Atrioventricular septal defect following blunt chest trauma

The authors describe an acquired atrioventricular septal defect that has resulted from a blunt chest trauma. Besides being an uncommon traumatic heart injury, this case has the particularities of the non-involvement of other adjacent anatomical structures and the long delay between the accident and the occurrence of the myocardial rupture.     

Atrioventricular septal defect complicated by right ventricular outflow tract obstruction. Analysis of risk factors regarding surgical repair

Eighteen patients with complete atrioventricular septal defect (AVSD) were found to have either associated tetralogy (n = 15) or pulmonary atresia (n = 3). Their pre- and post-operative course was reviewed focusing attention on risk factors for complete repair. These included right ventricular (RV) hypoplasia, identified by cineangiographic volume determinations in two cases (11%) and inadequate pulmonary artery size in one patient. In the 2 cases with RV hypoplasia and in one case, in whom all chordae of the AV valve were connected to a single right ventricular papillary muscle (AVSD type Rastelli B), complete repair was not feasible. In addition, angiography revealed coronary artery variations in 5/18 (28%), which did not preclude surgical repair. Palliative surgery was undertaken in 10 patients and complete repair carried out in five. Six of 18 patients died, 2 among those after complete repair.     

Surgical repair of complete atrioventricular septal defect.

BACKGROUND: The objective of this study was to assess the outcome of complete atrioventricular septal defect repair from 1981 to 2000. METHODS: One hundred seventy-two consecutive patients with atrioventricular septal defect were operated on by a single surgeon using a consistent operative technique (single patch; "cleft" closure). The patients' age range was from 5 weeks to 9 years (mean, 10.8 +/- 1.2 months). RESULTS: Overall operative mortality was 15 of 172 (8.7%) and this decreased significantly from 12 of 73 (16.4%) in the first decade to 3 of 99 (3.0%) in the second decade (p = 0.0021) with no operative deaths in the last 51 patients. Operative mortality was related to decade of operation (p = 0.0021) and to use of crystalloid cardioplegia (p = 0.0047) by univariate analysis, and to decade of operation (p = 0.0016) and postoperative time on ventilator (p = 0.0023) by multivariate analysis. Actuarial long-term survival including operative deaths was 79.0% +/- 3.8% at 15 years. Ten of 157 (6.4%) operative survivors have undergone reoperation for late mitral regurgitation (9 mitral valve repair, 1 mitral valve replacement) with one death. Four of 8 patients surviving late mitral valve replacement have subsequently required mitral valve repair. Freedom from late reoperation for severe mitral regurgitation was 89.9% +/- 3.1% at 15 years. Freedom from late reoperation for mitral regurgitation did not decrease in the second decade (84.2% +/- 6.6% at 10 years) versus the first decade (94.5% +/- 3.1%) (p = 0.0679). CONCLUSIONS: Although operative mortality for repair of atrioventricular septal defect has decreased dramatically during the past decade, the incidence of late reoperation for mitral regurgitation has not improved, and better techniques to eliminate late mitral regurgitation are needed.     

右美托咪定对室间隔缺损修补术婴儿心肌损伤的影响

目的 评价右美托咪定对室间隔缺损修补术婴儿心肌损伤的影响.方法 择期拟行室间隔缺损修补术婴儿40例,3～6月龄,体重4～6 kg,ASA分级Ⅱ或Ⅲ级,采用随机数字表法,将其分为2组(n=20):对照组(C组)和右美托咪定组(D组).入室后开放静脉通路,麻醉诱导后经鼻气管插管,行机械通气.D组在麻醉诱导后持续静脉输注右美托咪定0.5 μg· kg-1 ·h-1至术毕,C组相同速率持续静脉输注生理盐水至术毕.于术前10 min(T1)、切皮(T2)、胸骨劈开即刻(T3)、主动脉开放后10min(T4)和术毕(T5)时记录HR和BP.于T1、T5和术后24 h(T6)时采集右颈内静脉血样,测定血浆肌酸酶同工酶(CK-MB)活性和心肌肌钙蛋白T(cTnT)浓度.结果 与T1时比较,D组各时点HR和BP差异无统计学意义(P＞0.05),C组T2-5时HR和BP升高,2组T5.6时血浆CK-MB活性及cTnT浓度升高(P＜0.05).与C组比较,D组T2-5时HR和BP、T56时血浆CK-MB活性及cTnT浓度降低(P＜0.05).结论 麻醉诱导后静脉输注右美托咪定0.5 μg·kg-1·h-1可减轻室间隔缺损修补术婴儿的心肌损伤程度.     

Primary repair of complete atrioventricular septal defect in infancy.

Forty infants with complete atrioventricular septal defect have undergone primary repair within their 1st year of life. The mean age at time of surgery was 4 months (range 1-12 months) and the mean weight 4.2 kg (range 2.9-7.0 kg). Either the one- or the two-patch method was used. Four patients died (10%). There were no late deaths. Three patients needed reoperation due to mitral valve insufficiency. Postoperative complications were: 1 total atrioventricular block in an infant with an absent ventricular septum 3 weeks after surgery, 9 complete right bundle branch blocks, 3 small residual ventricular septal defects. Mean follow-up of the 36 survivors is 22 months (3-46 months). Thirty (83%) are in NYHA functional class I, 4 (11%) in NYHA class II and 2 (6%) in NYHA class III. No atrioventricular valve regurgitation is detectable by the color Doppler technique in 19 (53%) patients. Mitral incompetence is mild in 13 cases (36%) and moderate in 4 (11%). In ten recatheterized patients the average systolic pulmonary to systemic artery pressure ratio dropped from 1.0 to 0.42 and the average pulmonary arteriolar resistance was reduced from 5.5 to 3.9 U/m2. All but one patient gained weight and underwent adequate statomotoric development. Primary repair should be performed at the age of 5-6 months or even earlier, if pulmonary arteriolar resistance exceeds 5 U/m2.     

