Heart rate is increasingly being considered as a prognostic factor in cardiovascular disease, and the
need to measure and control heart rate in all coronary patients is clear. When comparisons of heart
rate and life expectancy are adjusted for body weight in mammals, it appears that life span is pre-determined
by the basic energetics of living cells. This inverse relationship between heart rate and life expectancy
reflects an epiphenomenon, in which heart rate is a marker for, or a determinant of, metabolic
rate and energetic needs. The heart rate is controlled by the If current, which plays a central role
as a pacemaker in the sinoatrial node. Ivabradine, the first representative of a new class of exclusive
heart rate-reducing agents, selectively inhibits the If current in the sinoatrial node. The direct electrophysiological
consequence of this inhibition is a reduction in the slope of the diastolic depolarization
curve and a decrease in heart rate. Pharmacological inhibition of the If current with ivabradine has
been shown to preserve coronary vasodilation upon exercise, i.e. myocardial perfusion, with no negative
inotropic effects and maintenance of cardiac contractility. Ivabradine also protects the myocardium
during ischaemia, improves left ventricular function in congestive heart failure, and reduces remodeling
subsequent to myocardial infarction. Pure heart rate reduction by specific and selective If inhibition
decreases oxygen demand and improves myocardial energetics, and so we can expect distinc