Tag Archives: lipids

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 Cholesterol is a key risk factor for atheroma and coronary heart disease. The evidence-base for high-intensity lipid-lowering therapy in secondary prevention of cardiovascular disease is unequivocal.1-4 Despite the introduction of novel drugs, including ezetimibe5,6 and monoclonal antibodies,7 statins remain first-line therapy.8,9 Statins decrease hepatic cholesterol synthesis by competitively inhibiting 5-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase receptors, as they have an affinity up to 10,000 times greater than the natural substrate.10 Through reducing intra-cellular cholesterol concentration, statins up-regulate

Detecting undiagnosed familial hypercholesterolaemia (FH) in the community and helping families manage the condition before it leads to a cardiovascular disease (CVD) event was one of the key themes of the conference. A second important theme was taking action on the risk factors and behaviours that are linked to CVD and other non-communicable diseases (NCDs). These risk factors and behaviours have been understood for decades, yet the challenges of finding effective ways to help the population change to healthier behaviours, and how to assess and monitor this in clinical practice, remain. Professor Huon Gray, National ClinicalDirector for He

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Introduction Since their discovery in the 1970s, statins are widely used in clinics for the treatment of atherosclerosis and other cardiovascular diseases (CVD). Statins attenuate the intracellular levels of cholesterol by inhibiting the rate-limiting enzyme 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, either by competing with the normal substrate in the enzyme’s active site, or by altering the conformation of the enzyme by binding to its active site. Lipid-mediated effects Statins exert their lipid-mediated action by decreasing the production of cholesterol and low-density lipoproteins (LDL), by up-regulation of LDL-receptors and uptake

Background Statins are first choice for treatment of dyslipidaemia in both secondary and primary cardiovascular disease prevention. For every 1.0 mmol/L reduction in low-density lipoprotein cholesterol (LDL‑C), the risk of coronary heart disease (CHD) mortality decreases by 19% and overall mortality decreases by 12%.1 Despite statin treatment, a substantial number of cardiovascular events still occur, and one reason may be persistent lipid abnormalities including total cholesterol and LDL-C not at target, or low levels of high-density lipoprotein cholesterol (HDL-C) or elevated triglycerides. Results from the DYSlipidaemia International Stu

Highlights of this year’s European Society of Cardiology Congress, held in Stockholm, Sweden, from August 28th to September 1st included a new drug which benefits heart failure by slowing heart rate, and more exciting results from oral compounds that could replace warfarin in various indications. Highlights of this year’s European Society of Cardiology Congress, held in Stockholm, Sweden, from August 28th to September 1st included a new drug which benefits heart failure by slowing heart rate, and more exciting results from oral compounds that could replace warfarin in various indications. SHIFT: ivabradine shows benefit in heart failure

Introduction Bile acid sequestrants (BAS) were the first class of lipid-lowering drug to be developed for reducing blood cholesterol levels.1 Now, after their introduction 30 years ago, BAS still continue to command a position in the treatment of hyperlipidaemia.2 How do BAS work? Figure 1. Mode of action of bile acid sequestrants BAS bind to negatively charged bile acids in the intestine and impede their absorption (figure 1). This process depletes the bile acid pool and disrupts the enterohepatic circulation of bile acids, thus, increasing the synthesis of bile acids. Cholesterol is, therefore, diverted to bile acid synthesis, thereby reduc

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