More details about beta blockers and heart failure

The sympathetic nervous system accelerates the frequency of the heartbeat, strengthens heart contractions, it contracts veins, increases blood pressure, widens respiratory tracts, widens the pupils and increases the formation of glucose in the liver. All this is urgently necessary when the organism is under stress, is defending itself or fleeing. For some diseases, especially heart diseases and those with high blood pressure it is desired that the effect on the sympathetic nervous system is reduced. For this purpose we use blockers for beta receptors. With heart weakening because of less effective blood pumping adrenaline secretion occurs which forces heart to work harder. In this case beta blockers relieve and slow down the heart and prevent and irregular heartbeat. This allows the heart to revive itself from excessive activity and the size of the heart is reduced, which helps the heart muscles to function more effectively.

The effect of beta blockers depends on the structure of the beta receptors on which they have an impact on. The gene ADRB1 contains information on the structure of the beta-1 adrenergic receptor. Little variability in this gene or SNP in the location rs1801253 has an impact on the effect of the beta blocker bucindol.

Research on 1040 patients with heart failure showed that bucindol decreased mortality by 38% in patients with rs1801253(C;C) compared to the placebo. The drug did not have an impact on mortality in patients with rs1801253(C;G) and rs1801253(G;G). Otherwise, bucindol is not used in clinical practice but the data is important because the effect of the drug metoprol (Lopressor, Toprol-XL, Betaloc, Apo-Metoprol, Nu-Metop) also depends on polymorfism instead of rs1801253.

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