Turitto Gioia, Saponieri Cesare, Onuora Afamefuna, El-Sherif Nabil
Cardiac Electrophysiology Services, New York Methodist Hospital, 506 Sixth Street, Brooklyn, NY 11215, USA.
Pacing Clin Electrophysiol. 2007 Nov;30(11):1311-5. doi: 10.1111/j.1540-8159.2007.00863.x.
Atrial standstill is a rare heterogeneous arrhythmia characterized by electrical and mechanical standstill and electrical inexcitability. A long-lasting progressive form is seen with cardiac and neuromuscular diseases, and a familial or idiopathic form may have a genetic basis. A transient form was described secondary to drug intoxication, electrolyte imbalance, cardiac inflammation, and ischemia.
We investigated three patients with long-standing atrial tachyarrhythmia (AT) (atrial flutter in two, and focal atrial tachycardia in one). All patients underwent a complete electrophysiological study with mapping of right and left atrial activity and radiofrequency ablation (RF Abl) of AT.
Following RF Abl of AT, all three patients manifested transient atrial electrical silence in the absence of known reversible causes. Atrial electrical silence was observed when, following AT termination, an escape atrioventricular (AV) junctional rhythm (in two patients) and an escape VVI pacemaker rhythm (in one patient) showed transient ventriculo-atrial (VA) conduction block (up to 30 seconds). A dominant sinus rhythm was observed to return 30 minutes, 90 minutes, and 12 hours, respectively, in the three patients. Two patients received a dual chamber pacemaker and a decision was made not to upgrade the patient with VVI pacemaker.
The present report expands the spectrum of the syndrome of atrial standstill and raises interesting questions regarding possible electrophysiologic mechanism(s) of prolonged post overdrive atrial standstill. The report suggests that chronic overdrive of sinus and subsidiary atrial pacemakers may result in calcium overloading of cardiac cells, which is known to cause suppression of pacemaker activity as well as increased intracellular resistance. These mechanisms can possibly result in either prolonged suppression of sinus and atrial pacemaker activity and/or pacemaker exit block.
心房静止是一种罕见的异质性心律失常,其特征为电活动和机械活动静止以及电不可兴奋性。在心脏和神经肌肉疾病中可见到一种持久的进行性形式,而家族性或特发性形式可能有遗传基础。曾有文献描述过继发于药物中毒、电解质失衡、心脏炎症和缺血的短暂性形式。
我们研究了3例长期存在房性快速心律失常(AT)的患者(2例为心房扑动,1例为局灶性房性心动过速)。所有患者均接受了完整的电生理检查,包括右心房和左心房活动标测以及AT的射频消融(RF Abl)。
在AT进行RF Abl后,所有3例患者在无已知可逆病因的情况下均出现了短暂的心房电静止。当AT终止后,在出现逸搏房室(AV)交界性心律(2例患者)和逸搏VVI起搏器心律(1例患者)时观察到心房电静止,同时伴有短暂的室房(VA)传导阻滞(长达30秒)。3例患者分别在30分钟、90分钟和12小时后观察到窦性主导心律恢复。2例患者接受了双腔起搏器治疗,对于植入VVI起搏器的患者则决定不进行升级。
本报告扩展了心房静止综合征的范围,并就超速起搏后心房静止延长的可能电生理机制提出了有趣的问题。该报告表明,窦性和附属心房起搏器的慢性超速起搏可能导致心肌细胞钙超载,已知这会导致起搏器活动受抑制以及细胞内电阻增加。这些机制可能导致窦性和心房起搏器活动的长期抑制和/或起搏器传出阻滞。