M3C-Necker, Congenital and Pediatric Cardiology, Hôpital Universitaire Necker-Enfants malades, Paris, France.
Adult Congenital Heart Disease Unit, Cardiology Department, Hôpital Européen Georges Pompidou, Centre de référence des Malformations Cardiaques Congénitales Complexes, M3C, Assistance Publique-Hôpitaux de Paris, Paris, France; INSERM U970, PARCC, Paris Descartes University, Sorbonne Paris Cité, Paris, France.
Int J Cardiol. 2020 Feb 1;300:121-126. doi: 10.1016/j.ijcard.2019.10.032. Epub 2019 Oct 21.
Children with repaired congenital heart disease (CHD) have impaired maximal aerobic capacity (VO2max). Determining the causes of their VO2max alteration remains challenging. Cardiac output measure using thoracic impedancemetry during cardiopulmonary exercise tests (CPET) can help to understand the determinants of VO2max in children with open-heart repaired CHD.
We analyzed CPET in 77 children with repaired CHD. Among them, 55 patients had residual lesions. Patients with repaired CHD were compared with 44 age-matched healthy individuals. Maximal oxygen content brought to capillaries (QO2max) and oxygen muscle diffusion capacity (DO2) were assessed using cardiac output measure, Fick principle and simplified Fick law.
In the 55 patients with residual lesion, VO2max, QO2max and DO2 were lower than those of controls (76.1 vs 86% of theoretical value, p < 0.01; 2.15 vs 2.81 L/mn, p < 0.001; 24.7 vs 28.8 ml/min/mmHg, p < 0.05). Decrease in QO2max was due to both impaired stroke volume and chronotropic insufficiency (48 vs 53 ml/m and p < 0.05; 171 vs 185/min p < 0.001). Patients without residual lesion (22/77) had normal VO2max with lower maximal heart rate compensated by higher SV (p < 0.05).
Aerobic capacity was normal in children without residual lesions after CHD repair. Patients with residual lesion have impaired VO2max due to both lower central and peripheral determinants. Measuring cardiac performance during CPET allowed a better selection of patients with altered cardiac reserve that can benefit from residual lesion treatment and find the good timing for intervention. Detection of peripheral deconditioning can lead to a rehabilitation program.
患有先天性心脏病（CHD）修复的儿童有氧能力（VO2max）受损。确定其 VO2max 改变的原因仍然具有挑战性。心肺运动测试（CPET）期间使用胸部阻抗法测量心输出量有助于了解心胸修复 CHD 患儿 VO2max 的决定因素。
我们分析了 77 例修复性 CHD 患儿的 CPET。其中 55 例患者有残余病变。将修复性 CHD 患者与 44 名年龄匹配的健康个体进行比较。使用心输出量测量、Fick 原理和简化 Fick 定律评估最大氧含量输送至毛细血管（QO2max）和氧肌肉扩散能力（DO2）。
在 55 例有残余病变的患者中，VO2max、QO2max 和 DO2 均低于对照组（76.1%对理论值的 86%，p<0.01；2.15 对 2.81 L/min，p<0.001；24.7 对 28.8 ml/min/mmHg，p<0.05）。QO2max 的降低归因于射血分数和变时性不足（48 对 53 ml/m，p<0.05；171 对 185/min，p<0.001）。无残余病变的患者（22/77）VO2max 正常，最大心率较低，但通过更高的 SV 进行代偿（p<0.05）。
CHD 修复后无残余病变的儿童有氧能力正常。有残余病变的患者 VO2max 受损，原因是中心和外周决定因素均较低。在 CPET 期间测量心脏功能可以更好地选择心脏储备功能改变的患者，从而受益于残余病变的治疗并找到干预的最佳时机。检测外周功能不全可导致康复计划。
