Atrial stunning: determinants and cellular mechanisms.
BACKGROUND
Atrial stunning is a transient depression of atrial and atrial-appendage mechanical function after successful cardioversion of atrial fibrillation compared with its precardioversion state.


METHODS
Atrial stunning associated with different methods of cardioversion of atrial fibrillation and the determinants and cellular mechanisms of atrial stunning were elaborated by thoroughly examining the studies on the subject identified through a comprehensive literature search.


CONCLUSIONS
Atrial stunning has been reported with all methods of cardioversion of atrial fibrillation, including transthoracic electrical, low-energy internal electrical, pharmacological, and spontaneous. It is a function of the underlying atrial fibrillation becoming apparent at the restoration of sinus rhythm, regardless of the method used for conversion. Unsuccessful cardioversion does not result in atrial stunning. The duration of the preceding atrial fibrillation, atrial size, and underlying structural heart disease are the determinants of atrial stunning. A shorter duration of atrial fibrillation and smaller atrial diameters are associated with a relatively less severe stunning, lasting for a shorter duration. Atrial stunning after cardioversion of atrial fibrillation of <1 week usually resolves within 24 hours, and atrial stunning after cardioversion of chronic atrial fibrillation usually resolves within 4 weeks. Tachycardia-induced atrial cardiomyopathy, atrial cytosolic calcium alterations with down-regulation of the L-type Ca2+ channels and up-regulation of the Na+/Ca2+ exchanger, atrial hibernation with myocyte dedifferentiation and myolysis, and atrial fibrosis are the suggested mechanisms underlying atrial stunning. Atrial stunning determines the risk of postcardioversion thrombus formation in atria and atrial appendages, the duration of postcardioversion anticoagulation therapy, the recovery of the atrial contribution to the ventricular function, and the functional recovery of the patients after successful cardioversion of atrial fibrillation.
Khan
Ijaz A
IA
Division of Cardiology, Creighton University School of Medicine, Omaha, Neb 68131-2044, USA. ikhan@cardiac.creighton.edu
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy*; D016275:Atrial Function / Q000502:physiology*; D004554:Electric Countershock / Q000009:adverse effects*; D006325:Heart Atria / Q000033:anatomy & histology; D006801:Humans; D009200:Myocardial Contraction; D017682:Myocardial Stunning / Q000209:etiology* / Q000503:physiopathology; D012075:Remission, Spontaneous; D013610:Tachycardia / Q000150:complications; D013997:Time Factors
D000889:Anti-Arrhythmia Agents