对“用EHRA(评估心瓣膜、风湿性或人工)分类评估心房颤动患者是否存在先天性瓣膜疾病”的评论

IF 2.3 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Arooha Javed, Syed Muhammad Savez, Syed Muhammad Rayyan
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Sicker patients or those with less access to monitoring may prefer to stay on VKA, which could explain the apparent protective correlation of DOACs vs VKAs. Causal inference would be strengthened by using instrumental variable techniques, inverse probability weighting, or propensity matching [<span>4</span>]. Only baseline measurements of CHA₂DS₂-VASc and HAS-BLED were made; events and comorbidity accrual over ~2.5 years may change treatment and risk choices. Updated analysis would more accurately represent clinical practice [<span>1</span>].</p><p>Future research should (a) record the kind and severity of echocardiographic lesions, (b) conduct lesion-specific outcome analyses, (c) compare anticoagulants using propensity/causal approaches, and (d) take time-updated risk ratings into account. 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引用次数: 0

摘要

我们饶有兴趣地阅读了Escolar Conesa等人的文章《用EHRA(评估心瓣膜、风湿或人工)分类评估心房颤动患者存在原生瓣膜疾病》[10]。Escolar Conesa等人研究了一个关键的临床问题:在抗凝房颤(AF)患者中,患有先天性瓣膜疾病(EHRA-2)的患者与没有瓣膜受累(EHRA-3)的患者预后是否不同?作者报告了一个大型多中心队列(n = 1399)中位随访约910天的EHRA-2患者的大出血、心血管死亡率、心力衰竭和MACE发生率显著升高。他们还证明,EHRA-2状态在多变量调整后仍然是一个独立的预测因子。作者使用了大量真实世界的数据,并公布了每100例患者年的发病率,这是一个有临床价值的统计数据,值得称赞。他们对基线差异和Cox模型的直截了当的解释使得主要观点非常明显:房颤的原生瓣膜受累不是无害的,在确定风险和选择抗凝治疗时应考虑到这一点。这些发现在日常实践中的直接应用受到一些挑战的限制。轻度退行性反流、主动脉狭窄、既往生物假体等病变均归为EHRA-2类。这些实体在病理生理上是不同的,可能构成不同的风险;如果没有病变特异性亚组研究[2],观察者无法确定哪个瓣膜病变是信号的主要驱动因素。该研究承认缺乏标准化的超声心动图分级。预后和治疗取决于严重程度(例如,轻度vs中度主动脉狭窄或反流);将所有原发病变归为一类有误诊临床风险b[1]的危险。EHRA-2患者的ha - bled和CHA₂DS₂-VASc评分较高,且年龄较大。即使调整后的模型部分地解决了这一问题,这种联系也可能部分地被未测量的混杂因素(虚弱、功能不全状态和与瓣膜相关的血流动力学)所解释。经过大量修正后,以往的研究表明EHRA-2信号衰减[3]。病情较重的患者或较少获得监测的患者可能更愿意继续使用VKA,这可以解释DOACs与VKA之间明显的保护性相关性。通过使用工具变量技术、逆概率加权或倾向匹配[4],可以加强因果推理。仅基线测量CHA₂、DS₂、vasc和ha - bled;超过2.5年的事件和合并症可能改变治疗和风险选择。更新的分析将更准确地代表临床实践[1]。未来的研究应该(a)记录超声心动图病变的种类和严重程度,(b)进行病变特异性结果分析,(c)使用倾向/因果方法比较抗凝剂,(d)考虑时间更新的风险评级。这些措施如果得到验证,将有助于提高目前接近推荐临界值的患者的抗凝阈值,正如2020年ESC房颤管理指南所强调的那样。总之,Escolar Conesa等人提供了一个关键的指标,即“非瓣膜性”房颤是多种多样的:天然瓣膜受累可以识别出少数血栓和出血风险增加的患者,需要更仔细的检查和专门的治疗。房颤与瓣膜性心脏病之间的相互作用及其对抗凝治疗的影响在最近的综述中得到了强调[6,7]。为了指导临床治疗,这项工作应该刺激前瞻性的、病变分层的研究。作者没有什么可报告的。作者没有什么可报告的。作者声明无利益冲突。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Critique on “Evaluation of the Presence of Native Valvular Disease in Patients With Atrial Fibrillation Using the EHRA (Evaluated Heartvalves, Rheumatic, or Artificial) Classification”

