Heart rate is a fundamental determinant of cardiac oxygen consumption and plays a
pivotal role in the pathophysiology of chronic stable angina (CSA). Ivabradine selectively and
specifically inhibits the sino-atrial If current, slowing selectively heart rate without other significant
haemodynamic effects. The consequent clinical effects are a sinus rate reduction similar to that
obtained with beta-blockers, but without the related haemodynamic side effects.
Ivabradine clinical benefits have been demonstrated both in patients with stable coronary artery
disease (CAD) with associated systolic left ventricular dysfunction or in patients with congestive heart failure (HF). In
this review we focused on the pharmacology and clinical research about ivabradine in the context of anti-ischemic therapy
for CAD patients. Actually most guidelines suggest ivabradine therapy as last resort antianginal drugs in patients with
uncontrolled symptoms or excessive heart rate despite maximum tolerated beta-blockade. However, the peculiar
pharmacologic effects of the drug suggest that most patients with CAD might benefit from adding ivabradine to their
therapeutic schemata. In fact, even if the recently released main analysis of the SIGNIFY study seems not to support an
employ of ivabradine in primary prevention, it is easy to imagine a future wider use of this drug in elderly patients with
incomplete myocardial revascularization and in patients with total chronic coronary occlusions and failure or unacceptable
risk for percutaneous or surgical coronary revascularization.