The present review summarizes the experimental and clinical evidence for the anti-ischemic action of the selective bradycardic agent ivabradine. Improvements in myocardial blood flow and contractile function during experimental myocardial ischemia and the clinical anti-anginal effect are largely mediated by heart rate reduction. However, a significant reduction in infarct size by ivabradine persists in the absence of heart rate reduction, and such protection can also be recruited when ivabradine is given only during early reperfusion. The mechanisms for such pleiotropic action of ivabradine remain to be resolved.