Abstract
The goal of pharmacotherapy of dyslipidemias (DLP) is to reduce the risk of atherosclerotic cardiovascular diseases (CVD), and cardiovascular and overall mortality. The purpose of DLP pharmacotherapy is to achieve the desired LDL-C concentrations i.e. 1.40 mmol/L for patients at very high-risk, 1.80 mmol/L for patients at high-risk.
The individuals at moderate (respectively low) risk desired levels of LDL-C are 2.60 and 3.00 mmol/L. An overview of conventional hypocholesterolemic drugs (statins, ezetimibe, bile acid sequestrants) as well as new drugs that block PCSK9 activity (monoclonal antibodies, specific antisense oligonucleotides, small interfering RNA molecules), inhibitor of microsomal triglyceride transfer protein and bempedic acid (inhibitor ATP: citrate lyase) are reviewed.
Conventional drugs with hypotriglyceridemic activity include statins, fibrates, niacin and omega-3 fatty acids (EPA). New drugs with hypotriglyceridemic effects include pradigastat (an intestinal diacylglycerol transferase inhibitor).
In familial lipoprotein lipase deficiency, gene therapy is possible by application of human hyperfunctional mutations of the LPL gene (alipogen tiparvovek). This group is complemented by selective modulators of PPARα receptors (pemafibrate), specific antisense oligonucleotides that bind to APOC3 mRNA (volanosersen), and ANGPTL3 mRNA, as well as small interfering RNA against ANGPTL3 and APOC3.
Moreover, pronounced hypotriglyceridemic effect reveals monoclonal antibodies against ANGPTL3 (evinacumab).