Department of Pediatric Cardiovascular Surgery, National Cerebral and Cadiovascular Center, Suita, Japan.
Department of Radiology, National Cerebral and Cardiovascular Center, Suita, Japan.
Eur J Cardiothorac Surg. 2021 Sep 11;60(3):526-533. doi: 10.1093/ejcts/ezab112.
The present study was conducted to investigate the decrease in left ventricular stroke volume index (LVSVI) that is caused by pulmonary regurgitation-induced right heart dysfunction and its clinical implications before and after pulmonary valve replacement (PVR).
Between January 2010 and December 2019, 30 adults who underwent surgical PVR for chronic pulmonary regurgitation with right ventricular dilation late after tetralogy of Fallot (TOF) repair were included. All patients were evaluated using cardiac magnetic resonance before PVR. The median interval from TOF repair to PVR was 29 [25th, 75th percentile: 25, 37] years. The median pulmonary regurgitation fraction and right ventricular end-diastolic volume index were 56 [48, 66] % and 203 [187, 239] ml/m2. Twenty-three patients (76.7%) were re-evaluated 1 year after PVR.
Before PVR, the median LVSVI was 40 [35, 46] ml/beat/m2. A lower LVSVI was associated with a longer interval from TOF repair to PVR (r = -0.40, P = 0.029) and a lower right ventricular ejection fraction (r = 0.52, P = 0.004). A lower LVSVI was not associated with a higher right ventricular end-diastolic volume index. LVSVI remained unchanged after PVR. The patients were subdivided into Normal-stroke volume index (SVI) and Subnormal-SVI groups using the preoperative LVSVI cut-off value of 35 mL/beat/m2. Compared with the Normal-SVI group, the Subnormal-SVI group had a higher incidence of ablation therapy before PVR (4.7 vs 2.3 patient-years, P = 0.044). After PVR, LVSVI in the Subnormal-SVI group was still lower (40 [34, 42] vs 44 [42, 47] ml/beat/m2, P = 0.038) despite the right ventricular end-diastolic volume index normalization. There was no difference in the clinical event incidence between the 2 groups during the follow-up period. Brain natriuretic peptide level in the Subnormal-SVI group was higher within 3 years after PVR (P = 0.046).
Reduced left ventricular stroke volume did not fully recover after PVR. PVR for patients with repaired TOF should be performed before the left ventricular stroke volume begins to decrease.
本研究旨在探讨肺动脉瓣置换术(PVR)前、后因肺动脉瓣反流引起的右心功能障碍导致的左心室每搏输出量指数(LVSVI)降低及其临床意义。
2010 年 1 月至 2019 年 12 月,30 例因法洛四联症(TOF)修复后右心室扩张导致慢性肺动脉瓣反流而接受 PVR 的成人患者纳入研究。所有患者均在 PVR 前接受心脏磁共振检查。TOF 修复至 PVR 的中位时间间隔为 29 年[25 百分位数,75 百分位数:25,37]。肺动脉瓣反流分数和右心室舒张末期容积指数中位数分别为 56%[48%,66%]和 203 ml/m2[187 ml/m2,239 ml/m2]。23 例(76.7%)患者在 PVR 后 1 年接受了重新评估。
在 PVR 前,LVSVI 的中位数为 40 ml/beat/m2[35 ml/beat/m2,46 ml/beat/m2]。较低的 LVSVI 与 TOF 修复至 PVR 的时间间隔较长(r=-0.40,P=0.029)和右心室射血分数较低(r=0.52,P=0.004)相关。较低的 LVSVI 与较高的右心室舒张末期容积指数无关。PVR 后 LVSVI 保持不变。使用术前 LVSVI 截断值 35 ml/beat/m2 将患者分为正常 LVSVI 组和亚正常 LVSVI 组。与正常 LVSVI 组相比,亚正常 LVSVI 组在 PVR 前有更高的消融治疗发生率(4.7 患者年 vs 2.3 患者年,P=0.044)。尽管右心室舒张末期容积指数恢复正常,但在 PVR 后,亚正常 LVSVI 组的 LVSVI 仍然较低(40 ml/beat/m2[34 ml/beat/m2,42 ml/beat/m2] vs 44 ml/beat/m2[42 ml/beat/m2,47 ml/beat/m2],P=0.038)。在随访期间,两组的临床事件发生率无差异。PVR 后 3 年内,亚正常 LVSVI 组的脑钠肽水平更高(P=0.046)。
PVR 后左心室每搏输出量未完全恢复。对于接受过修复的 TOF 患者,应在左心室每搏输出量开始下降之前进行 PVR。