We read with great interest the article “Evaluation of the Presence of Native Valvular Disease in Patients With Atrial Fibrillation Using the EHRA (Evaluated Heartvalves, Rheumatic, or Artificial) Classification” by Escolar Conesa et al [1]. A critical clinical question is examined by Escolar Conesa et al that: Does a patient with native valvular disease (EHRA-2) have a different prognosis than a patient without valve involvement (EHRA-3) in anticoagulated patients with atrial fibrillation (AF)? The authors report significantly higher rates of major bleeding, cardiovascular mortality, heart failure, and MACE in EHRA-2 patients in a large multicenter cohort (n = 1399) with a median follow-up of approximately 910 days. They also demonstrate that EHRA-2 status remained an independent predictor following multivariable adjustment [1].

The authors' use of a large, real-world data set and their publication of incident rates per 100 patient-years, a clinically valuable statistic, are commendable. Their straightforward explanation of baseline differences and Cox models makes the main point very evident: native valve involvement in AF is not harmless and should be taken into consideration when determining risk and selecting anticoagulation.

The immediate application of these discoveries to routine practice is limited by several challenges. Mild degenerative regurgitation, aortic stenosis, previous biological prosthesis, and other lesions are all grouped under the EHRA-2 category. These entities are pathophysiologically distinct and probably pose different risks; the observer cannot determine which valve lesions are the main drivers of the signal without lesion-specific subgroup studies [2]. The study acknowledges the lack of standardized echocardiographic grading. Prognosis and treatment depend on severity (e.g., mild vs. moderate aortic stenosis or regurgitation); combining all native lesions into one category runs the danger of misclassifying clinical risk [1]. EHRA-2 patients had higher HAS-BLED and CHA₂DS₂-VASc scores and were older. The connection may be partially explained by unmeasured confounders (frailty, frail-functional status, and hemodynamics related to the valves), even if adjusted models partially address this. After substantial correction, previous research indicated that the EHRA-2 signal attenuated [3]. Sicker patients or those with less access to monitoring may prefer to stay on VKA, which could explain the apparent protective correlation of DOACs vs VKAs. Causal inference would be strengthened by using instrumental variable techniques, inverse probability weighting, or propensity matching [4]. Only baseline measurements of CHA₂DS₂-VASc and HAS-BLED were made; events and comorbidity accrual over ~2.5 years may change treatment and risk choices. Updated analysis would more accurately represent clinical practice [1].

Future research should (a) record the kind and severity of echocardiographic lesions, (b) conduct lesion-specific outcome analyses, (c) compare anticoagulants using propensity/causal approaches, and (d) take time-updated risk ratings into account. These actions, if verified, would assist in improving anticoagulation thresholds for patients who are currently close to recommended cutoffs, as also emphasized in the 2020 ESC guidelines on atrial fibrillation management [5]. In summary, Escolar Conesa et al. offer a crucial indication that “non-valvular” AF is diverse: native valvular involvement can identify a minority at increased risk for thrombosis and hemorrhage, necessitating more careful examination and specialized treatment. This interplay between AF and valvular heart disease, and its implications for anticoagulation, has been highlighted in recent reviews [6, 7]. To inform clinical treatment, the work should stimulate prospective, lesion-stratified research.

The authors have nothing to report.

The authors have nothing to report.

The authors declare no conflicts of interest.

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来源期刊
Clinical Cardiology
Clinical Cardiology 医学-心血管系统
CiteScore
5.10
自引率
3.70%
发文量
189
审稿时长
4-8 weeks
期刊介绍: Clinical Cardiology provides a fully Gold Open Access forum for the publication of original clinical research, as well as brief reviews of diagnostic and therapeutic issues in cardiovascular medicine and cardiovascular surgery. The journal includes Clinical Investigations, Reviews, free standing editorials and commentaries, and bonus online-only content. The journal also publishes supplements, Expert Panel Discussions, sponsored clinical Reviews, Trial Designs, and Quality and Outcomes.
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