Background:Individuals with left ventricular (LV) hypertrophy and elevated cardiac biomarkers in middle age are at increased risk for the development of heart failure with preserved ejection fraction. Prolonged exercise training reverses the LV stiffening associated with healthy but sedentary aging; however, whether it can also normalize LV myocardial stiffness in patients at high risk for heart failure with preserved ejection fraction is unknown. In a prospective, randomized controlled trial, we hypothesized that 1-year prolonged exercise training would reduce LV myocardial stiffness in patients with LV hypertrophy.Methods:Forty-six patients with LV hypertrophy (LV septum >11 mm) and elevated cardiac biomarkers (N-terminal pro-B-type natriuretic peptide [>40 pg/mL] or high-sensitivity troponin T [>0.6 pg/mL]) were randomly assigned to either 1 year of high-intensity exercise training (n=30) or attention control (n=16). Right-heart catheterization and 3-dimensional echocardiography were performed while preload was manipulated using both lower body negative pressure and rapid saline infusion to define the LV end-diastolic pressure-volume relationship. A constant representing LV myocardial stiffness was calculated from the following: P=S×[Exp {a (V–V₀)}–1], where “P” is transmural pressure (pulmonary capillary wedge pressure – right atrial pressure), “S” is the pressure asymptote of the curve, “V” is the LV end-diastolic volume index, “V₀” is equilibrium volume, and “a” is the constant that characterizes LV myocardial stiffness.Results:Thirty-one participants (exercise group [n=20]: 54±6 years, 65% male; and controls (n=11): 51±6 years, 55% male) completed the study. One year of exercise training increased max by 21% (baseline 26.0±5.3 to 1 year later 31.3±5.8 mL·min^–1·kg^–1, P<0.0001, interaction P=0.0004), whereas there was no significant change in max in controls (baseline 24.6±3.4 to 1 year later 24.2±4.1 mL·min^–1·kg^–1, P=0.986). LV myocardial stiffness was reduced (right and downward shift in the end-diastolic pressure-volume relationship; LV myocardial stiffness: baseline 0.062±0.020 to 1 year later 0.031±0.009), whereas there was no significant change in controls (baseline 0.061±0.033 to 1 year later 0.066±0.031, interaction P=0.001).Conclusions:In patients with LV hypertrophy and elevated cardiac biomarkers (stage B heart failure with preserved ejection fraction), 1 year of exercise training reduced LV myocardial stiffness. Thus, exercise training may provide protection against the future risk of heart failure with preserved ejection fraction in such patients.Registration:URL: https://www.clinicaltrials.gov; Unique identifier: NCT03476785.

中文翻译：

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为期一年的承诺运动训练可逆转 B 期心力衰竭患者的左心室心肌异常僵硬并保留射血分数

背景：中年左心室 (LV) 肥大和心脏生物标志物升高的个体发生射血分数保留的心力衰竭的风险增加。长时间的运动训练可以逆转与健康但久坐老化相关的 LV 僵硬；然而，它是否还能使射血分数保留的心力衰竭高风险患者的左室心肌僵硬度正常化尚不清楚。在一项前瞻性、随机对照试验中，我们假设 1 年的长期运动训练会降低 LV 肥大患者的 LV 心肌僵硬度。方法：46 名 LV 肥大（LV 隔膜 >11 mm）和升高的心脏生物标志物（N -末端B型利钠肽前体[>40 pg/mL]或高敏肌钙蛋白T[>0。6 pg/mL]）被随机分配到 1 年的高强度运动训练（n=30）或注意力控制（n=16）。进行右心导管插入术和 3 维超声心动图检查，同时使用下半身负压和快速盐水输注来控制 LV 舒张末期压力-容积关系。代表 LV 心肌硬度的常数由以下公式计算得出：P=S×[Exp {a (V–V₀ )}–1]，其中“P”是透壁压（肺毛细血管楔压-右心房压），“S”是曲线的压力渐近线，“V”是左室舒张末期容积指数，“V” ₀ ”是平衡体积，“a”是表征 LV 心肌僵硬度的常数。结果：31 名参与者（运动组 [n=20]：54±6 岁，65% 男性；对照组（n=11） ：51±6 岁，55% 男性）完成了研究。一年的运动训练最大增加了 21%（基线 26.0±5.3 至 1 年后 31.3±5.8 mL·min ^–1 ·kg ^–1，P <0.0001，交互作用P =0.0004），而最大没有显着变化对照组（基线 24.6±3.4 至 1 年后 24.2±4.1 mL·min ^–1·kg ^–1 , P =0.986)。LV 心肌硬度降低（舒张末期压力-容积关系向右和向下移动；LV 心肌硬度：基线 0.062±0.020 至 1 年后 0.031±0.009），而对照组没有显着变化（基线 0.061±0.033至 1 年后 0.066±0.031，交互作用P =0.001)。结论：在左室肥大和心脏生物标志物升高（射血分数保留的 B 期心力衰竭）患者中，1 年的运动训练降低了左室心肌僵硬度。因此，运动训练可以保护此类患者在射血分数保持不变的情况下未来发生心力衰竭的风险。注册：URL：https://www.clinicaltrials.gov；唯一标识符：NCT03476785。