Pharmacologic Approach to Sinoatrial Node Dysfunction

Author:

Mesirca Pietro12,Fedorov Vadim V.34,Hund Thomas J.35,Torrente Angelo G.12,Bidaud Isabelle12,Mohler Peter J.346,Mangoni Matteo E.12

Affiliation:

1. Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France;

2. LabEx Ion Channels Science and Therapeutics (ICST), 06560 Nice, France

3. Frick Center for Heart Failure and Arrhythmia at the Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA

4. Department of Physiology and Cell Biology, The Ohio State University College of Medicine, Wexner Medical Center, Columbus, Ohio 43210, USA

5. Department of Biomedical Engineering, The Ohio State University, Columbus, Ohio 43210, USA

6. Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA

Abstract

The spontaneous activity of the sinoatrial node initiates the heartbeat. Sino-atrial node dysfunction (SND) and sick sinoatrial (sick sinus) syndrome are caused by the heart's inability to generate a normal sinoatrial node action potential. In clinical practice, SND is generally considered an age-related pathology, secondary to degenerative fibrosis of the heart pacemaker tissue. However, other forms of SND exist, including idiopathic primary SND, which is genetic, and forms that are secondary to cardiovascular or systemic disease. The incidence of SND in the general population is expected to increase over the next half century, boosting the need to implant electronic pacemakers. During the last two decades, our knowledge of sino-atrial node physiology and of the pathophysiological mechanisms underlying SND has advanced considerably. This review summarizes the current knowledge about SND mechanisms and discusses the possibility of introducing new pharmacologic therapies for treating SND.

Publisher

Annual Reviews

Subject

Pharmacology,Toxicology

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