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Heart Rhythm. 2019 Feb 14. pii: S1547-5271(19)30139-0. doi: 10.1016/j.hrthm.2019.02.017. [Epub ahead of print]

Autoimmune and inflammatory K+ channelopathies in cardiac arrhythmias: Clinical evidence and molecular mechanisms.

Author information

1
Department of Medical Sciences, Surgery and Neurosciences, University of Siena, Siena, Italy.
2
VA New York Harbor Healthcare System, SUNY Downstate Medical Center, New York, New York.
3
NewYork-Presbyterian Brooklyn Methodist Hospital, Brooklyn, New York.
4
VA New York Harbor Healthcare System, SUNY Downstate Medical Center, New York, New York; NYU School of Medicine, New York, New York.
5
Department of Medical Sciences, Surgery and Neurosciences, University of Siena, Siena, Italy. Electronic address: lazzerini7@unisi.it.

Abstract

Cardiac K+ channelopathies account for a significant proportion of arrhythmias and sudden cardiac death (SCD) in subjects without structural heart disease. It is well recognized that genetic defects are key factors in many cases, and in practice, the term cardiac channelopathies currently coincides with inherited cardiac channelopathies. However, mounting evidence demonstrate that not only genetic alterations but also autoimmune and inflammatory factors can cause cardiac K+-channel dysfunction and arrhythmias in the setting of a structurally normal heart. In particular, it has been demonstrated that specific autoantibodies as well as inflammatory cytokines can modulate expression and/or function of different K+ channels in the heart, resulting in a disruption of the cardiac action potential and arrhythmias/sudden cardiac death. Awareness about the existence of these newly recognized forms is essential to identify and adequately manage affected patients. In the present review, we focus on autoimmune and inflammatory K+ channelopathies as a novel mechanism for cardiac arrhythmias and analyze the recent advancements in this topic, providing complementary basic, clinical, and population health perspectives.

KEYWORDS:

Autoantibodies; Autoimmunity; Cardiac K(+) channels; Cardiac arrhythmias; Cytokines; Inflammation; Sudden cardiac death

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