In 1997, Levine1 reviewed the theory of the relationship between heart rate and life span. From observations in the animal kingdom, smaller animals have higher heart rates and shorter life spans than do large animals. This is simply explained by a biophysical imperative in which the ratio of heat loss, which is a function of body mass, increases as body size decreases. Calculations also show that the number of heart beats per lifetime is unexpectedly constant among mammals, despite a 40-fold difference in life span. The difference in body weight is even greater, of the order of 500,000-fold, from hamster to whale. Azbel2 stressed the concept and suggested that life expectancy is predetermined by the basic energetics of living cells, and the inverse relationship between longevity and heart rate reflects an epiphenomenon in which heart rate is a marker or a determinant of metabolic rate and energetic requirements. This linear inverse relationship between heart rate and life expectancy is valid for all mammals except humans. Humans have a mean heart rate of 70 beats/min and a life expectancy of 80 years.1 The reason why the relationship does not apply to humans may reside in advances in science, medicine and technology. The observation that lowering heart rate just from 70 to 60 beats/min would increase life expectancy from 80 to 93.3 years in humans is surprising. In contrast, in the general population it has been observed that the risk for death from all causes, including cardiovascular diseases, increases with resting heart rate. Several clinical studies have shown that increased heart rate is an important risk factor for cardiovascular morbidity and mortality, not only in patients with established heart disease3 and cardiovascular risk factors such as hypertension,4 but also in the general population.5 Heart rate is a major determinant of myocardial oxygen consumption and metabolic demand, and consequently of cardiac workload. A reduction in heart rate would therefore elevate the ischaemic threshold and improve cardiac performance. Several drugs are used in the treatment of cardiovascular diseases but only two classes at present can reduce the heart rate, namely the beta-blockers and some of the calcium channel blockers. It is interesting that reduction in heart rate by beta-blockers has two favourable consequences: first, a decrease in blood pressure, with consequent reduced myocardial oxygen requirements; and, second, a longer diastolic filling time associated with a slower heart rate, allowing for increased coronary perfusion. Betablockers have been consistently shown to reduce cardiovascular mortality, sudden death and reinfarction in patients recovering from acute myocardial infarction.6—8 The primary actions of beta-blockers are to reduce both resting heart rate and the response of heart rate to exercise. The magnitude of mortality reduction, non-fatal reinfarction and infarct size with beta-blockers is clinically meaningful. Diltiazem and verapamil, among the calcium channel blockers, lower heart rate by 6—7 beats/min and have both been shown to decrease the risk for death and non-fatal reinfarction in survivors of acute myocardial infarction with no clinical heart failure or impaired left ventricular function.9,10 Correspondence: Prof. Roberto Ferrari, Cattedra di Cardiologia, University of Ferrara and Fondazione S. Maugeri, IRCCS, Cardiovascular Pathophysiology Research Centre, Corso Giovecca, 203, 44100 Ferrara, Italy.