BACKGROUND There are currently no therapies that can improve prognosis in cases of heart failure (HF) with preserved ejection fraction (EF). We hypothesized that there is a point of no return after which no response to treatment is noted and that for the prevention of hypertensive HF this point may be determined by left ventricle (LV) strain, in the prevention of hypertensive HF. Here an angiotensin-converting enzyme inhibitor (ACE-I) was initiated based on myocardial strain imaging and its effects were determined in an animal model. METHODS Thirty-two male Dahl salt-sensitive rats, age 6 weeks, were divided into six experimental groups and compared with low-salt (n = 8) and high-salt control groups (n = 8). In the early treatment group, ACE-I was administered from the age of 6 weeks (n = 4); in the longitudinal strain (LS) group, at 10-12 weeks when LS impairment was >-21% (n = 4); in the circumferential strain (CS) group, at 16-18 weeks when CS impairment was >-18% (n = 4); and in the EF group, at 20 weeks when EF was <55% (n = 4). Subsequently, all rats were sacrificed at 23 weeks age, the LV and lung weight were measured, and pathologic analyses were performed. RESULTS At 23 weeks of age, the lung and LV weights increased in the high-salt control, EF, and CS groups, whereas the lung and LV weights in the LS and early groups were similar to those in the low-salt control group. The percentage of area of subendocardial fibrosis was >6% in the high-salt control, EF, and CS groups and <3% in the LS, early, and low-salt groups. Serial echocardiography demonstrated LS improvement in the LS group; however, the CS and EF groups showed no differences. CONCLUSIONS Heart failure-related lung congestion was prevented when ACE-I was administered soon after LS impairment, accompanied by suppression of cardiac hypertrophy and fibrosis, thereby suggesting that the point of no return of myocardial remodeling due to hypertension was present after LS but before CS impairment.

中文翻译：

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左心室纵向应变是高血压心力衰竭治疗中不归位的标志。

背景技术当前，在保留射血分数（EF）的心力衰竭（HF）的情况下，尚无能够改善预后的疗法。我们假设有一个没有返回的点，之后没有注意到对治疗的反应，并且对于预防高血压性HF，这一点可以通过预防高血压性HF的左心室（LV）应变来确定。在此，基于心肌应变成像启动了血管紧张素转换酶抑制剂（ACE-1），并在动物模型中确定了其作用。方法将32只6周大的Dahl雄性盐敏感性雄性大鼠分为6个实验组，并与低盐（n = 8）和高盐对照组（n = 8）进行比较。在早期治疗组中，ACE-I从6周龄开始给药（n = 4）；在纵向应变（LS）组中，在10-12周时，当LS损伤> -21％（n = 4）时；在圆周应变（CS）组中，在16-18周时，CS损伤> -18％（n = 4）；而在EF组中，当EF低于55％（n = 4）时为20周。随后，在23周龄处死所有大鼠，测量LV和肺重量，并进行病理分析。结果在23周龄时，高盐对照组，EF和CS组的肺和LV重量增加，而LS组和早期组的肺和LV重量与低盐对照组相似。在高盐对照组，EF和CS组中，心内膜下纤维化的面积百分比> 6％，而在LS，早期和低盐组中，<3％。连续超声心动图显示LS组的LS改善。但是，CS和EF组没有差异。