Carrel T, Serraf A, Lacour-Gayet F, Bruniaux J, Demontoux S, Touchot A, Piot D, Losay J, Planché C
Department of Pediatric Cardiac Surgery, Marie-Lannelongue Surgical Center, University of Paris Sud, France.
Ann Thorac Surg. 1996 Mar;61(3):940-4. doi: 10.1016/0003-4975(95)01190-0.
Tricuspid valve insufficiency secondary to structural anomalies of the valve itself or to an iatrogenic complication of the Rashkind procedure is very rarely associated with transposition of the the great arteries. This condition represents an interesting perioperative challenge. Rapid restoration of the tricuspid valve to a low-pressure system by arterial switch operation associated with tricuspid repair should theoretically improve the outcome in terms of myocardial and valve function.
Thirteen of 839 patients who underwent an arterial switch operation for various forms of transposition of the great arteries presented with moderate to severe tricuspid insufficiency. Three of them had a ventricular septum defect. Nine experienced severe cardiac failure with profound hypoxemia. Ventilatory support was necessary in 7, 6 had renal or hepatic dysfunction, and 5 had coagulation disorders. Inotropic support was started preoperatively in 8 patients.
Tricuspid lesions were as follows: primary annular dilatation and lack of coaptation at the commissural level (n = 1), straddling tricuspid valve (n = 1) redundant tricuspid valve tissue leading to left ventricular outflow tract obstruction (n = 1), small cleft of the septal leaflet (n = 1), and dysplastic valve tissue with juxtacommissural regurgitation (n = 1). In 8 patients, the cause of the tricuspid valve insufficiency was most probably an iatrogenic lesion, with rupture of the papillary muscle (n = 2), rupture of the chordae (n = 1), or tear of the anterior leaflet (n = 5), whereas no clear cause could be found in 1 patient. Repair consisted of the arterial switch operation associated with tricuspid valve repair in 10 patients. In 2 patients with only discrete anomaly and in 1 without a clear cause of tricuspid regurgitation, no valve repair was performed. Three patients had their ventricular septal defect closed. There were only one early and one late death, both not related to the tricuspid lesions. Late postoperative (mean, 6.5 years) evaluation revealed normal left ventricular function in 10, with no tricuspid incompetence in 7 and trivial tricuspid insufficiency in 3.
Restoration of an incompetent tricuspid valve in a low-pressure system by the arterial switch operation combined with valve repair provides good ventricular and valvar results. Preoperative management and appropriate timing of operation seem to be of utmost importance.
继发于瓣膜本身结构异常或 Rashkind 手术医源性并发症的三尖瓣关闭不全很少与大动脉转位相关。这种情况代表了一个有趣的围手术期挑战。理论上，通过与三尖瓣修复相关的动脉调转手术将三尖瓣快速恢复至低压系统应能改善心肌和瓣膜功能方面的预后。
839 例因各种形式的大动脉转位接受动脉调转手术的患者中，13 例存在中度至重度三尖瓣关闭不全。其中 3 例合并室间隔缺损。9 例出现严重心力衰竭并伴有严重低氧血症。7 例需要通气支持，6 例有肾或肝功能障碍，5 例有凝血功能障碍。8 例患者术前开始使用正性肌力药物支持。
三尖瓣病变如下：原发性瓣环扩张及瓣叶联合处对合不良（n = 1）、跨瓣三尖瓣（n = 1）、多余的三尖瓣组织导致左心室流出道梗阻（n = 1）、隔叶小裂缺（n = 1）以及发育异常的瓣膜组织伴瓣叶联合处反流（n = 1）。8 例患者三尖瓣关闭不全的原因很可能是医源性病变，包括乳头肌破裂（n = 2）、腱索断裂（n = 1）或前叶撕裂（n = 5），而 1 例患者未发现明确病因。10 例患者的修复包括动脉调转手术联合三尖瓣修复。2 例仅有轻微异常且 1 例三尖瓣反流无明确病因的患者未进行瓣膜修复。3 例患者关闭了室间隔缺损。仅 1 例早期死亡和 1 例晚期死亡，均与三尖瓣病变无关。术后晚期（平均 6.5 年）评估显示，10 例患者左心室功能正常，7 例无三尖瓣关闭不全，3 例有轻微三尖瓣关闭不全。
通过动脉调转手术联合瓣膜修复将功能不全的三尖瓣恢复至低压系统可取得良好的心室和瓣膜预后。术前管理及合适的手术时机似乎至关重要。
