Abstract
The bradycardic agent ivabradine has proved to be of benefit in experimental models with the end points of ischaemic myocardial blood flow and contractile function, infarct size, post-infarct remodelling and atherosclerosis. The benefits to ischaemic myocardial blood flow and contractile function are strictly heart rate dependent; those on infarct size are partly heart rate independent. The heart rate dependency of ivabradine's benefit for atherosclerotic vascular function is contradictory, and that on post-infarct remodelling is entirely unclear.