Optimization of heart failure treatment

Optimization of heart failure treatment by heart rate reduction

Elevated resting heart rate (RHR) is associated with cardiovascular outcomes in the general population, while only in Heart Failure (HF), RHR represents a significantly modifiable risk factor. Physicians should achieve an optimal RHR of 50−60 bpm on treatment at which RHR associated risk is maximally reduced.

β-Blockers are associated with improved outcomes in patients with chronic HF representing guideline-recommended standard treatments. However, RHR reduction is achieved, often not sufficiently, by β-Blocker therapy, which beyond a negative chronotropic effect might also antagonize direct toxic effects of catecholamines and reduce oxygen consumption by negative inotropic effects. In addition, the average RHR and the lowest RHR achieved in β-Blockers trials was only 70 bpm, being only reached in the population that had high doses.

Ivabradine was the first clinically available drug to reduce RHR by inhibition of If—(f stands for “funny”) due to the unusual gating behavior this nonspecific cation current (I)—mediated by hyperpolarization-activated cyclic nucleotide–gated (HCN) channels, which are expressed exclusively in sinus nodal cells.

Results from SHIFT demonstrated that ivabradine safely lowers RHR in patients with sinus rhythm above 70 bpm, being associated with a reduction of the composite primary endpoint of cardiovascular death or hospital admission for worsening HF compared with placebo. Patients with the highest RHR had a greater reduction of RHR and a greater reduction of risk. Similarly, patients treated with Ivabradine, achieved RHR between 50−60 bpm (at 28 days) resulted in a 50% lower number of subsequent cardiovascular outcomes.

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Reference:

Michael Böhm, et al. Int J Heart Fail. 2020 Jan;2¹:1-11.