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首页> 外文期刊>The Journal of Thoracic and Cardiovascular Surgery >Persistent atrial fibrillation in a goat model of chronic left atrial overload.
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Persistent atrial fibrillation in a goat model of chronic left atrial overload.

机译:在慢性左心房超负荷的山羊模型中持续性心房颤动。

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OBJECTIVES: Atrial dilatation predisposes to atrial fibrillation. Although several animal models focus on the initiating mechanisms of atrial fibrillation in dilated atria, a model of left atrial overload resulting in persistent atrial fibrillation in nonanesthetized animals has not been presented thus far. METHODS: In 24 goats a vascular shunt was implanted between the aorta and the left atrium through a left thoracotomy. In 6 animals the shunt was ligated immediately (control group). Ultrasonic crystals were implanted to monitor atrial dilatation. Bipolar electrodes were positioned epicardially on the left atrium for measurement of the atrial effective refractory period, conduction times, and atrial fibrillation duration. RESULTS: Four weeks of overload resulted in an increase of left atrial pressure (23.1 +/- 6.8 mm Hg in the open-shunt group vs 7.0 +/- 1.9 mm Hg in the control group, P = .002) and a progressive dilatation of the left atrium (135% +/- 20% in the open-shunt group vs 98% +/- 8.0% in the control group, P = .002). Among the open-shunt group's long-term survivors (n = 12), 9 animals showed prolonged atrial fibrillation (>1 hour), and of these, 6 were in persistent atrial fibrillation (>1 week). The atrial effective refractory period increased during the first week and remained prolonged until death (182 +/- 11 ms in the open-shunt group vs 161 +/- 15 ms, P = .03). The conduction time did not change. An increase in collagen formation was noticed in both groups, without a significant difference between them. CONCLUSIONS: A chronic aortic to left atrial shunt is a feasible model in the goat. It induces progressive left atrial dilatation with an increased atrial fibrillation duration up to hours in the majority of animals. Prolonged atrial fibrillation duration could not be explained by a shortening of atrial effective refractory period or increase in fibrosis.
机译:目的:心房扩张易诱发房颤。尽管几种动物模型关注于扩张心房中心房纤颤的起始机制,但迄今为止,尚未提出导致非麻醉动物持续性房颤的左心房超负荷模型。方法:在24只山羊中,通过左胸廓切开术在主动脉和左心房之间植入血管分流器。立即将6只动物的分流结扎(对照组)。植入超声波晶体以监测心房扩张。双极电极位于左心房心外膜上,以测量心房有效不应期,传导时间和心房颤动持续时间。结果:超负荷四周导致左心房压力升高(开放分流组为23.1 +/- 6.8 mm Hg,对照组为7.0 +/- 1.9 mm Hg,P = .002)并进行性扩张(左分流组为135%+/- 20%,而对照组为98%+/- 8.0%,P = .002)。在开放式分流组的长期存活者中(n = 12),有9只动物表现出较长的心房纤颤(> 1小时),其中有6只处于持续性心房纤颤(> 1周)。心房有效不应期在第一个星期增加,一直持续到死亡为止(开放分流组为182 +/- 11毫秒,而161 +/- 15毫秒,P = .03)。传导时间没有改变。两组均发现胶原蛋白形成增加,但两组之间无显着差异。结论:慢性主动脉至左心房分流术是山羊可行的模型。在大多数动物中,它诱导进行性左心房扩张,心房纤颤持续时间增加,长达数小时。房颤持续时间的延长不能通过缩短房颤的有效不应期或增加纤维化来解释。

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