目的:法洛四联症(TOF)修复患者的近端肺动脉(PAs)血流高度紊乱,并伴有明显的反流。本研究的目的是评估4D-FlowMRI得出的粘性能量损失[公式:见正文])-由于非有效的流动传播,并将该参数与TOF修复患者的标准右心室(RV)大小和功能标志物相关联。
方法:对35例TOF患者和14例对照者进行了全面的4D-FlowMRI评估,以进行定性血流分析并计算[公式:见正文]。采样[公式:见正文]指数与MRI衍生的RV大小和功能指数相关。
结果:所有TOF患者均表现为异常,PA中的超生理螺旋/旋涡地层。TOF患者收缩压峰值显着增加[公式:参见正文](8.0vs0.5mW,p<0.001),时间平均[公式:见正文](2.5与0.2mW,p<0.001),和收缩压峰值[公式:见正文]索引为每搏输出量(0.082vs.0.012mW/mL,p<0.001)。[公式:见正文]以每搏输出量与右心室舒张末期容积相关(R=0.68,p<0.001),收缩末期容积(R=0.62,p<0.001),射血分数(R=-0.45,p=0.002),和心脏指数(R=0.45,p=0.002)。关于输入RV机械功率的由于[公式:见正文]的平均估计能量损耗为4.7%。
结论:这项研究表明,修复TOF的患者通过PA的流量传导高度异常,导致大量的粘性能量损失。这种显著的流动介导的能量损失与RV体积和功能有关,并且可能代表每个心动周期产生的机械动力的相当大的损失。需要进一步的研究来评估异常的流量传导是否会增加RV的后负荷和重塑。
结论:•TOF患者通过近端肺动脉的异常血流模式与过多的粘性能量损失有关。•低效的流量传导与RV扩张和功能降低有关,并可能有助于RV适应性重塑。
OBJECTIVE: Flow through the proximal pulmonary arteries (PAs) of patients with repaired Tetralogy of Fallot (TOF) is known to be highly disordered and associated with significant regurgitation. The purpose of this study was to evaluate 4D-Flow MRI-derived viscous energy loss [Formula: see text])-as a result of non-efficient flow propagation, and relate this parameter to standard right ventricular (RV) size and function markers in patients with repaired TOF.
METHODS: Thirty-five patients with TOF and 14 controls underwent comprehensive 4D-Flow MRI evaluation for qualitative flow analysis and to calculate [Formula: see text] in the main and right pulmonary arteries. Sampled [Formula: see text] indices were correlated with the MRI-derived RV size and functional indices.
RESULTS: All patients with TOF exhibited abnormal, supra-physiologic helical/vortical formations in the PAs. Patients with TOF had significantly increased peak systolic [Formula: see text] (8.0 vs 0.5 mW, p < 0.001), time-averaged [Formula: see text] (2.5 vs. 0.2 mW, p < 0.001), and peak systolic [Formula: see text] indexed to stroke volume (0.082 vs. 0.012 mW/mL, p < 0.001). [Formula: see text] indexed to stroke volume correlated with the RV end-diastolic volume (R = 0.68, p < 0.001), end-systolic volume (R = 0.62, p < 0.001), ejection fraction (R = -0.45, p = 0.002), and cardiac index (R = 0.45, p = 0.002). The mean estimated energy loss due to [Formula: see text] with regard to input RV mechanical power was 4.7%.
CONCLUSIONS: This study demonstrates that patients with repaired TOF have highly abnormal flow conduction through the PAs which result into extensive viscous energy loss. This significant flow-mediated energy loss is associated with the RV volume and function, and might represent considerable loss of mechanical power generated by each cardiac cycle. Future studies are required to assess whether the abnormal flow conduction adds to the RV afterload and remodeling.
CONCLUSIONS: • Abnormal flow patterns through proximal pulmonary arteries in patients with TOF are associated with excessive viscous energy loss. • Inefficient flow conduction is associated with the RV dilation and reduced function and might contribute to the RV adaptive remodeling.