Heart rate (HR) is an independent predicting factor of cardiovascular events in patients with advanced heart failure. Clinical trials conducted with beta-blockers have demonstrated that reduction of HR is a fundamental mechanism to explain the reduction of morbidity-mortality in such a disease. Trials conducted with ivabradine, the first selective inhibitor of the I(f) current in cardiac pacemaker cells, have also clearly confirmed that reduction of HR lead to powerful and sustained favourable effects in patients with cardiac failure and post-infarcted myocardial diseases. These effects are not only due to the reduction of the risk factors associated with myocardial ischemia but also to the reduction of cardiac and perivascular fibrosis associated with the remodelling process at the ventricular level. Although the mechanisms associated with reduction of HR following administration of beta-blockers and ivabradine are to a large extent similar, others like their effects on post-systolic contraction are totally opposed. So, new clinical trials are necessary to know whether it is possible to substitute these drugs or conversely to associate them for an optimal therapeutic strategy in patients with advanced heart failure and post-infarcted myocardium.