Tag Archives: inflammation

Introduction Stroke is defined as an acute neurological deficit of cerebrovascular origin lasting longer than 24 hours. In the UK each year, stroke affects approximately 100,000 people, is a leading cause of mortality, causing over 30,000 deaths in 2020, and is a significant contributor to severe disability.1 Caring for patients with stroke in the UK costs approximately £2.5 million each year and leads to significant production losses. Clearly, preventing stroke has many benefits. Strokes can be ischaemic (85%), where tissue damage is due to occlusion of blood supply, or haemorrhagic (15%), due to a ruptured vessel.2 Ischaemic stroke can be

Introduction Originally, icosapent ethyl (IPE) was developed as a treatment for hypertriglyceridaemia.2 However, in the Reduction of Cardiovascular Events With Icosapent Ethyl–Intervention Trial (REDUCE-IT),3 IPE significantly decreased the risk of ischaemic events (including cardiovascular [CV] death) by ~25% after a median follow-up of 4.9 years. The study included patients with fasting triglyceride (TG) levels of 1.7 to 5.6 mmol/L (150 to 499 mg/dL) and low-density lipoprotein cholesterol (LDL-C) levels of 1.1 to 2.6 mmol/L (41 to 100 mg/dL) who were on optimum statin treatment. Interestingly, this reduction in CV risk was independent of

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

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

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

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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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

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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