主动脉缩窄或主动脉弓中断合并心内畸形一期修复

目的 探讨采用经胸骨正中切口一期修复主动脉缩窄(CoA)或主动脉弓中断(IAA)合并心内畸形的治疗效果.方法 2002年7月至2009年6月,经胸骨正中切口行降主动脉远端和主动脉弓下缘端侧吻合术一期修复CoA或IAA合并心内畸形病儿43例,其中CoA 34例,IAA 9例(A型6例、B型3例),合并心内畸形包括室间隔缺损42例、动脉导管未闭34例、房间隔缺损12例、主动脉瓣下隔膜狭窄5例、二尖瓣关闭不全2例,右心室双出口1例.结果 手术死亡1例,为术后肺动脉高压和严重低心排血量综合征者.术后并发症包括严重低心排血量综合征3例,低氧血症6例,肺部炎症11例,肺不张14例,声音嘶哑19例,室上性心动过速23例.8例失访.34例随访3个月～5年,生活质量明显改善,心脏超声心动图和CT检查显示吻合口无明显再缩窄发生.结论 经胸骨正中切口,采用主动脉远端和主动脉弓下缘端侧吻合技术一期修复CoA或IAA合并心内畸形的手术早、中期效果良好,能明显减少术后再狭窄.     

降主动脉-升主动脉吻合术矫治婴儿期主动脉缩窄合并心内畸形15例

目的探讨降主动脉-升主动脉吻合术治疗婴儿期主动脉缩窄合并主动脉弓发育不良及心内畸形的疗效。方法选取2011-05—2015-05间治疗的主动脉缩窄合并主动脉弓发育不良、心内畸形的患儿15例。患儿均采用胸骨正中切口、开胸后先游离出主动脉弓、头臂干、动脉导管、弓降部等血管。建立体外循环、选择性脑灌注下行降主动脉-升主动脉端侧吻合术,恢复全身灌注后完成心内畸形的矫治。体外循环时间86~132 min,主动脉阻断时间51~94 min。结果术后早期死亡2例,低心排出量综合征6例,室上性心动过速6例,肺炎7例。13例患儿随访2个月~3 a,无死亡及再次主动脉狭窄。结论降主动脉-升主动脉吻合术治疗婴儿期主动脉缩窄合并主动脉弓发育不良及心内畸形的临床效果满意。     

主动脉缩窄合并心内畸形的一期手术治疗

１９９３年６月至１９９４年８月为５例主动脉缩窄合并先天性心内畸形病儿施行了一期手术治疗。男４例，女１例，年龄１．５～１３岁，体重７．５～４５ｋｇ。除主动脉缩窄外，合并的心内畸形有室间隔缺损、主动脉瓣及瓣下狭窄、主动脉瓣关闭不全等。手术采用左后外侧第４肋间切口，矫治主动脉缩窄后，同期行胸骨正中切口体外循环下心内畸形矫治。本组无手术死亡和并发症，取得了满意的治疗效果。作者认为，对主动脉缩窄合并心内畸形施行一期手术矫治是完全可行的。     

一期手术矫治主动脉弓缩窄合并心内畸形

目的：探讨主动脉弓缩窄合并心内畸形病人的一期手术矫治方法及治疗效果。方法：自１９８９年１２月至１９９８年２月,运用一期手术方法为１０例主动脉弓缩窄合并心内畸形病人进行外科矫治。合并的心内畸形有室间隔缺损７例,二尖瓣关闭不全２例,主动脉瓣狭窄１例;６例同时合并动脉导管未闭。采用左后外侧切口矫治主动脉弓缩窄,正中切口行心内畸形矫治６例、正中切口采用主肺动脉内隧道同时矫治主动脉弓缩窄及合并心内畸形３例;     

