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. Given that the benefits of ivabradine were somewhat attenuated in the subgroup of patients on at least half-dose beta blocker therapy, this raises the question of whether ivabradine truly benefits patients already on target dose beta blocker therapy. These guidelines also recommend consideration of ivabradine in patients with HFrEF and beta blocker intolerance.

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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. Such an inconsistency warrants the need for a meta-analysis to consider the effectiveness and efficacy of Ivabradine in the treatment of coronary artery disease and heart failure. Each eligible study was assessed for risk of bias by using the Cochrane Risk of Bias Assessment tool. The outcomes assessed in this study included: all cause mortality, cardiovascular-related mortality, hospitalization for new or worsening heart failure, and adverse events.


Kimi Between December,and December,we screened 12 patients at centres in 33 countries. Provide sufficient details of any financial or non-financial competing interests to enable users to assess whether your comments might lead a reasonable person to question your impartiality. You must be a registered member of The Cardiology Advisor to post a comment. The use of certain tools provided by this website is subject to additional Terms and Conditions. Over 6, patients were randomized and followed for about Ivabradine is the only selective I f ivabracine inhibitor to date. Digoxin may also be used in concomitant atrial fibrillation, whereas ivabradine cannot.

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