Author + information
- Received June 5, 2017
- Revision received August 1, 2017
- Accepted August 16, 2017
- Published online September 25, 2017.
- Jacob S. Koruth, MDa,
- Anuradha Lala, MDb,c,
- Sean Pinney, MDb,
- Vivek Y. Reddy, MDa and
- Srinivas R. Dukkipati, MDa,∗ ()
- aHelmsley Electrophysiology Center, Icahn School of Medicine at Mount Sinai, New York, New York
- bDivision of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York
- cPopulation Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, New York
- ↵∗Address for correspondence:
Dr. Srinivas R. Dukkipati, Helmsley Electrophysiology Center, Mount Sinai Hospital and School of Medicine, One Gustave L. Levy Place, P.O. Box 1030, New York, New York 10029.
The clinical use of ivabradine has and continues to evolve along channels that are predicated on its mechanism of action. It selectively inhibits the funny current (If) in sinoatrial nodal tissue, resulting in a decrease in the rate of diastolic depolarization and, consequently, the heart rate, a mechanism that is distinct from those of other negative chronotropic agents. Thus, it has been evaluated and is used in select patients with systolic heart failure and chronic stable angina without clinically significant adverse effects. Although not approved for other indications, ivabradine has also shown promise in the management of inappropriate sinus tachycardia. Here, the authors review the mechanism of action of ivabradine and salient studies that have led to its current clinical indications and use.
Dr. Pinney has received consulting fees from Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Roberto Ferrari, MD, PhD, served as Guest Editor for this paper.
- Received June 5, 2017.
- Revision received August 1, 2017.
- Accepted August 16, 2017.
- 2017 American College of Cardiology Foundation
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