婴幼儿主动脉缩窄合并心内畸形的外科治疗

目的 探讨婴幼儿主动脉缩窄合并心内畸形的外科治疗经验.方法 2000年1月至2006年12月,84例主动脉缩窄合并心内畸形患儿接受了外科手术治疗,手术年龄1个月～3岁(平均13.5个月),体重3.3～15.0 kg(平均7.3 kg).12例合并复杂心内畸形,72例合并室间隔缺损和其他简单心内畸形,23例伴有主动脉弓发育不良.一期手术62例,49例正中开胸同时矫治主动脉缩窄和心内畸形,13例左侧开胸矫治主动脉缩窄,正中开胸修补心内畸形;分期手术22例.主动脉缩窄的手术方式包括补片成形42例,切除端端吻合30例,锁骨下动脉翻转6例,血管旁路3例,球囊扩张1例.在49例正中切口一期手术中,43例应用选择性脑灌注加下半身停循环,4例应用全身低流量灌注,2例应用深低温停循环.结果 围手术期死亡8例,死亡率9.5%,其中3例为术前漏诊主动脉缩窄.结论 婴幼儿主动脉缩窄合并心内畸形的外科治疗可获得良好的近期疗效,绝大部分患儿可采取正中切口一期手术.选择性脑灌注和下半身停循环可以有效地保护脑和重要脏器.     

经胸骨正中切口一期矫治小儿主动脉缩窄及合并畸形

目的探讨经胸骨正中切口一期矫治小儿主动脉缩窄(CoA)及合并畸形的手术方法和治疗效果。方法2002年6月至2005年8月手术治疗CoA及合并畸形36例,其中男27例,女9例;年龄18d~8岁,平均(14·3±9·5)个月,其中小于1岁27例,小于3月龄18例;体重3~23kg,平均(6·6±3·0)kg。有症状的婴儿型27例,无症状的大儿童型8例,经左胸切口矫治CoA后再狭窄1例;合并室间隔缺损、动脉导管未闭、房间隔缺损、主动脉弓发育不良、完全性大动脉转位及主动脉瓣下狭窄等心内畸形。36例均经胸骨正中切口以扩展端端吻合术一期矫治CoA及合并畸形。结果手术死亡1例,系术前反复心力衰竭及充血性肺炎,术后15d死于心肺功能衰竭。35例随访4~36个月,晚期死亡1例。生存34例恢复良好,无再缩窄发生。结论经胸骨正中切口一期矫治CoA及合并畸形效果良好;扩展端端吻合法是一种值得推荐的技术。     

一期矫治合并主动脉弓病变的心内畸形

1993年以来，我们收治了14例合并多种心内畸形的主动脉弓发育不良或主动脉缩窄病儿，均经胸骨正中切口在体外循环下行同期矫治，取得了满意疗效，现报道如下。     

婴儿主动脉缩窄合并心内畸形的一期矫治

目的总结婴儿主动脉缩窄（CoA）合并心内畸形一期矫治的手术方法和临床经验。方法2001年1月至2006年1月，对28例CoA合并心内畸形患者行一期手术矫治。CoA为导管前型18例，邻近或正对导管处10例；伴主动脉弓发育不良6例，动脉导管未闭22例。合并的心内畸形包括：室间隔缺损16例、室间隔缺损＋房间隔缺损5例、完全性房室间隔缺损3例，完全型大动脉错位伴室间隔缺损（D—TGA／VSD）2例，右心室双出口2例。采用左胸后外侧联合胸骨正中切口（双切口）径路手术12例，胸骨正中切口径路（单一切口）手术16例。采用缩窄段切除端端吻合术20例，Gore—Tex补片扩大成形术4例，左锁骨下动脉翻转扩大成形术4例。结果全组无手术死亡，术后呼吸机辅助呼吸时间7h～13d，住ICU时间3～18d。因术后心脏扩大延迟48～72h关胸4例，术后发生急性肾功能衰竭行腹膜透析3例，吸入一氧化氮（NO）治疗重度肺动脉高压3例。术后下肢收缩压高于上肢10～20mmHg18例（64．3％），收缩压上、下肢相差不大8例（28．6％），上肢分别高于下肢15mmHg和20mmHg2例（7．1％）。所有患者均得到随访，随访时间3～50个月，1例D—TGA／VSD患者因重度三尖瓣反流、肺部严重感染和呼吸功能衰竭于术后3个月死亡；其余27例患者恢复顺利。心脏超声心动图提示：1例采用端端吻合法、1例采用Gore～Tex补片扩大成形术的患者在CoA纠治处仍存在压差，分别为25mmHg、28mmHg，均未再次手术。结论一期手术矫治CoA合并心内畸形可以缩短疗程，有利于患者术后心、肺功能的恢复，避免二次手术的痛苦，降低治疗费用。可采用单一胸骨正中切口或胸骨正中联合左胸后外侧切口完成手术。     