Transaortic repair of ventricular septal defect

A technique is described for repairing defects of the interventricular septum using an aortotomy incision. This approach allows excellent access to the membranous septum, where more than 80% of defects occur. While the standard transventricular or transatrial approach serves best in most instances, the transaortic exposure may be a useful alternative in the small defect, to avoid ventriculotomy, or in some complicated anomalies.     

Complete repair of atrioventricular septal defect

We report our experience with 103 consecutive children who underwent repair of complete atrioventricular septal defect between 1971 and 1990. Ninety-one patients were less than 18 months old (mean age, 6.2 months; mean weight, 5.8 kg) and were repaired using deep hypothermia and circulatory arrest. There were 15 perioperative deaths. Twelve patients were older (mean age, 40.2 months; mean weight, 18.9 kg) and were repaired using moderate hypothermia and cardiopulmonary bypass. There were two perioperative deaths. Repairs were performed with the single-patch technique. Four younger patients required repeat repair to control residual mitral regurgitation. Two of the older children required late reoperation to replace one or both atrioventricular valves. Three younger children underwent pulmonary artery banding initially; 1 died after complete repair. Three older children underwent initial pulmonary artery banding; 2 died at definitive repair, and the survivor required pulmonary artery reconstruction, which was repeated subsequently. Since 1977 our policy has been to perform primary definitive repair whenever possible. Two patients died late from unrelated causes. At the most recent follow-up the majority of patients had no or minimal symptoms. We continue to advocate primary definitive repair whenever possible using the single-patch technique in symptomatic patients with complete atrioventricular septal defect.     

完全性房室间隔缺损的外科治疗

目的回顾性总结手术治疗完全性房室间隔缺损的经验。方法112例病儿,≤6个月43例(38%,X组),>6个月69例(62%,Y组)。85例行心导管检查。Rastelli A型89例,Rastelli B型10例,Ras- telli C型13例。手术技术分单片法,双片法和简化单片法。术中经食管超声检查发现异常而即刻再次手术者7例(二尖瓣反流4例,二尖瓣狭窄2例,左室流出道梗阻1例)。术后入重症监护室,左房压8～21 mm Hg,中心静脉压7～12mm Hg。呼吸机平均应用47h,监护室平均滞留6.3d。结果室间隔缺损残余分流(直径>2mm)13例,二尖瓣中度反流12例,完全性房室传导阻滞4例。院内死亡6例(X组1例,Y组5例)。术后随访91例(81%),随访1～5年,平均2.3年。1例术后1年因肺炎心衰死亡,1例术后2年因二尖瓣中-重度反流而换瓣。结论院内死亡率提示,小于6月龄完全性房室间隔缺损病婴手术是安全的。随着年龄增大,瓣膜成形效果、肺动脉高压的预后可能会更差。双片法修补室间隔缺损较易发生残余漏(9例,18%),简化单片法出院时二尖瓣关闭不全发生率明显高于另外两种方法(6例,16%)。     

Intraventricular repair of transposition complexes with ventricular septal defect.

Repair of transposition of the great arteries by the technique developed by Mustard is the method routinely used for correction of such anomalies. Intraventricular repair of transposition complexes associated with a large ventricular septal defect can prevent some of the limitations and late complications of the intra-atrial operation. A technique is described of intraventricular repair of an unusual Taussig-Bing type of anomaly with a pericardial patch as a baffle to channel left ventricular outflow to the aorta and right ventricular outflow to the pulmonary artery.     

Surgical repair of inferior sinus venosus atrial septal defect.

A 9-year-old girl presented for cardiac evaluation with symptoms of dyspena, fatigue, and cyanosis with exercise. Cardiac catheterization demonstrated an atrial septal defect; an anomalous right superior pulmonary vein was suspected but not confirmed. Operation disclosed anomalous drainage of the right superior and inferior pulmonary veins into the right atrium, an intact fossa ovalis, and an inferior sinus venosus defect. Repair was accomplished by detaching the posterior edge of the atrial septum and suturing it to the right of the pulmonary veins, so that the defect was closed and all the pulmonary venous blood was directed to the left atrium.     

Coronary embolism following atrial septal defect repair

To our knowledge, coronary embolism following repair of atrial septal defect has not been reported previously. A 29-year-old woman had an angiographically documented embolus to the circumflex coronary artery on the fifth postoperative day after pericardial patch repair of a secundum atrial septal defect. This complication might have been prevented by temporary postoperative anticoagulation.     

Transatrial repair of post-infarction ventricular septal defect

A 72-year-old woman presented with a post-infarction ventricular septal defect, presumably within 10 days after the onset of acute myocardial infarction. An emergency surgery was performed because of hemodynamic instability. Using the sandwich patch technique, we approached the posteriorly oriented defect through a right atriotomy and detached tricuspid valve. By avoiding either left or right ventriculotomy, additional damage to the already infarcted ventricle and risk of bleeding were avoided. The patient showed an uneventful postoperative recovery, with no residual shunt detected. A transatrial approach combined with a sandwich patch technique is a good alternative in cases where the pathological anatomy is suitable.