Dyslipidaemia Clinical Practice

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The aim of the present study was to assess the positioning of clinical guidelines as regards atherogenic dyslipidaemia.

High-density lipoprotein HDL cholesterol, triglycerides, atherogenic dyslipidaemia, non-HDL cholesterol, and apolipoprotein apo B were gathered from the 10 selected guidelines, and it was assessed whether these parameters were considered a cardiovascular risk factor, a therapeutic target, or proposed a pharmacological strategy. The NLA emphasises the relevance of atherogenic dyslipidaemia.

Dyslipidaemia in Clinical Practice

The Canadian guidelines introduced non-HDL cholesterol and ApoB as alternative targets, and proposes non-statin treatment in the presence of low HDL cholesterol and hypertriglyceridaemia. European, Brazilian and Japanese guidelines highlight HDL cholesterol and triglycerides, but with the limitation that the main evidence comes from sub-analysis of clinical studies.

Dyslipidemia: Statin Treatment -2016 Guidelines

The clinical guidelines analysed do not consider, or unconvincingly address, the importance of atherogenic dyslipidaemia. Read Article at publisher's site.

Atherogenic Dyslipidemia

How does Europe PMC derive its citations network? Protein Interactions. Some drugs interfere with intestinal cholesterol absorption and play a role in lowering blood cholesterol levels. Once absorbed by the intestinal cells, dietary lipids are packaged into lipid-rich lipoproteins known as chylomicrons through a process resembling that of VLDL synthesis in the liver Chylomicrons differ from VLDL in that their major apolipoprotein is apo B48 instead of B and their lipid content is much greater than the liver-derived particles.

Once in the bloodstream, chylomicrons are acted upon by the enzyme LPL exactly as VLDL , which hydrolyzes the triglyceride moiety of chylomicrons to produce fatty acids that are then taken up by the various tissues containing LPL Figure 7. The resulting particle, the chylomicron remnant, is thus depleted of triglycerides and relatively richer in cholesterol. It has become small enough to leave the blood capillaries and come into contact with a receptor, LDL-related protein LRP , located Lon the surface of liver cells. The chylomicron remnant is then internalized and degraded, delivering to the liver its load of dietary cholesterol.

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The basic processes of fasting lipoprotein metabolism continue in the postprandial state. However, in healthy people, several adaptations take place upon food ingestion, mainly to reduce the output of endogenous lipids into the circulation and route dietary lipids to the appropriate tissues.


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Insulin plays a key role in these adaptations. As seen above, insulin tends to reduce VLDL secretion. This is amplified by the postprandial rise in insulin. After a meal, the liver therefore puts out fewer triglycerides, making LPL more available for hydrolysis of chylomicron-bound dietary triglycerides.

Dyslipidaemia in Clinical Practice (2nd ed.)

The new guidelines call for treating low-density lipoprotein cholesterol LDL-C levels in specific patient groups to lower goals than previously recommended. They also support the use of coronary artery calcium scores and inflammatory markers to help clinicians better stratify risk. Another notable feature is that the guidelines call for special consideration when it comes to patients with diabetes or familial hypercholesterolemia, women, and pediatric patients with dyslipidemia. The Extreme Risk category includes patients who have progressive cardiovascular disease, such as patients with unstable angina who have achieved a lowered LDL-C level and patients who have established cardiovascular disease accompanied by diabetes mellitus, chronic kidney disease stages 3 or 4 , or familial hypercholesterolemia.


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