Abstract

Dyslipidemia is a potent risk factor for the genesis and progression of cardiovascular disease (CVD), and both the concentration and type of low-density lipoproteins (LDL) augment this association. The small, dense LDL (sdLDL) subfraction is the subtype which is most strongly predictive of atherosclerosis and cardiovascular events. In addition to the traditionally available lipid-lowering treatment options, certain novel therapies have been shown to favorably impact sdLDL, among them the antidiabetic class of agents known as glucagon-like peptide 1 receptor agonists (GLP1-RAs). These drugs seem to alter the pathophysiologic mechanisms responsible for the formation and accumulation of atherogenic lipoprotein particles, thus potentially reducing cardiovascular outcomes. They represent a uniquely targeted therapeutic approach to reduce cardiometabolic risk and warrant further study for their beneficial nonglycemic actions.

Highlights

  • Accepted: 26 October 2021Cardiovascular disease (CVD) is the leading cause of death globally, causing an estimated 18 million deaths each year [1], and hyperlipidemia is a major risk factor for the development and progression of atherosclerotic cardiovascular disease (CVD) [1]

  • Clinical interest has focused recently on a common human atherogenic lipoprotein phenotype characterized by a moderate increase in plasma triglycerides, a decrease in high density lipoprotein (HDL) cholesterol and the prevalence of small dense Low-density lipoprotein (LDL)

  • Discussions on LDL subclasses [20]. It seems the all the metabolic changes associated with the production of small dense LDL (sdLDL) collectively contribute to cardiometabolic risk, and increased number of atherogenic LDL particles must be present for disease risk to be evident

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Summary

New Therapeutical Options

Rizvi 1,2 , Anca Pantea Stoian 3 , Andrej Janez 4 and Manfredi Rizzo 2,3,5, *. Division of Endocrinology, Diabetes and Metabolism University of South Carolina School of Medicine

Introduction
VLDL in exchange of cholesteryl estersoffrom
Conclusions
Full Text
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