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优化心房颤动合并心脏瓣膜病患者的抗凝策略:一项基于证据的全面综述

Optimizing Anticoagulation Strategies in Patients With Atrial Fibrillation and Valvular Heart Disease: A Comprehensive Evidence-Based Review.

作者信息

Deiveegan Dharani S, Salahie Mohamed, Subhan Muhammad, Ismail Sulman, Khan Muhammad Abdullah, Raval Darshankumar M, Abbas Usama, Betsy Baiju Beyla, Abuasaker Husam K, Bibi Ruqiya

机构信息

Internal Medicine, The Tamil Nadu Dr. M. G. R. Medical University, Tiruchirappalli, IND.

Pediatrics, Upstate University Hospital, Syracuse, USA.

出版信息

Cureus. 2025 Mar 27;17(3):e81319. doi: 10.7759/cureus.81319. eCollection 2025 Mar.

DOI:10.7759/cureus.81319
PMID:40291263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12033385/
Abstract

Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, significantly increases the risk of thromboembolism and stroke. Its coexistence with valvular heart disease (VHD) further complicates management due to elevated risks of thromboembolism, bleeding, and mortality. This review explores the pathophysiology of AF and its interaction with VHD, focusing on diagnostic tools like echocardiography and risk stratification scores such as CHA2DS2-VASc and HAS-BLED. Vitamin K antagonists (VKAs) remain the cornerstone of anticoagulation therapy in high-risk VHD populations, particularly in patients with mechanical heart valves or moderate-to-severe mitral stenosis (MS). VKAs have demonstrated proven efficacy in reducing thromboembolic events in these subgroups, supported by decades of clinical evidence. However, their use requires frequent international normalized ratio (INR) monitoring and is associated with higher bleeding risks, posing challenges in long-term management. Despite these limitations, VKAs are indispensable in these populations due to the lack of robust evidence supporting the safety and efficacy of direct oral anticoagulants (DOACs) in these high-risk groups. Ongoing clinical trials, such as the RIVER trial, aim to evaluate the role of DOACs in VHD. However, current guidelines continue to recommend VKAs as the standard of care for these patients. In contrast, DOACs offer significant advantages in non-valvular AF and selected VHD populations. Their predictable pharmacokinetics, fewer dietary restrictions, and lower risks of intracranial hemorrhage make them a preferred choice for many patients. Landmark trials and meta-analyses, including RE-LY, ROCKET-AF, and ARISTOTLE, have demonstrated the safety and efficacy of DOACs in non-valvular AF and certain VHD subgroups. However, DOACs are contraindicated in high-risk VHD populations, such as those with mechanical valves or moderate-to-severe MS, due to insufficient evidence and potential risks of thromboembolic events. Evolving guidelines from leading societies emphasize individualized approaches and collaborative decision-making in anticoagulation therapy. While DOACs are preferred for most AF patients, VKAs remain essential for high-risk VHD patients. Future advancements, such as factor XIa inhibitors, hold promise for improving outcomes and safety in these complex populations. This review provides a comprehensive framework for clinicians to navigate the complexities of anticoagulation in AF and VHD, ensuring evidence-based, patient-centered care.

摘要

心房颤动(AF)是最常见的持续性心律失常,会显著增加血栓栓塞和中风的风险。它与心脏瓣膜病(VHD)共存会使管理更加复杂,因为血栓栓塞、出血和死亡风险都会升高。本综述探讨了AF的病理生理学及其与VHD的相互作用,重点关注超声心动图等诊断工具以及CHA2DS2-VASc和HAS-BLED等风险分层评分。维生素K拮抗剂(VKAs)仍然是高危VHD人群抗凝治疗的基石,特别是对于机械心脏瓣膜或中重度二尖瓣狭窄(MS)患者。数十年来的临床证据表明,VKAs在降低这些亚组的血栓栓塞事件方面已证明有效。然而,使用VKAs需要频繁监测国际标准化比值(INR),且出血风险较高,这给长期管理带来了挑战。尽管存在这些局限性,但由于缺乏有力证据支持直接口服抗凝剂(DOACs)在这些高危人群中的安全性和有效性,VKAs在这些人群中仍是不可或缺的。正在进行的临床试验,如RIVER试验,旨在评估DOACs在VHD中的作用。然而,目前的指南仍继续推荐VKAs作为这些患者的标准治疗方法。相比之下,DOACs在非瓣膜性AF和特定VHD人群中具有显著优势。其可预测的药代动力学、较少的饮食限制和较低的颅内出血风险使其成为许多患者的首选。包括RE-LY、ROCKET-AF和ARISTOTLE在内的标志性试验和荟萃分析已证明DOACs在非瓣膜性AF和某些VHD亚组中的安全性和有效性。然而,由于证据不足以及存在血栓栓塞事件的潜在风险,DOACs在高危VHD人群中,如机械瓣膜或中重度MS患者中是禁忌的。主要学会不断更新的指南强调在抗凝治疗中采用个体化方法和共同决策。虽然DOACs是大多数AF患者的首选,但VKAs对高危VHD患者仍然至关重要。未来的进展,如因子Xa抑制剂,有望改善这些复杂人群的治疗效果和安全性。本综述为临床医生应对AF和VHD抗凝治疗的复杂性提供了一个全面的框架,确保以证据为基础、以患者为中心的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f66/12033385/45fc3d49c424/cureus-0017-00000081319-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f66/12033385/92d9760c094e/cureus-0017-00000081319-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f66/12033385/45fc3d49c424/cureus-0017-00000081319-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f66/12033385/92d9760c094e/cureus-0017-00000081319-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f66/12033385/45fc3d49c424/cureus-0017-00000081319-i02.jpg

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