新生儿主动脉弓中断合并心内畸形的一期手术矫治长期结果

目的探讨新生儿主动脉弓中断(IAA)合并心内畸形的一期手术矫治效果。方法回顾性分析2003年5月至2014年9月我院采用经胸骨正中切口下一期手术矫治IAA合并心内畸形新生儿21例的临床资料,其中男18例、女3例,年龄6~26(15.9±5.8)d。A型14例,B型7例。手术均采用胸骨正中切口,端侧吻合降主动脉及主动脉弓,同期矫治合并心内畸形。结果机械通气时间14~809(237.8±179.7)h,体外循环时间92~174(132.6±27.1)min,主动脉阻断时间48~118(70.9±18.8)min,深低温停循环时间5~60(28.8±15.5)min,住院时间4~52(28.0±12.1)d。住院期间死亡3例(14.3%),分别因手术后败血症、肺动脉高压危象、心脏骤停而死亡。18例新生儿生存,随访3个月至11年,超声检查示患儿术后心功能良好。结论新生儿IAA合并心内畸形采用经胸骨正中切口一期手术矫治减少了手术次数,提高了患儿生活质量,手术效果良好。     

升主动脉-降主动脉心包内旁路术治疗成人主动脉缩窄及主动脉弓中断合并心脏畸形的临床分析

目的探讨经正中切口行升主动脉-降主动脉心包内旁路术治疗成人主动脉缩窄及主动脉弓中断合并心脏畸形的技术要点。方法 2010年4月至2015年1月2例成人主动脉缩窄和1例成人主动脉弓中断合并心脏畸形患者行手术治疗,其中男2例,女1例;年龄35.6(27~46)岁。患者的疾病包括先天性主动脉弓缩窄、二尖瓣前叶脱垂伴中度关闭不全1例,先天性主动脉瓣二瓣化畸形伴主动脉瓣重度关闭不全、升主动脉瘤及主动脉弓缩窄1例,先天性主动脉瓣二瓣化畸形伴主动脉瓣轻度狭窄、房间隔缺损(继发孔)及主动脉弓中断(A型)1例。患者均在升主动脉及股动脉,上下腔静脉插管建立体外循环,经正中切口行升主动脉-降主动脉心包内旁路术及合并心脏畸形矫治手术。结果本组无围术期死亡病例,术后患者症状明显好转,出院随访2~59个月,除1例患者仍有上肢高血压需服用药物控制外,其他患者血压恢复到正常水平,术后下肢乏力症状消失。主动脉CTA检查示人工血管通畅,无人工血管扭曲压缩及假性动脉瘤形成等并发症。结论经正中切口行升主动脉-降主动脉心包内旁路术治疗成人主动脉缩窄及主动脉弓中断,同时行合并心脏畸形矫治的一期手术,患者手术安全及疗效确切,临床可选择性应用。     

Surgical treatment of coarctation and interrupted aortic arch complex in infants

One hundred forty-two consecutive neonates or early infants with coarctation and interrupted aortic arch complex who underwent biventricular repair at the Fukuoka Children's Hospital between January 1991 and December 2000 were reviewed. One-stage repair was performed in 33 patients (35%) with coarctation complex and in 41 patients (85%) with interrupted aortic arch complex. The overall mortality rate was 6.1% in one-stage repair and 6.6% in two-stage repair of coarctation complex patients and 9.8% in one-stage repair and 28.6% in two-stage repair of interrupted aortic arch complex patients. The recoarctation rate was 5.3% in coarctation complex and 2.1% in interrupted aortic arch complex. All patients with recoarctation underwent successful catheter intervention and required no reoperation. In conclusion, one-stage repair of interrupted aortic arch and coarctation complex with the anterior approach resulted in good outcomes. Then descending aorta cannulation through a median sternotomy combined with the cerebral perfusion technique enables complete avoidance of circulatory arrest and is a useful technique. However, a two-stage procedure can be useful in the patients whose condition has deteriorated substantially or in whom intracardiac anomalies are severe.     

Off pump repair of aortic arch anomalies with concomitant intracardiac defects via anterior approach

BACKGROUND: The authors evaluated the surgical treatment of aortic arch anomalies associated with intracardiac pathologies, through median sternotomy on beating heart without using cardiopulmonary bypass (CPB). METHODS: A consecutive series of 10 patients with aortic coarctation were operated upon. Median age at repair was 3.5 months (range, 5 days to 72 months), median weight was 4 kg (range, 2.2 to 30 kg). All aortic obstruction repairs were done via midsternotomy without using CPB and it is used only for repair of intracardiac defects. The aortic reconstruction included resection and end-to-side anastomosis in six patients and pulmonary autograft patch aortoplasty in four patients. RESULTS: There was no operative mortality. Mean follow-up value was 17.6 +/- 8.07 months. There was no restenosis. CONCLUSION: Most of the aortic coarctation and interrupted aorta type A can be well-treated surgically through median sternotomy without using CPB. Thus, the need for profound hypothermia and circulatory arrest and its potential neurological and other side effects are removed and CPB is reserved only for associated intracardiac defects, if present.     

