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Low-density lipoprotein cholesterol target achievement in patients surviving an acute coronary syndrome in Hong Kong and Taiwan - findings from the Dyslipidemia International Study II.

08:00 EDT 15th August 2018 | BioPortfolio

Summary of "Low-density lipoprotein cholesterol target achievement in patients surviving an acute coronary syndrome in Hong Kong and Taiwan - findings from the Dyslipidemia International Study II."

Individuals are at increased risk for cardiovascular events following an acute coronary syndrome (ACS). Effective management of hyperlipidemia, an associated risk factor, is essential for improving outcomes. We aimed to quantify the extent of hyperlipidemia and its treatment in ACS survivors in Hong Kong and Taiwan.

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This article was published in the following journal.

Name: International journal of cardiology
ISSN: 1874-1754
Pages: 1-5

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Medical and Biotech [MESH] Definitions

An abnormal lipoprotein present in large amounts in patients with obstructive liver diseases such as INTRAHEPATIC CHOLESTASIS. LP-X derives from the reflux of BILE lipoproteins into the bloodstream. LP-X is a low-density lipoprotein rich in free CHOLESTEROL and PHOSPHOLIPIDS but poor in TRIGLYCERIDES; CHOLESTEROL ESTERS; and protein.

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.

An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.

The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

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