The role of ivabradine in improving myocardial perfusion, adding to the antianginal benefits

The most common cause of oxygen demand/supply mismatch is atherosclerotic narrowing of the coronary artery, resulting in decreased coronary blood flow. However, endothelial dysfunction and/or microvascular dysfunction may be responsible for myocardial ischaemia and importantly may often coexist in patients with angina. Coronary flow reserve reflects the functional capacity of coronary circulation to adapt to the blood demand during increased cardiac work. In addition, coronary flow reserve predicts long-term adverse cardiovascular outcome. Therefore, a clear understanding of myocardial perfusion pathophysiology and a knowledge of the antianginal–anti-ischaemic drugs effect on coronary circulation are crucial for the judicious use of medications for the treatment of angina patients with coronary artery disease. This article discusses the role of ivabradine in improvement of myocardial perfusion based on data drawn from relevant preclinical and clinical investigations. Experimental data suggest that heart rate reduction with ivabradine causes greater increase in duration of diastolic perfusion time and coronary flow compared with β-blockade due to absence of impairing of left ventricular contractility and coronary vasomotion. In consequence, the full benefits of heart rate reduction for improved coronary perfusion could be realized with ivabradine. Following experimental data, clinical studies demonstrated anti-ischaemic and antianginal efficacy of ivabradine in patients with stable coronary artery disease. These clinical benefits have been supported by recent clinical data on improvement of coronary flow reserve, and coronary collateral circulation with ivabradine supports the role of ivabradine as an important anti-ischaemic and antianginal agent in patients with angina in addition to other recommended therapies or revascularization.