Stoddard M F
Department of Medicine, University of Luisville, KY 40292, USA.
Echocardiography. 2000 May;17(4):393-405. doi: 10.1111/j.1540-8175.2000.tb01155.x.
Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia, predominating in the elderly, with stroke as a potentially devastating complication. Prevention of the thromboembolic sequelae from AF remains a central focus of practicing clinicians. Although the risk of thromboembolism in chronic AF is well recognized, less is known about the potential risk of systemic embolism in acute AF. In addition, recent data support the notion of a group at considerable risk of embolism from atrial flutter, an arrhythmia typically believed to bestow little increased risk of thromboembolism. The mechanism of thrombus formation, embolization, and resolution in atrial arrhythmias is not well defined, particularly in that of acute AF or atrial flutter. The traditional concept proposes that atrial thrombus forms only after > 2 days of AF and embolizes by being dislodged from increases in shear forces. This widely accepted concept further holds that newly formed atrial thrombus, in the setting of AF, organizes over a span of 14 days. The results of studies based on observations from transesophageal echocardiography examinations have provided provocative insight into the temporal sequence of atrial thrombus formation, embolization, and resolution in AF or atrial flutter and have expanded the traditional concept of thromboembolism in these atrial dysrhythmias. Namely, left atrial thrombus may form before the onset of AF in the face of sinus rhythm. Conversion to sinus rhythm may increase the thrombogenic milieu of the left atrium. Importantly, atrial thrombus may form in the acute phase of AF. Last, thrombi may require > 14 days to become immobile or to resolve. Findings similar to those of acute AF have been reported in patients with atrial flutter and coexisting cardiac pathology. On the basis of these emerging insights fostered by the use of transesophageal echocardiography, it appears appropriate to consider anticoagulation in patients presenting with acute AF or atrial flutter with coexisting cardiac pathology predisposing to left atrial thrombus.
心房颤动（AF）是最常见的持续性心律失常，在老年人中占主导地位，中风是其潜在的毁灭性并发症。预防房颤的血栓栓塞后遗症仍然是临床医生关注的核心问题。虽然慢性房颤的血栓栓塞风险已得到充分认识，但对于急性房颤的全身栓塞潜在风险了解较少。此外，最近的数据支持这样一种观点，即心房扑动患者存在相当大的栓塞风险，而心房扑动这种心律失常通常被认为血栓栓塞风险增加不多。房性心律失常中血栓形成、栓塞和溶解的机制尚不清楚，尤其是急性房颤或心房扑动。传统观念认为，心房血栓仅在房颤发作超过2天后形成，并因剪切力增加而脱落导致栓塞。这一被广泛接受的观念还认为，在房颤情况下新形成的心房血栓会在14天内机化。基于经食管超声心动图检查观察结果的研究，为房颤或心房扑动中心房血栓形成、栓塞和溶解的时间顺序提供了有启发性的见解，并扩展了这些房性心律失常中血栓栓塞的传统概念。也就是说，在窦性心律时，左心房血栓可能在房颤发作前就已形成。转为窦性心律可能会增加左心房的血栓形成环境。重要的是，心房血栓可能在房颤急性期形成。最后，血栓可能需要超过14天才能变得固定或溶解。在患有心房扑动和并存心脏疾病的患者中也报告了与急性房颤类似的发现。基于经食管超声心动图带来的这些新见解，对于患有急性房颤或心房扑动且并存易导致左心房血栓形成的心脏疾病的患者，考虑进行抗凝治疗似乎是合适的。
