-reactive protein (CRP), interleukin-6, and N-terminal prohormone B-type natriuretic peptide (NTproBNP) correlating closely with subsequent cardiac

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January 2009 Br J Cardiol 2009;16(Suppl 2):S1-S2

Maximising safety and efficacy in the treatment of wet AMD

Rachel Arthur

Abstract

Vascular endothelial growth factor (VEGF) plays a critical role in stimulating abnormal neovascularisation, inflammation and vascular permeability, all factors involved in the pathogenesis of wet AMD. Inhibition of VEGF with intravitreal ranibizumab, pegaptanib and (off-licence) bevacizumab is currently first-line therapy for this condition. However, VEGF plays a pivotal role in maintaining vascular integrity, particularly under conditions of ischaemia and hypoxia. This is particularly significant since most (but not all) studies have suggested that patients with wet AMD have a higher incidence of coronary heart disease and stroke, and becaus

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January 2007 Br J Cardiol 2007;14:37-40

Coronary artery calcification is associated with alcohol intake but not oxidative stress or inflammation

Natalie C Ward, Kevin D Croft, Henrietta Headlam, Trevor A Mori, Keith Woollard, Ian B Puddey

Abstract

No content available

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March 2004 Br J Cardiol 2004;11:144-7

Thermography of the human arterial system

Christodoulos Stefanadis

Abstract

No content available

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