一期手术纠治婴幼儿主动脉缩窄或离断合并心内畸形

目的 总结婴幼儿主动脉缩窄或离断合并心内畸形胸骨正中切口一期纠治的外科治疗策略.方法 2004年5月至2010年3月,采用胸骨正中切口一期纠治主动脉缩窄或离断合并心内畸形患儿52例.其中男性32例,女性20例;年龄25 d～7个月,平均(2.03±0.15)个月;体质量3.5～8.0 kg,平均(3.9±0.5)kg.采用自体心包片修补心内缺损;主动脉缩窄者40例,34例采用端侧吻合或扩大端侧吻合术,3例行纵切横缝术,3例假性主动脉缩窄行导管韧带切断主动脉松解;主动脉离断12例,均采用扩大端侧吻合.结果 所有病例心肺转流时间平均为(98±41)min,术中出血量(78±13)ml.1例主动脉离断合并右心室双出口患儿术后因左侧支气管狭窄,脱离呼吸机困难,于术后43 d死亡.其余病例术后生存良好,随访1～6年,术后再缩窄率为11%.结论 采用胸骨正中一期切口纠治主动脉缩窄或离断近期手术效果显著,可避免二次手术.

Abstract：

Objective To sum up one-stage complete correction of infantile aortic coarctation (CoA) or interrupted aortic arch (IAA) associated with intracardiac anomailes through median sternotomy.Methods The clinical data of 52 infants with CoA or IAA associated with intracardiac anomalies from May 2004 to March 2010 was analyzed. There were 32 male and 20 female, aged from 25 d to 7 months with a mean of (2.03 ±0. 15) months, weighted from 2.5 to 8.0 kg with a mean of (3.9 ±0.5) kg. All of intracardia defect were corrected by self-arcula cordisand. Forty cases with CoA were underwent by operative techniques, including resection with end to side anastomosis, extented end to side anastomosis (n = 34),and vertical incision and cross joint ( n = 3). Three cases of pseudo-CoA were cuted and ductus arterissus or ligamentum arteriosus and dissected aorch. Twelve cases of IAA were underwent by extented end to side anastomosis. Results The time of cardiopulmonary bypass was (98 ± 41 ) min, and all patients hemorrhaged (78 ± 13) ml during operation. One case of IAA associated with double outlet right ventricle died after 43 d post-operation because of left bronchinal stenosis. The other patients were in good condition.The rate of aneurysm formation was 11% in 1 to 6 years' follow-up. Conclusions One-stage complete correction of infantile CoA or IAA associated with intracardiac anomailes through median sternotomy yieldes excellent intermediate surgical results. This operative approach is beneficial, not only with shorten period of therapy and loss operative cost.     

Repair of interrupted aortic arch and associated malformations in infancy: indications for complete or partial repair

There is uncertainty regarding the best method of repair of interrupted aortic arch. The question is whether to perform primary definitive repair of this anomaly plus the associated defects versus arch repair only and palliation of the intracardiac defects, usually by pulmonary artery banding. Since 1976, 16 infants with interrupted aortic arch have been treated surgically. They were seen at 5.2 +/- 3 days of age and weighed 3.2 +/- 0.7 kg. The interruption occurred between the left carotid and left subclavian arteries (type B) in 9 and between the left subclavian artery and the descending aorta in 7 (type A). Isolated ventricular septal defect (VSD) was the only associated anomaly in 7 and aortopulmonary window, in 4. Two patients had truncus arteriosus type 1. Three had transposition of the great arteries: 1 with VSD and 2 with single ventricle. Prior to 1980, our policy was to palliate all patients. Between 1976 and 1980, 4 infants underwent left thoracotomy with arch repair plus pulmonary artery banding (3, VSD; 7, transposition of the great vessels and single ventricle) with only 1 (25%) survivor. Because of this high mortality, 8 patients with interrupted aortic arch and VSD or aortopulmonary window, seen since 1980, received complete repair with median sternotomy, end-to-end arch anastomosis, and closure of the VSD or aortopulmonary window utilizing profound hypothermia and circulatory arrest. All 8 survived.(ABSTRACT TRUNCATED AT 250 WORDS)     

