Selective heart rate (HR) reduction by I(f)-channel inhibition is a recently 
developed pharmacological principle in cardiovascular therapy. Among these newly 
identified HR-lowering drugs, only ivabradine has now become approved for 
clinical use. I(f)-channel inhibition mainly reduces HR, thereby improving 
myocardial oxygen supply, energy balance, and cardiac function. Ivabradine was 
well tolerated and revealed a good safety profile in the investigated study 
populations. The guiding experimental and clinical results of I(f)-channel 
inhibition were compared to those of beta-blockade as a HR reducing principle as 
well as cornerstone of heart failure standard therapy. Beside its use in therapy 
of coronary artery disease, I(f)-channel inhibition potentially exhibits 
beneficial effects in systolic and diastolic heart failure as well. Therefore, 
hemodynamic effects of ivabradine and its limitations in heart failure together 
with the biological impact of HR reduction will be considered in this context. 
Because no clinical data with specific heart-rate-reducing agents are available 
in heart failure patients until now, the prospective significance of 
I(f)-channel inhibition can only be speculated on. However, the presented 
results and considerations are encouraging: ivabradine may play a therapeutic 
role in the future protecting left ventricular function and structure from early 
deterioration in heart failure with reduced and preserved ventricular ejection 
fraction.