Ivabradine, the first representative of a new class of exclusive heart rate-reducing agents, selectively inhibits the I(f) current in the sinoatrial node. The direct electrophysiological consequence of this inhibition is a reduction in the slope of the diastolic depolarisation curve and a decrease in heart rate. Pharmacological inhibition of the I(f) current with ivabradine has been shown to preserve coronary vasodilatation upon exercise, i.e., myocardial perfusion, with no negative inotropic effects and maintenance of cardiac contractility. Ivabradine protects the myocardium during ischaemia, improves left ventricular function in congestive heart failure, and reduces remodelling subsequent to myocardial infarction. Pure heart rate reduction by specific and selective I(f) inhibition decreases oxygen demand, improves myocardial energetics and improves perfusion of the ischaemic myocardium. We can expect distinct clinical benefits from long-term heart rate reduction in patients with chronic ischaemic disease.