End-to-side anastomosis for coarctation of the aorta and type a aortic arch interruption with hypoplastic aortic arch

Objective: We investigated the advantages of reconstructing the aortic arch in neonates and infants by end-to-side anastomosis (ESA) in aortic coarctation and type A aortic arch interruption. Subjects and Methods: The patients were 28 neonates and infants who underwent median full sternotomy for correction of aortic coarctation (CoA) and type A interrupted aortic arch (IAA), at our institute, from October 1997 to September 2002. The cases were divided into two groups: ESA was performed in 16 cases (group A) and extended end to end anastomosis in 12 cases (group B). All repairs were made using simple clamping of the descending aorta under cardiac arrest. We compared groups A and B with regard to duration of simple clamping, postoperative blood pressure in the upper and lower extremities, echocardiographic pressure gradient, and the presence or absence of tracheal stenosis as diagnosed by postoperative clinical symptoms and chest radiography. Results: No significant difference between the groups was found in age, gender, body weight, or the ratio of CoA to IAA. In addition, there was no defference between the two groups in the duration of simple clamping or the difference in blood pressure between the lower and upper extremities. However, the echocardiographic pressure gradient at the site of anastomosis in group A was significantly lower than that in group B. There were no cases with symptoms of bronchial stenosis in either group. Conclusion: ESA is a relatively simple method for treating CoA or IAA with hypoplastic aortic arch, and was found to be effective for the elimination of residual stenosis.     

End-to-side anastomosis for coarctation of the aorta and type a aortic arch interruption with hypoplastic aortic arch

Objective: We investigated the advantages of reconstructing the aortic arch in neonates and infants by end-to-side anastomosis (ESA) in aortic coarctation and type A aortic arch interruption. Subjects and Methods: The patients were 28 neonates and infants who underwent median full sternotomy for correction of aortic coarctation (CoA) and type A interrupted aortic arch (IAA), at our institute, from October 1997 to September 2002. The cases were divided into two groups: ESA was performed in 16 cases (group A) and extended end to end anastomosis in 12 cases (group B). All repairs were made using simple clamping of the descending aorta under cardiac arrest. We compared groups A and B with regard to duration of simple clamping, postoperative blood pressure in the upper and lower extremities, echocardiographic pressure gradient, and the presence or absence of tracheal stenosis as diagnosed by postoperative clinical symptoms and chest radiography. Results: No significant difference between the groups was found in age, gender, body weight, or the ratio of CoA to IAA. In addition, there was no defference between the two groups in the duration of simple clamping or the difference in blood pressure between the lower and upper extremities. However, the echocardiographic pressure gradient at the site of anastomosis in group A was significantly lower than that in group B. There were no cases with symptoms of bronchial stenosis in either group. Conclusion: ESA is a relatively simple method for treating CoA or IAA with hypoplastic aortic arch, and was found to be effective for the elimination of residual stenosis.     

One stage repair of aortic arch anomalies and intracardiac defects

Between August 1985 and May 1990, 27 neonates and infants underwent combined correction of intracardiac and aortic arch anomalies through a median sternotomy. Coarctation (CoA) was combined with VSD (6), AVSD (2), Taussig-Bing (TB) heart (5), transposition of the great arteries (TGA) (1), TGA + VSD (2), congenitally corrected TGA + VSD (1) and VSD + myxoid stenotic outlet valves (1). Interrupted aortic arch (IAA) was combined with VSD (10) and TB heart (1). Two patients had IAA type B as well as CoA. Age at operation varied from 2 to 243 days with a mean age of 51 days. Twenty patients (70%) were younger than 30 days. One TGA + VSD and all TB hearts had maligned outlet septum and right ventricular outflow tract obstruction (RVOTO). Posterior outlet septum deviation and left ventricular outflow tract obstruction (LVOTO) occurred in 8 patients with malalignment VSD and IAA (7) or CoA (1). Aortic arch reconstruction was performed using extended end-to-end anastomoses. In 3 patients, arch hypoplasia necessitated patch implantation. VSDs were closed through the right atrium unless the anatomy dictated otherwise. One TB heart was reconstructed with a Kawashima procedure. All other TB hearts and all TGAs were corrected with arterial switch operation. Obstructing outlet septum was resected whenever necessary. Follow-up was complete and included echo-Doppler control. Eleven patients had postoperative heart catheterisation. Early mortality was 18.5% (5 patients). Persisting LVOTO or RVOTO was responsible. There was no late mortality. Five patients were reoperated upon: 3 for stenotic anastomoses and 2 for a subaortic membranous stenosis. Successful balloon dilatation of recoarctation was performed four times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coarctation of the aorta with right aortic arch: surgical technique and new classification.

