Regional cardiac dysfunction and dyssynchrony in a murine model of afterload stress.
Regional cardiac dysfunction and dyssynchrony in a murine model of afterload stress.
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DOI：
10.1371/journal.pone.0059915
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Liao R
中科院分区：
文献类型：
--
作者：
Bauer M;Cheng S;Unno K;Lin FC;Liao R
后负荷应激的小动物模型对我们目前对高血压到心力衰竭的进展的理解做出了很大贡献。用于体内心脏功能表型的高灵敏度方法，特别是在代偿性心脏肥大的情况下，可能会增加有关心脏性能改变的新信息，即使在暴露于压力超负荷的最早阶段也可能发生这种改变。我们已经开发了一种超声心动图分析方法，基于斑点跟踪应变分析，并使用此工具快速表型心脏的变化所造成的后负荷应力在小动物模型。成年小鼠接受升主动脉缩窄，随后有和没有逆转的压力梯度。在这种代偿性肥厚性心脏重塑模型中，常规超声心动图测量在检查的早期时间点没有检测到左心室（LV）功能的变化。然而，应变分析显示，主动脉缩窄引起的基底纵向肌纤维缩短减少，并在压力梯度缓解后得到改善。此外，我们观察到压力超负荷导致LV节段性不同步，随着后负荷恢复到基线水平而减弱。在此，我们描述了使用超声心动图应变分析的心脏表型在小鼠模型的压力超负荷。这种方法提供了不同步和局部心肌功能障碍的证据，这些不同步和局部心肌功能障碍在代偿性肥大早期发生，并在主动脉收缩缓解后得到改善。重要的是，这些发现说明了一种快速，非侵入性的方法来表征早期心脏功能障碍，不能检测到的常规超声心动图，后负荷应激的效用。
Small animal models of afterload stress have contributed much to our present understanding of the progression from hypertension to heart failure. High-sensitivity methods for phenotyping cardiac function in vivo, particular in the setting of compensated cardiac hypertrophy, may add new information regarding alterations in cardiac performance that can occur even during the earliest stages of exposure to pressure overload. We have developed an echocardiographic analytical method, based on speckle-tracking-based strain analyses, and used this tool to rapidly phenotype cardiac changes resulting from afterload stress in a small animal model. Adult mice were subjected to ascending aortic constriction, with and without subsequent reversal of the pressure gradient. In this model of compensated hypertrophic cardiac remodeling, conventional echocardiographic measurements did not detect changes in left ventricular (LV) function at the early time points examined. Strain analyses, however, revealed a decrement in basal longitudinal myofiber shortening that was induced by aortic constriction and improved following relief of the pressure gradient. Furthermore, we observed that pressure overload resulted in LV segmental dyssynchrony that was attenuated with return of the afterload to baseline levels. Herein, we describe the use of echocardiographic strain analyses for cardiac phenotyping in a mouse model of pressure overload. This method provides evidence of dyssynchrony and regional myocardial dysfunction that occurs early with compensatory hypertrophy, and improves following relief of aortic constriction. Importantly, these findings illustrate the utility of a rapid, non-invasive method for characterizing early cardiac dysfunction, not detectable by conventional echocardiography, following afterload stress.