Westerman G R, Lang P, Castaneda A R, Norwood W I
Circulation. 1982 Aug;66(2 Pt 2):I197-202.
From August 1974 through April 1981, 23 patients, ages 5 months to 40 years (median 11 years) with corrected transposition of the great arteries (C-TGA), underwent repair of associated intracardiac defects: 20 for ventricular septal defect (VSD), 19 for pulmonary outflow tract obstruction, and five for anatomic tricuspid valve regurgitation. Segmental anatomy was [S,L,L] in 18 or [I,D,D] in 5. Pulmonary outflow tract obstruction was resected in 10 and bypassed with a left ventricle-to-main pulmonary artery conduit in nine patients. Hospital mortality was 9% (two of 23). One patient died from arrhythmia and one from sepsis and arrhythmia. The late mortality rate was 14% (three patients). Two patients died from severe pulmonary vascular obstructive disease (5 months and 2 years postoperatively) and one from arrhythmia (2 months postoperatively). Fourteen have undergone cardiac catheterization 3 days to 4 years (mean 12 months) postoperatively. Three had a small residual VDS (Qp/Qs less than 1.5). Five had residual pulmonary outflow tract obstruction (peak systolic ejection gradient 30-130 mm Hg) after resection or pulmonary valvotomy. One patient had reresection and four had placement of a secondary left ventricular-pulmonary artery conduit. Anatomic tricuspid valve regurgitation became severe in three patients after VSD closure, two of whom required valve replacement; the other died of coexisting pulmonary vascular obstructive disease. Five with [S,L,L] segmental anatomy had complete atrioventricular block preoperatively and six developed complete atrioventricular block at surgery. Eleven of 18 patients with [S,L,L] anatomy had atrioventricular spontaneous or iatrogenic complete block; none of the five patients with [I,D,D] anatomy had atrioventricular block. Pulmonary outflow tract obstruction in [S,L,L] segmental anatomy required conduit interposition in 12 of 14 of our patients to significantly decompress the ventricle. Postoperative development or exacerbation of anatomic tricuspid valve regurgitation occurs in TGA [S,L,L] and may be causally related to surgical complete atrioventricular block.
从1974年8月至1981年4月，23例年龄在5个月至40岁（中位年龄11岁）的矫正型大动脉转位（C-TGA）患者接受了相关心内缺损的修复：20例为室间隔缺损（VSD），19例为肺动脉流出道梗阻，5例为解剖性三尖瓣反流。节段性解剖结构为[S，L，L]的有18例，[I，D，D]的有5例。10例患者切除了肺动脉流出道梗阻，9例患者通过左心室至主肺动脉管道进行了旁路手术。住院死亡率为9%（23例中有2例）。1例患者死于心律失常，1例死于败血症和心律失常。晚期死亡率为14%（3例患者）。2例患者死于严重的肺血管阻塞性疾病（术后5个月和2年），1例死于心律失常（术后2个月）。14例患者在术后3天至4年（平均12个月）接受了心导管检查。3例有小的残余VDS（肺循环血流量/体循环血流量小于1.5）。5例在切除或肺动脉瓣切开术后有残余肺动脉流出道梗阻（收缩期射血峰值梯度为30 - 130 mmHg）。1例患者再次切除，4例放置了二级左心室 - 肺动脉管道。3例患者在VSD闭合后解剖性三尖瓣反流变得严重，其中2例需要瓣膜置换；另1例死于并存的肺血管阻塞性疾病。5例[S，L，L]节段性解剖结构的患者术前有完全性房室传导阻滞，6例在手术时发生完全性房室传导阻滞。18例[S，L，L]解剖结构的患者中有11例有房室自发性或医源性完全性传导阻滞；5例[I，D，D]解剖结构的患者中无一例有房室传导阻滞。在我们的14例[S，L，L]节段性解剖结构的患者中，12例肺动脉流出道梗阻需要插入管道以显著减轻心室压力。解剖性三尖瓣反流在TGA [S，L，L]中术后会发生或加重，可能与手术导致的完全性房室传导阻滞有因果关系。
