The Labatt Family Heart Centre, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
J Thorac Cardiovasc Surg. 2011 Aug;142(2):326-35.e2. doi: 10.1016/j.jtcvs.2010.11.060. Epub 2011 May 17.
This study was to determine whether atrioventricular valve repair modifies natural history of single-ventricle patients with atrioventricular valve insufficiency and to identify factors predicting survival and reintervention.
Fifty-seven (13.5%) of 422 single-ventricle patients underwent atrioventricular valve repair. Valve morphology, regurgitation mechanism, and ventricular morphology and function were analyzed for effect on survival, transplant, and reintervention with multivariate logistic and Cox regression models. Comparative analysis used case-matched controls.
Atrioventricular valve was tricuspid in 67% and common in 28%. Ventricular morphology was right in 83%. Regurgitation mechanisms were prolapse (n = 24, 46%), dysplasia (n = 18, 35%), annular dilatation (n = 8, 15%), and restriction or cleft (n = 2, 4%). Postrepair insufficiency was none or trivial in 14 (26%), mild in 33 (61%), and moderate in 7 (13%). Survival in repair group was lower than in matched controls (78.9% vs 92.7% at 1 year, 68.7% vs 90.6% at 3 years, P = .015). Patients with successful repair and normal ventricular function had equivalent survival to matched controls (P = .36). Independent predictors for death or transplant included increased indexed annular size (P = .05), increased cardiopulmonary bypass time (P = .04), and decreased postrepair ventricular function (P = .01). Ventricular dilation was a time-related factor for all events, including failed repair.
Survival was lower in single-ventricle patients operated on for atrioventricular valve insufficiency than in case-matched controls. Patients with little postoperative residual regurgitation and preserved ventricular function had equivalent survival to controls. Lower grade ventricular function and ventricular dilation correlated with death and repair failure, suggesting that timing of intervention may affect outcome.
本研究旨在确定房室瓣修复是否改变了伴有房室瓣关闭不全的单心室患者的自然病程，并确定预测生存和再干预的因素。
422 例单心室患者中有 57 例（13.5%）接受了房室瓣修复。使用多变量逻辑回归和 Cox 回归模型分析瓣膜形态、反流机制以及心室形态和功能对生存、移植和再干预的影响。采用病例匹配对照进行比较分析。
房室瓣为三尖瓣者占 67%，共同房室瓣者占 28%。83%的心室形态为右心室。反流机制为脱垂（n=24，46%）、发育不良（n=18，35%）、瓣环扩张（n=8，15%）和限制或裂孔（n=2，4%）。修复后无或轻度关闭不全者占 14 例（26%），轻度关闭不全者占 33 例（61%），中度关闭不全者占 7 例（13%）。修复组的生存率低于匹配对照组（1 年时分别为 78.9%和 92.7%，3 年时分别为 68.7%和 90.6%，P=0.015）。修复成功且心室功能正常的患者与匹配对照组的生存率相当（P=0.36）。死亡或移植的独立预测因素包括指数化瓣环大小增加（P=0.05）、体外循环时间延长（P=0.04）和术后心室功能下降（P=0.01）。心室扩张是所有事件（包括修复失败）的时间相关因素。
接受房室瓣关闭不全手术的单心室患者的生存率低于匹配对照组。术后残余反流少且心室功能保留的患者与对照组的生存率相当。较低的心功能分级和心室扩张与死亡和修复失败相关，提示干预时机可能影响结局。
