Atrial stunning: basics and clinical considerations.
Conversion of atrial fibrillation and flutter to sinus rhythm results in a transient mechanical dysfunction of atrium and atrial appendage, termed atrial stunning. Atrial stunning has been reported with all modes of conversion of atrial fibrillation and flutter to sinus rhythm including both transthoracic and low energy internal electrical, pharmacological, and spontaneous cardioversion, and conversion by overdrive pacing and by radiofrequency ablation. Atrial stunning is a function of the underlying arrhythmia becoming apparent at the restoration of sinus rhythm, not the function of the mode of conversion, and does not develop after the unsuccessful attempts of cardioversion or the delivery of electric current to the heart during rhythms other than atrial fibrillation or flutter. Tachycardia-induced atrial cardiomyopathy, cytosolic calcium accumulation, and atrial hibernation are the suggested mechanisms of atrial stunning. Atrial stunning is at maximum immediately after cardioversion and improves progressively with a complete resolution within a few minutes to 4-6 weeks depending on the duration of the preceding atrial fibrillation, atrial size, and structural heart disease. Atrial stunning causes postcardioversion thromboembolism despite restoration of sinus rhythm. Duration of anticoagulation therapy after successful cardioversion should depend on the duration of atrial stunning. Lack of improvement in cardiac output and functional recovery of patients immediately after cardioversion is attributed to the atrial stunning. Verapamil, acetylstrophenathidine, isoproterenol, and dofetilide have been reported to protect from atrial stunning in animal and small human studies. Right atrium stunning is less marked and improves earlier than that of left atrium, resulting in a differential atrial stunning explaining the rare occurrence of pulmonary edema after cardioversion.
Khan
Ijaz A
IA
Divisions of Cardiology, Creighton University School of Medicine, 3006 Webster Street, Omaha, NE 68131, USA. ikhan@cardiac.creighton.edu
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001281:Atrial Fibrillation / Q000628:therapy; D001282:Atrial Flutter / Q000628:therapy; D016275:Atrial Function / Q000502:physiology*; D016279:Atrial Function, Left / Q000502:physiology; D016280:Atrial Function, Right / Q000502:physiology; D017115:Catheter Ablation; D004554:Electric Countershock; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D017682:Myocardial Stunning / Q000209:etiology / Q000503:physiopathology*; D010627:Phenethylamines / Q000494:pharmacology; D013015:Sotalol / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology; D013923:Thromboembolism / Q000209:etiology; D013997:Time Factors; D014700:Verapamil / Q000494:pharmacology
D000889:Anti-Arrhythmia Agents; D010627:Phenethylamines; D013449:Sulfonamides; D013015:Sotalol; D014700:Verapamil; D007545:Isoproterenol; C063533:dofetilide