Despite profound advances in the treatment of ischemic heart disease with medications or invasive procedures during the past 30 years, ischemic heart disease remains the main cause of mortality and morbidity in developed countries. Elevated resting heart rate is a well-known and easily measured risk factor, but too little attention is paid to decreasing it. A person’s heart rate depends on the metabolic rate and is defined by pace maker cells in the sinoatrial node. Both the sympathetic and parasympathetic nervous systems exert control on it through changes in the membrane potential across the ion channels (which also include the newly discovered f channels). An elevated resting heart rate can result from irregular functioning of the autonomic nervous system. Its unfavourable consequences include shortening of the diastolic time and elevated oxygen consumption in the myocardium, which in turn lead to an earlier occurrence of cardiovascular events. Several epidemiological studies have demonstrated that there is an association between elevated heart rate and cardiovascular mortality and morbidity in healthy subjects, as well as in patients with previous myocardial infracttions and heart failure. The target values of resting heart rate depend on the presen ce of heart failure. Patients with a significantly lowered left ventricular ejection fraction need higher heart rates, as these work as compensatory mechanisms for maintaining sufficient cardiac output. Lowering the heart rate can be done by changing one’s life-style, as well as with medical treatment, i.e. by administering adrenergic beta blockers, calcium channel antagonists which act on the cardiac electrical conduction system, digoxin, and the newest drug available in this field called ivabradin, which selectively and specifically inhibits f channels in sinoatrial pacemaker cells.