This report describes general characteristics of diseases classified as cardiac arrhythmias. The term "arrhythmia" refers to any change from the normal sequence of electrical impulses in the heart, such as atrial fibrillation, bradycardia (slow heartbeat), tachycardia (rapid heart rate), conduction disorders, rhythm disorders, ventricular fibrillation, premature contractions. Many of the genes associated with cardiac arrhythmias encode ion channels; these diseases are described as cardiac channelopathies.
Atrial remodeling is long-term result of various cardiac diseases and conditions, including atrial fibrillation. Structural remodeling is characterized by atrial enlargement and tissue fibrosis; other processes of remodeling include electrical remodeling, autonomic nervous system changes, and Ca[+2] handling abnormalities.
[updated Feb. 2018 by FlyBase; FBrf0222196]
The term "arrhythmia" refers to any change from the normal sequence of electrical impulses in the heart, such as atrial fibrillation, bradycardia (slow heartbeat), tachycardia (rapid heart rate), conduction disorders, rhythm disorders, ventricular fibrillation, premature contractions. Arrhythmias may be completely harmless or life-threatening. (http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/About-Arrhythmia_UCM_002010_Article.jsp)
Any persistent change in atrial structure or function constitutes atrial remodeling. Structural remodeling is characterized by atrial enlargement and tissue fibrosis; other processes of arrhythmogenic remodeling include electrical remodeling, autonomic nervous system changes, and Ca[+2] handling abnormalities. Atrial fibrillation (AF) is a final common endpoint of atrial remodeling caused by a variety of cardiac diseases and conditions and itself causes important remodeling that contributes to the progressive nature of the arrhythmia. Intracellular Ca[+2] plays a key role in this process. (Nattel and Harada, 2014; pubmed:24613319)
Mutations in calcium, sodium, potassium, and TRP channel genes have been identified to cause a variety of cardiac arrhythmic disorders; polymorphisms have been suggested to be risk factors (Kim, 2014; pubmed:24578711).