Dyslipidemias and Cardiovascular Prevention: Tailoring Treatment According to Lipid Phenotype

Curr Cardiol Rep. 2017 Jul;19(7):61. doi: 10.1007/s11886-017-0869-3.

Abstract

Purpose of review: This study aimed to present the current information on the genetic background of dyslipidemias and provide insights into the complex pathophysiological role of several plasma lipids/lipoproteins in the pathogenesis of atherosclerotic cardiovascular disease. Furthermore, we aim to summarize established therapies and describe the scientific rationale for the development of novel therapeutic strategies.

Recent findings: Evidence from genetic studies suggests that besides lowering low-density lipoprotein cholesterol, pharmacological reduction of triglyceride-rich lipoproteins, or lipoprotein(a) will reduce risk for coronary heart disease. Dyslipidemia, in particular hypercholesterolemia, is a common clinical condition and represents an important determinant of atherosclerotic vascular disease. Treatment decisions are currently guided by the causative lipid phenotype and the presence of other risk factors suggesting a very high cardiovascular risk. Therefore, the identification of lipid disorders and the optimal combination of therapeutic strategies provide an outstanding opportunity for reducing the onset and burden of cardiovascular disease.

Keywords: Coronary heart disease; Dyslipidemia; Genetic phenotype; Treatment options.

Publication types

  • Review

MeSH terms

  • Atherosclerosis / complications
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / prevention & control*
  • Coronary Disease / etiology
  • Coronary Disease / prevention & control
  • Dyslipidemias / complications*
  • Dyslipidemias / genetics*
  • Humans
  • Hypolipidemic Agents / therapeutic use
  • Lipids / genetics*
  • Lipoprotein(a) / blood
  • Lipoproteins / genetics
  • Lipoproteins, LDL / blood
  • Phenotype
  • Risk Factors

Substances

  • Hypolipidemic Agents
  • Lipids
  • Lipoprotein(a)
  • Lipoproteins
  • Lipoproteins, LDL