Khan Ijaz A
Division of Cardiology, Creighton University School of Medicine, Omaha, Neb 68131-2044, USA.
Am Heart J. 2003 May;145(5):787-94. doi: 10.1016/S0002-8703(03)00086-3.
Atrial stunning is a transient depression of atrial and atrial-appendage mechanical function after successful cardioversion of atrial fibrillation compared with its precardioversion state.
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.
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.
心房顿抑是指心房颤动成功转复后,与其转复前状态相比,心房及心耳机械功能出现的短暂性降低。
通过全面检索文献,对已识别的关于心房颤动不同转复方法以及心房顿抑的决定因素和细胞机制的研究进行深入分析,阐述心房顿抑相关情况。
所有心房颤动转复方法,包括经胸电转复、低能量心内电转复、药物转复和自行转复,均有关于心房顿抑的报道。它是潜在心房颤动在恢复窦性心律时显现出的一种功能,与所用转复方法无关。转复不成功不会导致心房顿抑。心房颤动的持续时间、心房大小以及潜在的结构性心脏病是心房顿抑的决定因素。心房颤动持续时间较短和心房直径较小与相对较轻的顿抑相关,且持续时间较短。心房颤动持续时间<1周转复后的心房顿抑通常在24小时内恢复,慢性心房颤动转复后的心房顿抑通常在4周内恢复。心动过速诱导的心房心肌病、L型钙通道下调和钠/钙交换体上调导致的心房胞浆钙改变、伴有心肌细胞去分化和溶解的心房冬眠以及心房纤维化是心房顿抑的潜在机制。心房顿抑决定心房颤动成功转复后心房和心耳内血栓形成的风险、转复后抗凝治疗的持续时间、心房对心室功能贡献的恢复情况以及患者的功能恢复情况。