Making Best Practice, Every Day Practice
The new NICE guideline enables us to individualise care bearing in mind the needs of the person in front of us. It is concerned with clinical efficacy, and – for once – the cost of care has not noticeably influenced its recommendations. In contrast, QOF does the exact opposite, demanding that we drive our patients’ HbA1c down to low […]
In patients with both homozygous and heterozygous familial hypercholesterolaemia (FH), statins with or without ezetimibe are now the mainstay pharmacological therapy for lowering low-density lipoprotein cholesterol (LDL-C) levels, combined with lipoprotein apheresis in homozygotes and statin-refractory heterozygotes. These therapies have helped to improve outcomes, but new treatment options areurgently needed, as FH patients continue to be at high risk of premature death due to cardiovascular disease (CVD).
HEART UK – The Cholesterol Charity – has provided editorial support and review of this sponsored FH series.This article was made possible by an unrestricted educational grant by Sanofi, who had no control over content.
Homozygous familial hypercholesterolaemia (FH) is a rare disorder with a very high risk of premature cardiac death that must be diagnosed and treated from childhood onwards, usually with lifelong lipoprotein apheresis. Heterozygous FH is much commoner, with a high risk of cardiovascular disease in adults that can be prevented by early diagnosis and statin therapy.
HEART UK – The Cholesterol Charity – has provided editorial support and review of this sponsored FH series.This article was made possible by an unrestricted educational grant by Sanofi, who had no control over content.
Familial hypercholesterolaemia (FH) is under-diagnosed and under-treated, despite clear evidence-based guidelines for identification and management, and the availability of low-cost, generic, high-intensity statin treatment. Genetic cascade testing is the key to early diagnosis, which can help ensure that this treatment is no longer ‘too little, too late’.
HEART UK – The Cholesterol Charity – has provided editorial support and review of this sponsored FH series.This article was made possible by an unrestricted educational grant by Sanofi, who had no control over content.
“I like to think of medicine in our day as an ever-broadening and deepening river, fed by the limpid streams of pure science-
Christian A. Herter (1865-1910), US neurologist, New York.
This study shows that people living in London have better treatment rates with lipid lowering drugs than the general population. This observation may be explained in part by the fact that London is a highly mobile population, so new patient checks are more common.
7.5 mmol/L) should prompt clinicians to think of familial hypercholesterolaemia. A family history of premature heart disease should further raise suspicion. This dominantly inherited genetic abnormality deserves as much attention as the oncogenes such as BRAC 1 and 2. HEART UK – The Cholesterol Charity – has provided editorial support and review of this sponsored FH series.This article was made possible by an unrestricted educational grant by Sanofi, who had no control over content.
50% lowering of LDL-C from the baseline value. Half of all patients and 53% of women with CHD failed to achieve the target >50% reduction in LDL-C. There is a major lack of family “cascade” testing. Funding for DNA testing and cascade testing is lacking in many parts of the UK.
The benefit of treatment with HMG-CoA reductase inhibitors (statins) is unquestioned, with multiple studies over the last 20 years having shown that statins improve cardiovascular (CV) outcomes.1 Although all statins reduce low-density lipoprotein cholesterol (LDL-C), their potencies differ. The decreasing order of potency (per milligram) for LDL-C reduction is: rosuvastatin, atorvastatin, simvastatin and pravastatin.
Familial hypercholesterolaemia (FH)—an inherited genetic defect that causes high blood cholesterol—often goes unrecognised. It is therefore under-diagnosed and poorly managed. This can have devastating repercussions for affected families, since premature deaths from heart disease can occur in people in their 40s or even younger. This article looks at the causes of FH, how to recognise those at risk and how to implement National Institute for Health and Clinical Excellence (NICE) guidance in practice.
Dealing with the complexity of lipid metabolism, its outcomes and modification can easily seem overwhelming for primary healthcare professionals. This article aims to help you understand the fundamentals using a back-to-basics approach designed to enhance your practical management of the most important risk factor for the development of atherosclerotic cardiovascular disease. The focus will be on the cholesterol-carrying lipoproteins LDL and HDL but we will also review important issues concerning the use of the total cholesterol to HDL ratio, the significance of triglycerides and the perennial question: ‘to fast or not to fast?’
Cardiovascular disease (CVD), including coronary heart disease (CHD) and stroke, is the leading cause of mortality in the UK. In addition to the effect on quality of life, CHD imposes a huge annual burden with costs on healthcare relating to CHD estimated to be over £3.3 billion a year in the UK.1 Coupled with the obesity epidemic, costing the NHS an estimated £4.2 billion per year,2 this creates a huge burden upon healthcare resources. This article was sponsored by an educational grant from Alpro soya UK; however, the views expressed are the author’s own.
A unique new e-platform for primary care
By continuing to this site you are confirming that you are a healthcare professional and are opting into the use of cookies.
