Department of Cardiovascular Surgery, Mayo Clinic, Rochester, Minn.
Department of Cardiovascular Surgery, Mayo Clinic, Rochester, Minn.
J Thorac Cardiovasc Surg. 2018 Apr;155(4):1498-1508.e3. doi: 10.1016/j.jtcvs.2017.11.093. Epub 2017 Dec 19.
Given the paucity of available literature, we sought to evaluate the mechanisms of tricuspid regurgitation and the outcomes of tricuspid valve surgery in the presence of permanent pacemakers.
We retrospectively reviewed the records of 622 adult patients who underwent tricuspid valve surgery in the presence of permanent pacemakers between January 1993 and December 2013. Those with prosthetic tricuspid valve or tricuspid valve endocarditis and those undergoing concomitant heart transplant were excluded (n = 23). Patients were divided into 2 etiologic groups: pacemaker-associated tricuspid regurgitation (n = 349, 58%) and pacemaker-induced tricuspid regurgitation (n = 249, 42%). One patient was not categorized, because permanent pacemaker involvement was unknown.
Mean age was 69.5 ± 12.0 years; 312 patients (52%) were female. In pacemaker-associated tricuspid regurgitation, the most common cause was functional (n = 304, 87%). The most common mechanism leading to pacemaker-induced tricuspid regurgitation was restricted leaflet mobility (n = 101, 41%), followed by adherent leaflet to the leads (n = 93, 37%), leaflet perforation (n = 30, 12%), scarring of leaflets (n = 19, 8%), and chordal entrapment (n = 18, 7%). The most common leaflet involved was septal leaflet (n = 182, 73%). Tricuspid valve repair (n = 215, 62%) was higher in the pacemaker-associated tricuspid regurgitation group. In multivariable analysis, pacemaker-induced tricuspid regurgitation was found to be protective with improved survival (hazard ratio [HR], 0.79; 95% confidence interval [CI], 0.68-0.98). Other independent risk factors of mortality included tricuspid valve replacement (HR, 1.50; 95% CI, 1.20-1.87), nonelective surgery (HR, 1.66; 95% CI, 1.33-2.08), diabetes (HR, 1.37; 95% CI, 1.09-1.73), severe tricuspid regurgitation (HR, 1.42; 95% CI, 1.04-1.95), and older age when there was a concomitant aortic valve surgery (HR, 1.44; 95% CI, 1.15-1.79).
Several mechanisms lead to pacemaker-induced tricuspid regurgitation. Pacemaker-induced tricuspid regurgitation when compared with pacemaker-associated tricuspid regurgitation carries a better prognosis with improved survival.
鉴于相关文献资料有限,我们旨在评估在存在永久性起搏器的情况下三尖瓣反流的机制以及三尖瓣瓣膜手术的结果。
我们回顾性分析了 1993 年 1 月至 2013 年 12 月期间 622 例在存在永久性起搏器的情况下接受三尖瓣瓣膜手术的成年患者的记录。排除了存在人工三尖瓣或三尖瓣心内膜炎以及同时进行心脏移植的患者(n=23)。患者被分为 2 个病因组:与起搏器相关的三尖瓣反流(n=349,58%)和起搏器引起的三尖瓣反流(n=249,42%)。有 1 名患者未进行分类,因为永久性起搏器的参与情况未知。
平均年龄为 69.5±12.0 岁;312 名患者(52%)为女性。在与起搏器相关的三尖瓣反流中,最常见的原因是功能性(n=304,87%)。导致起搏器引起的三尖瓣反流的最常见机制是瓣叶活动受限(n=101,41%),其次是瓣叶与导丝粘连(n=93,37%)、瓣叶穿孔(n=30,12%)、瓣叶瘢痕形成(n=19,8%)和腱索嵌压(n=18,7%)。最常累及的瓣叶是隔瓣(n=182,73%)。与起搏器相关的三尖瓣反流组中,三尖瓣瓣膜修复(n=215,62%)更高。多变量分析发现,起搏器引起的三尖瓣反流是保护性的,可改善生存率(风险比[HR],0.79;95%置信区间[CI],0.68-0.98)。死亡率的其他独立危险因素包括三尖瓣瓣膜置换术(HR,1.50;95%CI,1.20-1.87)、非择期手术(HR,1.66;95%CI,1.33-2.08)、糖尿病(HR,1.37;95%CI,1.09-1.73)、严重三尖瓣反流(HR,1.42;95%CI,1.04-1.95)和同期行主动脉瓣手术时年龄较大(HR,1.44;95%CI,1.15-1.79)。
几种机制导致起搏器引起的三尖瓣反流。与与起搏器相关的三尖瓣反流相比,起搏器引起的三尖瓣反流具有更好的预后,可改善生存率。