Verheule Sander, Wilson Emily, Everett Thomas, Shanbhag Sujata, Golden Catherine, Olgin Jeffrey
Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Ind, USA.
Circulation. 2003 May 27;107(20):2615-22. doi: 10.1161/01.CIR.0000066915.15187.51. Epub 2003 May 5.
Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR).
Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09+/-0.45 cm, compared with 3.25+/-0.28 at baseline (P<0.01), corresponding to a volume of 205+/-61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF (>1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs (P<0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally.
Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.
临床上，慢性心房扩张与心房颤动（AF）发病率增加相关，但潜在机制尚不清楚。我们在二尖瓣反流（MR）所致慢性心房扩张的犬模型中研究了心房电生理和组织结构。
研究了13只对照犬和19只MR犬（二尖瓣部分撕脱术后1个月）。对MR组犬进行超声心动图和动态心电图监测。在开胸随访实验中，将电极阵列置于心房以研究传导模式、有效不应期和AF的诱发性。评估心房组织样本的组织结构和超微结构改变。随访时，MR犬左心房长度为4.09±0.45 cm，而基线时为3.25±0.28 cm（P<0.01），对应于基线体积的205±61%。随访时，对照犬和MR犬之间在心房传导模式和传导速度方面未发现差异。整个左、右心房的有效不应期均均匀增加。19只MR犬中有10只可诱发持续性AF（>1小时），而13只对照犬均未诱发（P<0.01）。在扩张的MR左心房中，间质纤维化和慢性炎症增加的区域在超微结构上伴有糖原增加。
在无明显心力衰竭的情况下，慢性心房扩张导致AF易感性增加，这并非基于波长缩短。
