[Cardioversion and atrial stunning].
Stunned atrium is defined as a state of temporary mechanic atrial dysfunction with preserved bioeletrical function. It may follow up to 38-80% successful cardioversions performed to convert atrial fibrillation to regular sinus rhythm. Lack of effective atrial contractility leads to hemodynamic changes, which may result in thrombus formation with subsequent thromboembolic events. It becomes a priority to research in depth the pathophysiology of stunned atrium phenomenon and form strategies to avoid complications associated with it. Studies have shown, that even patients who had no evidence of thrombotic material (as proven by transesophageal echocardiography performed prior to cardioversion), are still at increased risk of embolic events. This fact created basis for hypothesis, that conditions for clot formation may be met only when sinus rhythm is restored. 93% of thrombi are accompanied by so-called spontaneous contrast phenomenon. The purpose of our study was to find relations between factors contributing to stunned atrium and its cellular mechanisms. It is suggested, that stunned atrium results from changes in atrial muscular membrane which occur during atrial fibrillation. Stunned atrium is encountered more frequently in patients with coronary artery disease than in hypertensive heart disease or even lone atrial fibrillation. It is also associated with rheumatic valvular abnormalities and left ventricular dysfunction from other causes. Studies have shown no correlation between the frequency of stunned atrium and the mode of cardioversion. It was observed, that duration of atrial fibrillation and dimensions of atria have substantial impact on time to mechanical function recovery and magnitude of atrial stunning. Studies on subjects undergoing cardioversion due to atrial fibrillation proved that there is a higher tendency to stunned atrium in patients with atrial enlargement. Due to significant delay until full mechanical function recovery, it is of prominent importance to continue anticoagulation for at least 4 weeks after cardioversion.
Slaska Akademia Medyczna w Katowicach, II Katedra i Klinika Kardiologii.
Józefa
J
Dabek
Zbigniew
Z
Gasior
Barbara
B
Monastyrska-Cup
Daniel
D
Jakubowski
D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D000925:Anticoagulants / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000628:therapy*; D016279:Atrial Function, Left / Q000187:drug effects / Q000502:physiology; D017548:Echocardiography, Transesophageal; D004554:Electric Countershock / Q000009:adverse effects*; D004617:Embolism / Q000000981:diagnostic imaging / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D009200:Myocardial Contraction; D017682:Myocardial Stunning / Q000000981:diagnostic imaging / Q000209:etiology* / Q000517:prevention & control*; D015912:Thrombolytic Therapy
D000889:Anti-Arrhythmia Agents; D000925:Anticoagulants