风湿性二尖瓣疾病患者三尖瓣反流的处理。

R Kalasipudi, S Gupta, A Meghdadi, S Gupta, Y Abu-Omar, A Al-Akhtar, M El-Diasty
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引用次数: 0

摘要

背景:风湿性心脏病(RHD)仍然是低收入和中等收入国家心血管疾病发病率和死亡率的主要原因,三尖瓣反流(TR)经常并发风湿性二尖瓣病理。虽然轻度TR在二尖瓣矫正后通常会稳定下来,但在这种情况下,中度和重度TR的处理仍然存在争议,因为证据有限,指南的适用性主要来自退行性病因。本综述综合了风湿性tr的诊断策略、手术决策和结果的最新数据。方法:在PubMed、谷歌Scholar和OMNI数据库(2010-2024)中进行全面的文献检索,检索关键词为“风湿性二尖瓣疾病”、“三尖瓣反流”和“管理”。符合条件的研究包括临床试验、病例系列、综述和荟萃分析,重点关注与风湿性二尖瓣疾病相关的TR。提取数据并对研究设计、人群和结果相关性进行严格评估。结果:风湿性二尖瓣疾病治疗TR的证据主要来自回顾性队列和小型前瞻性研究,很少有随机试验。TR进展的预测因素包括环扩张(>21 mm/m²)、右心室功能障碍、肺动脉高压和心房颤动。轻度TR一般在二尖瓣手术后消退,需保守处理。对于中度TR,虽然术后心律失常和起搏器植入的风险仍然存在,但伴随的修复可以防止晚期进展并改善血流动力学。严重的TR需要手术矫正,最好是硬环成形术,而瓣膜置换术用于晚期钙化疾病。新兴的经导管治疗显示出对高危患者的希望,但缺乏可靠的风湿病特异性数据。结论:由于高质量的证据有限,风湿性二尖瓣疾病TR的最佳管理需要个性化的、以心脏团队为基础的决策。未来的研究应优先考虑多中心试验,比较修复、置换和经导管入路,整合先进的成像技术进行风险分层,并解决资源有限环境下的准入差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Management of Tricuspid Regurgitation in Patients with Rheumatic Mitral Disease.

Background: Rheumatic heart disease (RHD) remains a major cause of cardiovascular morbidity and mortality in low and middle-income countries, with tricuspid regurgitation (TR) frequently complicating rheumatic mitral pathology. While mild TR often stabilizes after mitral correction, management of moderate and severe TR in this context remains controversial due to limited evidence and applicability of guidelines largely derived from degenerative etiologies. This review synthesizes current data on diagnostic strategies, surgical decision-making, and outcomes in rheumatic TR.

Methods: A comprehensive literature search was performed across PubMed, Google Scholar, and OMNI databases (2010-2024) using the keywords "rheumatic mitral disease," "tricuspid regurgitation," and "management." Eligible studies included clinical trials, case series, reviews, and meta-analyses focusing on TR associated with rheumatic mitral disease. Data was extracted and critically appraised for study design, population, and outcome relevance.

Results: Evidence for managing TR in rheumatic mitral disease primarily stems from retrospective cohorts and small prospective studies, with few randomized trials. Predictors of TR progression include annular dilation (>21 mm/m²), right ventricular dysfunction, pulmonary hypertension, and atrial fibrillation. Mild TR generally regresses following mitral surgery and is managed conservatively. For moderate TR, concomitant repair may prevent late progression and improve hemodynamics, though risks of postoperative arrhythmia and pacemaker implantation persist. Severe TR warrants surgical correction, preferably rigid ring annuloplasty, while valve replacement is reserved for advanced calcific disease. Emerging transcatheter therapies show promise for high-risk patients but lack robust rheumatic-specific data.

Conclusion: Optimal management of TR in rheumatic mitral disease requires individualized, Heart Team-based decision-making due to limited high-quality evidence. Future research should prioritize multicenter trials comparing repair, replacement, and transcatheter approaches, integrating advanced imaging for risk stratification and addressing access disparities in resource-limited settings.

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