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Modification of a Volume-Overload Heart Failure Model to Track Myocardial Remodeling and Device-Related Reverse Remodeling

机译:修改超负荷心力衰竭模型以追踪心肌重塑和与设备相关的逆向重塑

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摘要

Purpose. To provide an ovine model of ventricular remodeling and reverse remodeling by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). Methods. We induced volume-overload heart failure in 2 sheep; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. Results. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.
机译:目的。通过创建充血性心力衰竭(CHF),然后通过植入左心室辅助设备(LVAD)来提供绵羊的心室重塑和逆向重塑模型。方法。我们在两只绵羊中诱发了超负荷的心力衰竭。 20周后,我们植入了LVAD,并在11周后评估了恢复情况。我们检查了组织学和血液动力学数据以及CHF细胞标志物水平的变化。结果。 CHF诱导后,我们发现左室舒张末期压力,左室收缩和舒张期尺寸,壁厚,左心房直径,心房利钠蛋白(ANP)和内皮素1(ET-1)水平升高。 β-肾上腺素能受体(BAR)和肌营养不良蛋白的表达明显降低。活检证实左室重塑。 LVAD支持后,LV收缩和舒张尺寸,壁厚和质量以及ANP和ET-1水平降低。组织病理学和血液动力学标志改善,BAR和肌营养不良蛋白表达正常。结论。我们描述了一个成功的绵羊心室和反向重塑模型。

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