Tag Archives: atherosclerosis

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 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 Statins have proved beyond doubt the relevance of reducing low-density lipoprotein (LDL) in atherogenic cardiovascular disease (CVD), with the risk of a new CVD event reducing by one-fifth for each 1 mmol/L decrease in LDL-cholesterol (LDL-C) achieved.1 A typical patient experiencing an acute coronary event in the UK will do so with LDL-C of 3.8 mmol/L.2 Thus, introducing a statin to achieve a target of just under 2 mmol/L will decrease the risk of a future event by no more than 40%. Unlike more uncommon patients with much higher LDL-C levels, such as those with heterozygous familial hypercholesterolaemia,3 the pre-treatment LDL-

Introduction Renal artery stenosis (RAS), traditionally the preserve of the nephrologist, is a condition of increasing interest to the cardiologist. Ninety per cent of RAS is caused by atherosclerosis and the risk factors for renal atherosclerosis and coronary atherosclerosis are the same. Furthermore, the presence of RAS alters the prognosis of co-existent cardiac disease, most notably cardiac failure and ischaemic heart disease, both directly1–3 and via its sequelae of renal failure and hypertension. Finally, the treatments for the disease, both medical and interventional, are familiar to the cardiologist, who can employ much of the knowl

ENHANCE controversy dominates meeting The controversial ENHANCE (Ezetimibe and Simvastatin in Hypercholesterolaemia Enhances Atherosclerosis Regression) trial of ezetimibe dominated the ACC meeting, with a special session held to discuss the results, which were simultaneously published in the New England Journal of Medicine. The 720-patient trial showed no benefit of ezetimibe when added to simvastatin 80 mg in slowing the progression of atherosclerosis in the carotid artery (as measured by intima media thickness (IMT) in patients with familial hypercholesterolemia (FH), despite the fact that there were significantly greater reductions in lo

No content available

No content available

No content available

No content available