A major mechanism by which these agents are thought to provide benefit is by reducing myocardial oxygen demand by lowering heart rate through antagonism of sympathetic receptors in myocardial pacemaking tissue. This mechanism is supported by studies demonstrating strong associations between increasing resting heart rate HR and cardiovascular outcomes in patients with ischemic cardiomyopathy. The novel sinus node modifying agent ivabradine lowers heart rate by inhibiting the "funny current" If channel which is critical in determining the automaticity rate of pacemaking cells in the sinoatrial node. Given this very targeted mechanism of action, ivabradine may allow for further HR lowering despite maximally-tolerated doses of beta blocker therapy.

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Epub Aug Comment in Lancet. Cardiovasc J Afr. Curr Hypertens Rep. We aimed to test whether lowering the heart rate with ivabradine reduces cardiovascular death and morbidity in patients with coronary artery disease and left-ventricular systolic dysfunction. The primary endpoint was a composite of cardiovascular death, admission to hospital for acute myocardial infarction, and admission to hospital for new onset or worsening heart failure. We analysed patients by intention to treat.

The study is registered with ClinicalTrials. Median follow-up was 19 months IQR Ivabradine reduced heart rate by 6 bpm SE 0. Ivabradine did not affect the primary composite endpoint hazard ratio 1. In a prespecified subgroup of patients with heart rate of 70 bpm or greater, ivabradine treatment did not affect the primary composite outcome hazard ratio 0.

However, it did reduce secondary endpoints: admission to hospital for fatal and non-fatal myocardial infarction 0. INTERPRETATION: Reduction in heart rate with ivabradine does not improve cardiac outcomes in all patients with stable coronary artery disease and left-ventricular systolic dysfunction, but could be used to reduce the incidence of coronary artery disease outcomes in a subgroup of patients who have heart rates of 70 bpm or greater.



Abstract Background Although there are established drugs for treatment of cardiovascular diseases, due to adverse effects these drugs may not be clinically applicable to all patients. Recent trends have seen the emergence of drugs which act on funny current channels to induce selective heart rate reduction. Ivabradine is one such drug developed for coronary artery disease and heart failure. There is inconsistent evidence about the effect of this selective inhibitor in reduction of cardiovascular related mortality and morbidity.


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