oa SA Pharmaceutical Journal - Ivabradine - the first 1 inhibitor for the treatment of chronic stable angina : medifile

Volume 76, Issue 4
  • ISSN : 2221-5875
  • E-ISSN: 2220-1017



Coronary artery disease (CAD) is a highly prevalent condition with life-threatening consequences. The most common presenting symptom of CAD is the chest pain associated with angina.

Angina occurs when myocardial perfusion is inadequate to meet oxygen demand. An increased heart rate (HR) plays a vital role in CAD, not only as a trigger of most ischaemic events, but also as an important predictor of cardiovascular morbidity and mortality. Therefore HR reduction plays a central role in the management of patients with angina pectoris.
Current pharmacological management recommended by guidelines for the treatment of chronic stable angina includes β-blockers, calcium-channel blockers and organic nitrates. However, their use has limitations due to tolerance to the therapeutic effect, relative contraindications or side effects. In view of these limitations, a new pharmacological target was sought. This led to the launch of ivabradine, a selective and specific 1 inhibitor, which acts on the ionic currents for the regulation of pacemaker activity in the sinoatrial (SA) node cells. Ivabradine slows the slope of diastolic depolarisation of the action potential in the SA node cells and decreases HR at rest and during exercise.
Several clinical trials demonstrated dose-dependent anti-ischaemic and anti-anginal effects of ivabradine. There was no pharmacological tolerance or rebound phenomena upon withdrawal of ivabradine. Ivabradine was also found to have a good safety and tolerability profile with the main side effect being dose-related visual symptoms that were transient and mild in nature. Bradycardia may however be a problem with combination therapy.
Ivabradine is expected to give symptomatic relief to patients with chronic stable angina, especially those who have contra-indications or intolerance to current pharmacological options or who are insufficiently controlled on monotherapy. Long-term cardiovascular mortality benefits however need to be established.

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