Tag Archives: cardiovascular disease

Introduction Atrial fibrillation (AF) is encountered with increasing frequency in clinical practice,1 and is associated strongly with adverse clinical outcomes, including stroke, cardiovascular events and death.2,3 Concomitant atherosclerotic disease may increase the risk of adverse outcomes in people with AF. For example, peripheral arterial disease was present in 11% of a large cohort of European patients with AF, and increased the risk of all-cause and cardiovascular death, compared with patients with AF but no peripheral arterial disease.4 In addition, AF is associated with adverse outcomes in a range of other subgroups of patients, inclu

Frailty is strongly associated with cardiovascular disease (CVD) and, while the precise pathophysiological mechanisms linking frailty and CVD remain to be elucidated, it is likely that this association is bi-directional.4,6,7 Loss of muscle mass and function (sarcopaenia), insulin resistance and chronic low-level inflammation observed in the frailty state can predispose to CVD. On the other hand, the presence of CVD can lead to reduced activity, muscle loss and exhaustion, thus, predisposing to frailty. Large cross-sectional and longitudinal studies have shown that those with CVD were up to two to three times more likely to be frail than tho

Dr Sean L Zheng CVOTs The key studies evaluated sodium-glucose co-transporter 2 (SGLT2) inhibitors – empagliflozin (EMPA-REG OUTCOME)4 and canagliflozin (CANVAS)5 – and glucagon-like peptide 1 (GLP-1) receptor agonists – liraglutide (LEADER)6 and semaglutide (SUSTAIN-6)7 – in patients with type 2 diabetes and cardiovascular disease or elevated cardiovascular risk (table 1). In the EMPA-REG OUTCOME (Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients–Removing Excess Glucose) study, the use of empagliflozin resulted in 38% and 35% reductions in cardiovascular death and heart failure hospitalisation, r

The risk of developing type 2 diabetes is amplified among the South Asian population in the UK, with estimates suggesting a two- to fourfold increase in risk. Why is this? Hanif and Susarala review putative reasons why South Asian people represent at least 15% of the population of people with diabetes in this country, and who also carry higher microvascular complication rates than their European counterparts. Although the reasons for excess coronary heart disease (CHD) mortality risk in South Asians are not entirely clear, studies have found higher levels of conventional risk factors present at a younger age, which may be an explanation for

Introduction Individuals with diabetes are at increased risk of vascular outcomes, and their prognosis following an event remains worse compared with those having normal glucose metabolism.1 The relationship between glycaemia and vascular disease is complex as it is affected by multiple glucose parameters, including chronic hyperglycaemia, hypoglycaemia and, potentially, glycaemic variability.2 To add to the complexity, the type of hypoglycaemic agent used may also alter predisposition to vascular events. Over a decade ago, one hypoglycaemic agent, rosiglitazone, was implicated in increasing the risk of vascular disease, which prompted the U

Results from the PURE (Prospective Urban-Rural Epidemiology) study, carried out on 135,000 individuals aged 35 to 70 years from 18 low, middle and high-income countries (North America, Europe, South America, the Middle East, South Asia, China, South East Asia and Africa) has contrasted with current dietary advice, by finding that high carbohydrate intake is linked to worse total mortality and non-cardiovascular mortality outcomes, while high fat intake is associated with lower risk. “Our findings do not support the current recommendation to limit total fat intake to less than 30% of energy and saturated fat intake to less than 10% of energ

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Introduction Atherosclerosis is a systemic disease of the large- and medium-sized muscular arteries, which is characterised by endothelial dysfunction, vascular inflammation, and the build up of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This build up results in plaque formation, vascular remodelling, acute and chronic luminal obstruction, abnormalities of blood flow and diminished oxygen supply to target organs.1 Plaque rupture and thrombosis result in the acute clinical complications of atherosclerosis. The process of atherosclerosis begins early in life and progresses over many decades. Rupture

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

Promoting cardiovascular health is central to the national strategy to reduce premature mortality in our population. In this supplement, we offer a new approach to cardiovascular disease (CVD) prevention through the MyAction preventive cardiology programme, developed by Imperial College London. This nurse-led, multi-disciplinary, family-centred service embraces all patients with atherosclerotic disease – coronary heart disease, stroke and peripheral arterial disease – together with those identified through Health Checks to be at high risk of developing CVD in one community-based programme. In this supplement, we describe the studies that