European Heart Journal Advance Access originally published online on October 11, 2005
European Heart Journal 2005 26(23):2482-2483; doi:10.1093/eurheartj/ehi575
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
If at first you don't succeed try ... a new target in the treatment of angina
Department of Cardiology, King's College London, Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK
* Corresponding author. Tel: +44 207 188 1008; fax: +44 207 188 0970. E-mail address: mike.marber@kcl.ac.uk
This editorial refers to Efficacy of ivabradine, a new selective If inhibitor, compared with atenolol in patients with chronic stable angina
by J.-C. Tardiff et al., on page 2529
| The first 10% of the full text of this article appears below. |
Tardiff et al.1 describe a promising new treatment for angina, ivabradine, that appears to selectively reduce heart rate by blocking the cardiac pacemaker funny current, If. In contrast to the existing agents that slow heart rate, there is no accompanying intrinsic negative inotropic effect. Understanding the basis of this unique property requires a brief overview of the underlying physiology.
The cells of the sinoatrial node are the primary pacemaker of the heart. This function is the result of an upward, positive, depolarizing drift in their resting membrane potential during the diastolic phase of the action potential, known as the pacemaker current. Once this drift reaches a threshold potential, the next action potential is triggered by the opening of slow calcium channels and consequent influx of Ca2+ ions. Calcium antagonists reduce Ca2+ influx through slow (L-type) calcium channels and this leads to prolongation of the depolarization
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- Efficacy of ivabradine, a new selective If inhibitor, compared with atenolol in patients with chronic stable angina
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