One-Year Committed Exercise Training Reverses Abnormal Left Ventricular Myocardial Stiffness in Patients With Stage B Heart Failure With Preserved Ejection Fraction.
One-Year Committed Exercise Training Reverses Abnormal Left Ventricular Myocardial Stiffness in Patients With Stage B Heart Failure With Preserved Ejection Fraction.
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DOI：
10.1161/circulationaha.121.054117
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发表时间：
2021-09-21
期刊：
影响因子：
37.8
通讯作者：
Levine BD
中科院分区：
文献类型：
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作者：
Hieda M;Sarma S;Hearon CM Jr;MacNamara JP;Dias KA;Samels M;Palmer D;Livingston S;Morris M;Levine BD
中年左心室肥大（LVH）和心脏生物标志物升高的个体发生射血分数保留性心力衰竭（HFpEF）的风险增加。长期运动训练可逆转与健康但久坐不动的衰老相关的左心室僵硬;然而，它是否也能使HFpEF高危患者的左心室心肌僵硬正常化尚不清楚。在一项前瞻性随机对照试验中，我们假设1年的长期运动训练可以降低LVH患者的左室心肌硬度。46例LVH（左室间隔>1.1 mm）和心脏生物标志物升高[NT-proBNP（>40 pg/ml）或hsTnT（> 0.6 pg/ml）]的患者被随机分配到1年高强度运动训练组（N=30）或注意力控制组（N=16）。右心导管和三维超声心动图进行，同时使用下体负压和快速盐水输注来操纵前负荷，以定义LV舒张末期压力-容积关系（EDPVR）。代表LV心肌硬度的常数由下式计算：P = S * [Exp { a（V-V0）} - 1]，其中P是跨壁压[肺毛细血管楔压-右心房压]，S是曲线的压力渐近线，V是LVEDV指数，V0是平衡容积，“a”是表征LV心肌硬度的常数。31名参与者[运动组（N=20）; 54±6岁; 65%男性和对照组（N=11）：51±6岁，55%男性]完成了研究。一年的运动训练使V ~ O2 max增加了21%（训练前26.0±5.3 ml/min/kg，训练后31.3±5.8 ml/min/kg，P<0.0001，交互作用P=0.0004），而对照组的V ~ O2 max没有显著变化（训练前24.6±3.4 ml/min/kg，训练后24.2±4.1 ml/min/kg，P=0.986）。左心室心肌硬度降低（EDPVR右移和下移;左心室心肌硬度从术前0.062±0.020变为术后0.031±0.009），而对照组无显著变化（术前0.061±0.033变为术后0.066±0.031，相互作用P=0.001）。在LVH和心脏生物标志物升高（B期HFpEF）的患者中，1年的运动训练降低了LV心肌硬度。因此，运动训练可以保护这些患者免受HFpEF的未来风险。 https://clinicaltrials.gov/ct2/show/NCT03476785
Individuals with left ventricular hypertrophy (LVH) and elevated cardiac biomarkers in middle-age are at increased risk for the development of heart failure with preserved ejection fraction (HFpEF). 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 HFpEF is unknown. In a prospective, randomized-controlled trial, we hypothesized that 1-year prolonged exercise training would reduce LV myocardial stiffness in patients with LVH. Forty-six patients with LVH (LV septum >1.1 mm) and elevated cardiac biomarkers [NT-proBNP (>40 pg/ml) or hsTnT (>0.6pg/ml)] were randomly assigned to either 1 year of high-intensity exercise training (N=30) or attention control (N=16). Right-heart catheterization and 3D-echocardiography were performed while preload was manipulated using both lower body negative pressure and rapid saline infusion to the define LV end-diastolic pressure-volume relationship (EDPVR). A constant representing LV myocardial stiffness was calculated from: 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 LVEDV index, V0 is equilibrium volume, and “a” is the constant that characterizes LV myocardial stiffness. 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 V̇O2max by 21% (pre 26.0±5.3 to post 31.3±5.8 ml/min/kg, P<0.0001, interaction P=0.0004), whereas there was no significant change in V̇O2 max in controls (pre 24.6±3.4 to post 24.2±4.1 ml/min/kg, P=0.986). LV myocardial stiffness was reduced (right and downward shift in the EDPVR; pre LV myocardial stiffness 0.062±0.020 to post 0.031±0.009), whereas there was no significant change in controls (pre 0.061±0.033 to post 0.066±0.031, interaction P=0.001). In patients with LVH and elevated cardiac biomarkers (stage-B HFpEF), 1-year of exercise training reduced LV myocardial stiffness. Thus, exercise training may provide protection against the future risk of HFpEF in such patients. https://clinicaltrials.gov/ct2/show/NCT03476785