BACKGROUND We hypothesize that dobutamine-induced stress impacts intracardiac hemodynamic parameters and that this may be linked to decreased exercise capacity in Fontan patients. Therefore, the purpose of this study was to assess the effect of pharmacologic stress on intraventricular kinetic energy (KE), viscous energy loss (EL) and vorticity from four-dimensional (4D) Flow cardiovascular magnetic resonance (CMR) imaging in Fontan patients and to study the association between stress response and exercise capacity. METHODS Ten Fontan patients underwent whole-heart 4D flow CMR before and during 7.5 μg/kg/min dobutamine infusion and cardiopulmonary exercise testing (CPET) on the same day. Average ventricular KE, EL and vorticity were computed over systole, diastole and the total cardiac cycle (vorticity_volavg cycle, KEavg cycle, ELavg cycle). The relation to maximum oxygen uptake (VO2 max) from CPET was tested by Pearson's correlation or Spearman's rank correlation in case of non-normality of the data. RESULTS Dobutamine stress caused a significant 88 ± 52% increase in KE (KEavg cycle: 1.8 ± 0.5 vs 3.3 ± 0.9 mJ, P < 0.001), a significant 108 ± 49% increase in EL (ELavg cycle: 0.9 ± 0.4 vs 1.9 ± 0.9 mW, P < 0.001) and a significant 27 ± 19% increase in vorticity (vorticity_volavg cycle: 3441 ± 899 vs 4394 ± 1322 mL/s, P = 0.002). All rest-stress differences (%) were negatively correlated to VO2 max (KEavg cycle: r = - 0.83, P = 0.003; ELavg cycle: r = - 0.80, P = 0.006; vorticity_volavg cycle: r = - 0.64, P = 0.047). CONCLUSIONS 4D flow CMR-derived intraventricular kinetic energy, viscous energy loss and vorticity in Fontan patients increase during pharmacologic stress and show a negative correlation with exercise capacity measured by VO2 max.

中文翻译：

---

应力会增加源自心内4D流心血管磁共振的能量和涡度，并且与Fontan患者的VO2max有关。

背景我们假设多巴酚丁胺引起的压力会影响心脏内的血流动力学参数，并且这可能与Fontan患者运动能力下降有关。因此，本研究的目的是评估来自Fontan患者的三维（4D）流式心血管磁共振（CMR）成像对药理应激对脑室内动能（KE），粘性能量损失（EL）和涡度的影响。研究压力反应与运动能力之间的关系。方法10例Fontan患者在7.5μg/ kg / min多巴酚丁胺输注和心肺运动测试（CPET）之前和期间进行全心4D流CMR。计算平均心室KE，EL和涡度，计算收缩期，舒张期和总心动周期（vorticity_volavg周期，KEavg周期，ELavg周期）。在数据不正常的情况下，通过皮尔逊相关性或斯皮尔曼等级相关性来检验与CPET的最大摄氧量（VO2 max）的关系。结果多巴酚丁胺应力导致KE显着增加88±52％（KEavg周期：1.8±0.5 vs 3.3±0.9 mJ，P <0.001），EL显着增加108±49％（ELavg周期：0.9±0.4 vs 1.9± 0.9 mW，P <0.001），涡度显着提高27±19％（vorticity_volavg周期：3441±899 vs 4394±1322 mL / s，P = 0.002）。所有静息差异（％）与VO2 max负相关（KEavg周期：r =-0.83，P = 0.003; ELavg周期：r =-0.80，P = 0.006;涡度_volavg周期：r =-0.64，P = 0.047 ）。结论4D流CMR衍生的脑室内动能，