Development of new comprehensive heart failure treatment that takes into account the underlying disease and the stage of the heart failure

我们在犬心肌梗死模型和起搏诱导的失代偿性心力衰竭中检测AMPK激活是否可以调节心脏重塑和抑制心力衰竭的进展，这被认为与人类扩张型心肌病相似，可以叠加到人类心力衰竭的转化研究中。在心肌梗死或起搏性心力衰竭发生6周后，使用和不使用AICAR （AMPK激活剂）的两组之间的血压和心率均无差异。与未治疗组相比，AICAR治疗组左室射血分数升高，平均肺动脉压和肺毛细血管楔压降低。这些影响在两种模型中都可以观察到，甚至在心力衰竭发作后也是如此。因此，我们得出结论，AMPK激活是慢性心力衰竭的一个重要的新治疗靶点。

We examined whether AMPK activation can modulate cardiac remodeling and inhibit the progression of heart failure in the canine myocardial infarction model and pacing induced decompensated heart failure, which is considered to be similar to human dilated cardiomyopathy and can be superimposed on translational study for human heart failure. Neither blood pressure nor heart rate differed between the groups with and without AICAR (AMPK activator) at 6 weeks after the onset of myocardial infarction or pacing-induced heart failure. Left ventricular ejection fraction increased, and mean pulmonary arterial pressure and pulmonary capillary wedge pressure decreased in the AICAR treated group compared with the untreated group. These effects were observed in both models, even after the onset of heart failure. Thus, we conclude that AMPK activation is an important novel therapeutic target in chronic heart failure.