[Lipid lowering: new agents and new concepts]

Low-density lipoprotein (LDL) cholesterol (LDL-C) is a causal risk factor for cardiovascular complications. A target value is set according to risk, guideline-based and individual basis. We now have the means to lower LDL‑C levels to ranges that are even associated with plaque volume regression. Moreover, lipid treatment is an example of how pharmacotherapy has evolved from classical selective inhibition of enzymes by drugs (e.g. statins) to targeted neutralization of proteins by antibodies. The reduction of atherogenic lipoproteins by specific inhibition or reduction of mRNA of target proteins, e.g. PCSK‑9, ANGPLT3, ApoC-III or Apo (a), and possibly one day by vaccination or even CRISP-based gene therapy will in the long term lead to new concepts in the treatment and prevention of dyslipidemia and cardiovascular complications. The cumulative exposure of atherogenic lipoproteins to the vessel wall is determined by the time-averaged LDL‑C level. This essentially depends on patient adherence and prescribed treatment intensity by physicians. Therefore, it is likely that treatment adherence influences the cumulative benefit of treatment. Accordingly, the new therapeutic strategies mentioned above with presumably higher adherence rates could help to optimize cardiovascular prevention. Early and effective LDL‑C lowering could drastically reduce the incidence of cardiovascular complications in the long term and help to maintain the health of our patients.