Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Melchor Fernández Almagro, 3, 28029, Madrid, Spain.
Department of Cardiology, Heart Failure and Inherited Cardiac Diseases Unit, Puerta de Hierro University Hospital, Madrid, Spain.
J Cardiovasc Transl Res. 2017 Dec;10(5-6):499-501. doi: 10.1007/s12265-017-9765-x. Epub 2017 Aug 15.
Heart failure (HF) is a major cause of death and hospitalization worldwide. Despite advances in reducing mortality, prognosis remains poor and prevalence has reached epidemic proportions. The limitations of available preclinical models represent a major hurdle in the development of new therapies. Myocardial infarction (MI) is a main cause of HF in humans, and mouse models of MI are often used to study HF mechanisms and experimental treatments. We investigated whether MI in mice constitutes an appropriate model of HF. Permanent ligation of the left coronary artery induced severe and persistent systolic dysfunction and ventricular dilatation. Mouse follow-up for 10 months showed no significant evidence of lung congestion or other pulmonary defects associated with HF. No difference was observed in the capacity of infarcted mice to exercise compared to control animals. These results indicate that severe cardiac dysfunction in mice is not sufficient to demonstrate the presence of HF.
心力衰竭（HF）是全球范围内主要的死亡和住院原因。尽管在降低死亡率方面取得了进展，但预后仍然不佳，患病率已达到流行程度。现有临床前模型的局限性是新疗法发展的主要障碍。心肌梗死（MI）是人类 HF 的主要原因，MI 的小鼠模型常用于研究 HF 机制和实验治疗。我们研究了 MI 在小鼠中是否构成 HF 的合适模型。左冠状动脉的永久性结扎导致严重且持续的收缩功能障碍和心室扩张。对小鼠进行 10 个月的随访发现，没有 HF 相关的肺部充血或其他肺部缺陷的明显证据。与对照动物相比，梗死小鼠的运动能力没有差异。这些结果表明，小鼠严重的心脏功能障碍不足以证明 HF 的存在。
