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慢性心肌梗死大鼠室性心动过速的高分辨率光学标测

High-resolution optical mapping of ventricular tachycardia in rats with chronic myocardial infarction.

作者信息

Ding Chunhua, Gepstein Lior, Nguyen Duy Thai, Wilson Emily, Hulley George, Beaser Andrew, Lee Randall J, Olgin Jeffrey

机构信息

Cardiac Electrophysiology and Cardiovascular Research Institute, University of California, San Francisco, California 94143, USA.

出版信息

Pacing Clin Electrophysiol. 2010 Jun 1;33(6):687-95. doi: 10.1111/j.1540-8159.2010.02704.x. Epub 2010 Feb 18.

DOI:10.1111/j.1540-8159.2010.02704.x
PMID:20180914
Abstract

BACKGROUND

Ventricular tachycardia (VT) is a common cause of mortality in post-myocardial infarction (MI) patients, even in the current era of coronary revascularization treatment. We report a reproducible VT model in rats with chronic MI induced by ischemia-reperfusion and describe its electrophysiological characteristics using high-resolution optical mapping.

METHODS

An MI was generated by left anterior descending coronary ligation (25 minutes) followed by reperfusion in 20 rats. Electrophysiology study and optical mapping were performed 5 weeks later using a Langendorff-perfused preparation and compared to normal rats.

RESULTS

The conduction velocity of the MI border zone was decreased to 53% of the normal areas remote from the infarct (0.37 +/- 0.16 m/sec vs 0.70 +/- 0.09 m/sec, P < 0.0001). The rate of VT inducibility in MI rats was significantly greater than in normal control rats (70% vs 0%, P = 0.00002). VT circuits involving the infarct area were identified with optical mapping in 83% MI rats. In addition, fixed and functional conduction block were observed in the infarct border zone.

CONCLUSION

This ischemia-reperfusion MI rat model is a reliable VT model, which simulates clinical revascularization treatment. High-resolution optical mapping in this model is useful to study the mechanism of VT and evaluate the effects of therapies.

摘要

背景

室性心动过速(VT)是心肌梗死(MI)后患者死亡的常见原因,即使在当前冠状动脉血运重建治疗时代亦是如此。我们报告一种通过缺血再灌注诱导慢性MI的大鼠可重复性VT模型,并使用高分辨率光学标测描述其电生理特征。

方法

通过结扎左前降支冠状动脉(25分钟)然后再灌注,在20只大鼠中诱发MI。5周后使用Langendorff灌注标本进行电生理研究和光学标测,并与正常大鼠进行比较。

结果

MI边缘区的传导速度降至远离梗死的正常区域的53%(0.37±0.16米/秒对0.70±0.09米/秒,P<0.0001)。MI大鼠中VT诱发性发生率显著高于正常对照大鼠(70%对0%,P=0.00002)。在83%的MI大鼠中通过光学标测确定了涉及梗死区域的VT环路。此外,在梗死边缘区观察到固定和功能性传导阻滞。

结论

这种缺血再灌注MI大鼠模型是一种可靠的VT模型,模拟了临床血运重建治疗。该模型中的高分辨率光学标测有助于研究VT机制并评估治疗效果。

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