Abstract
Treatment of heart failure focuses on three areas - adjustment of hyperactivated regulatory mechanisms (beta blockers, ACE inhibitors, mineralocorticoid receptor antagonists and possibly AT1 receptor antagonists), adjustment of impaired contractility and improvement of tissue perfusion (particularly inotropes, possibly vasodilators) and reduction of fluid retention (diuretics). Genetic makeup certainly affects the incidence and course of heart failure.
However, our knowledge in this area remains insufficient and its direct application in clinical practice is not yet possible. On the other hand, polymorphisms at the level of drug absorption, transformation and elimination have already been generally mapped and pharmacogenetic principles are already taken into consideration during treatment.
In particular, the bioavailability and elimination as well as the duration of action of lipophilic beta-blockers and possibly digoxin depending on the pharmacogenetic makeup are all significant. Differences in pharmacodynamic responses to drugs based on the polymorphisms of drug target structures (enzymes, transport and ion channels, etc.) are less explored, but intensive research is at least being conducted at the level of beta-blockers and ACE inhibitors