BACKGROUND: The combination of right aortic arch and coarctation of the aorta has seldom been reported. This rare abnormality occurs as an isolated lesion or in association with other congenital defects, such as mixed gonadal dysgenesis and Turner's syndrome. METHODS: The medical records of 2 patients who underwent operation for right aortic arch and aortic coarctation in our institution were reviewed together with case reports in the literature. Various surgical options have been reported: synthetic grafts, subclavian flap, and end-to-end anastomosis. End-to-end anastomosis is our method of choice for coarctation of the aorta and for right aortic arch with coarctation, even though an excessive amount of dissection is needed. RESULTS: Both patients from our institution are doing well, with no sign of recoarctation in either patient. Our experience and recent advances in the understanding of the anatomy of this lesion led us to develop an alternative simplified classification for right aortic arch, which is presented here. CONCLUSIONS: Right aortic arch and coarctation of the aorta is a rare morphologic combination. On the basis of our experience with repair of coarctation of the aorta and our review of the literature, we think that end-to-end anastomosis is the operative technique of choice with the best long-term results. Our simplified classification is easy to understand when dealing with right aortic arch.     

Repair of Coarctation of the Aorta in Neonates and Young Infants

Abstract In repair of coarctation in neonates or young infants, inadequate removal of ductal tissue, failure to address hypoplasia of the aortic arch, and suture line tension have been reported to be important factors of residual or early recurrent stenosis at the coarctation repair site. In a consecutive series of neonates and young infants with coarctation, who were all operated without delay with extended resection, the clinical outcome regarding the development of restenosis and hypertension was studied. In addition, the resected specimens were investigated regarding the completeness of resection of ductal tissue. Twenty-five consecutive neonates and young infants (median age 22 days, range 5 to 39 days) who underwent surgical correction of coarctation were reviewed; the resected specimens were examined histologically to document the extent of ductal tissue in the aortic wall. Fifteen patients had a preductal coarctation with associated cardiovascular anomalies including a hypoplastic aortic arch (n = 11). The remaining 10 patients had a paraductal coarctation without associated intracardiac anomalies. In all patients, the isthmus was bypassed and an end-to-side anastomosis was constructed between the descending aorta and the undersurface of the proximal aortic arch (n = 13) or the distal ascending aorta (n = 12). In 13 patients without marked hypoplasia of tbe aortic arch, the coarctation repair was performed through a left thoracotomy. In the remaining 12 patients, the coarctation was repaired through a median sternotomy with CPB and hypothermic circulatory arrest, on the basis of an associated hypoplastic aortic arch (n = 4), hypoplastic aortic arch with intracardiac anomalies (n = 7), or a “bovine” innominate artery (n = 1). There was no perioperative or late mortality. At a median follow-up of 15 months, 1 patient (4%) developed a recurrent stenosis at the coarctation repair site; in the remaining 24 patients, echocardiograpby showed a widely patent anastomosis with no evidence of a hemodynamically significant gradient. None of the patients had hypertension. Histologic examination of the resected specimens demonstrated the presence of ductal tissue in the descending aorta with maximal extension into its lateral wall (mean 5.2 mm). In all specimens of the paraductal subtype, there was also extension of ductal tissue into the lateral wall of tbe isthmus (mean 3.9 mm). We conclude that: (1) in the absence of marked hypoplasia of the proximal aortic arch, coarctation can be repaired with low mortality and morbidity via a left thoracotomy; (2) in the presence of marked hypoplasia of the proximal aortic arch and/or if associated intracardiac defects also need to be repaired, we advocate repair of the coarctation and associated defects through a median sternotomy with circulatory arrest; (3) in view of the absence of postoperative hypertension in this series, early repair of aortic coarctation is recommended; and (4) because ductal tissue may extend not only into the descending aorta but also into the isthmus, complete excision of the coarctation and bypass of the isthmus are valuable techniques to avoid secondary constriction of the aorta by ductal tissue.