<p>We read with interest the recent article by Deng et al., which explored the association between renal function and left atrial low-voltage area (LVA) burden in patients with atrial fibrillation (Deng et al. <span>2025</span>). The authors report increased LVA prevalence among individuals with reduced estimated glomerular filtration rate (eGFR), suggesting a link between renal dysfunction and atrial substrate remodeling. Although the research addresses an important clinical question, several methodological considerations limit the strength of the conclusions.</p><p>A primary issue concerns the heterogeneity and intrinsic variability of bipolar voltage mapping. Voltage measurements are highly sensitive to catheter contact, mapping density, electrode configuration, and rhythm status during acquisition. The study does not clarify mapping stability parameters or point density across participants, factors known to influence LVA quantification and potentially introduce systematic misclassification (Huang et al. <span>2022</span>). Without standardized acquisition protocols, observed differences in LVA burden may partly reflect procedural variability rather than true substrate differences.</p><p>Another limitation arises from the distribution of renal function within the cohort. Only a small minority of subjects appear to have eGFR values in ranges typically associated with structural atrial remodeling. Prior studies have demonstrated that meaningful electrophysiologic atrial alterations are most evident in moderate-to-severe renal impairment, rather than in mild reductions of eGFR (Lee et al. <span>2021</span>). The limited representation of lower renal-function strata raises concerns regarding statistical power and the generalizability of the renal–atrial substrate association.</p><p>The multivariable models also may not sufficiently account for confounders that influence atrial fibrosis and LVA burden. Duration of atrial fibrillation, left atrial volume, hypertension severity, glycemic status, and systemic inflammatory markers are independently associated with voltage reduction and may overlap mechanistically with renal dysfunction. Omitting several of these parameters risks attributing substrate differences to renal function while partially reflecting unmeasured cardiac and metabolic remodeling pathways (Karakasis et al. <span>2024</span>).</p><p>Finally, the causal interpretability of the findings warrants caution. Atrial LVA represents a complex composite of fibrosis, anisotropy, and conduction heterogeneity, whereas renal dysfunction reflects systemic microvascular, neurohormonal, and inflammatory alterations. Although these processes may coexist, current evidence supports correlation rather than directional causality. The study would benefit from integration of imaging-based fibrosis quantification or biomarkers of extracellular matrix turnover to substantiate mechanistic claims (Pegoraro et al. <span>2025</span>). As it stands, the prognostic
我们饶有兴趣地阅读了Deng等人最近发表的一篇文章,该文章探讨了房颤患者肾功能与左房低压区(LVA)负担之间的关系(Deng et al. 2025)。作者报告肾小球滤过率(eGFR)降低的个体中LVA患病率增加,提示肾功能障碍与心房底物重塑之间存在联系。虽然这项研究解决了一个重要的临床问题,但一些方法学上的考虑限制了结论的强度。一个主要问题涉及双极电压映射的异质性和内在可变性。电压测量对导管接触、测绘密度、电极配置和采集期间的节律状态高度敏感。该研究没有阐明映射稳定性参数或参与者之间的点密度,已知影响LVA量化的因素,并可能引入系统的错误分类(Huang et al. 2022)。如果没有标准化的获取协议,观察到的LVA负担差异可能部分反映了程序的可变性,而不是真正的底物差异。另一个限制来自于队列中肾功能的分布。只有少数受试者的eGFR值出现在与结构性心房重构典型相关的范围内。先前的研究表明,有意义的心房电生理性改变在中度至重度肾功能损害中最为明显,而不是在轻度eGFR降低中(Lee et al. 2021)。较低肾功能层的有限代表性引起了对统计能力和肾-心房底物关联的普遍性的关注。多变量模型也可能不能充分考虑影响心房纤维化和LVA负担的混杂因素。房颤持续时间、左房容积、高血压严重程度、血糖状态和全身炎症标志物与电压降低独立相关,并可能与肾功能障碍有重叠机制。忽略这些参数有可能将底物差异归因于肾功能,同时部分反映了未测量的心脏和代谢重塑途径(Karakasis et al. 2024)。最后,研究结果的因果可解释性值得谨慎。心房LVA是纤维化、各向异性和传导异质性的复杂组合,而肾功能障碍反映了全身微血管、神经激素和炎症的改变。虽然这些过程可能共存,但目前的证据支持相关性而不是定向因果关系。该研究将受益于基于成像的纤维化量化或细胞外基质转换的生物标志物的整合,以证实机制主张(Pegoraro等人,2025)。目前,肾功能对基底引导消融策略的预后影响仍不确定。所有的作者都参与了计划、写作和修订。作者没有什么可报告的。作者声明无利益冲突。数据共享不适用于本文,因为在本研究中没有生成或分析数据集。
{"title":"Renal Function and Atrial Remodeling: Interpreting Voltage-Mapping Limitations","authors":"Mücahit Aker, Macit Kalçık, Lütfü Bekar","doi":"10.1111/anec.70144","DOIUrl":"10.1111/anec.70144","url":null,"abstract":"<p>We read with interest the recent article by Deng et al., which explored the association between renal function and left atrial low-voltage area (LVA) burden in patients with atrial fibrillation (Deng et al. <span>2025</span>). The authors report increased LVA prevalence among individuals with reduced estimated glomerular filtration rate (eGFR), suggesting a link between renal dysfunction and atrial substrate remodeling. Although the research addresses an important clinical question, several methodological considerations limit the strength of the conclusions.</p><p>A primary issue concerns the heterogeneity and intrinsic variability of bipolar voltage mapping. Voltage measurements are highly sensitive to catheter contact, mapping density, electrode configuration, and rhythm status during acquisition. The study does not clarify mapping stability parameters or point density across participants, factors known to influence LVA quantification and potentially introduce systematic misclassification (Huang et al. <span>2022</span>). Without standardized acquisition protocols, observed differences in LVA burden may partly reflect procedural variability rather than true substrate differences.</p><p>Another limitation arises from the distribution of renal function within the cohort. Only a small minority of subjects appear to have eGFR values in ranges typically associated with structural atrial remodeling. Prior studies have demonstrated that meaningful electrophysiologic atrial alterations are most evident in moderate-to-severe renal impairment, rather than in mild reductions of eGFR (Lee et al. <span>2021</span>). The limited representation of lower renal-function strata raises concerns regarding statistical power and the generalizability of the renal–atrial substrate association.</p><p>The multivariable models also may not sufficiently account for confounders that influence atrial fibrosis and LVA burden. Duration of atrial fibrillation, left atrial volume, hypertension severity, glycemic status, and systemic inflammatory markers are independently associated with voltage reduction and may overlap mechanistically with renal dysfunction. Omitting several of these parameters risks attributing substrate differences to renal function while partially reflecting unmeasured cardiac and metabolic remodeling pathways (Karakasis et al. <span>2024</span>).</p><p>Finally, the causal interpretability of the findings warrants caution. Atrial LVA represents a complex composite of fibrosis, anisotropy, and conduction heterogeneity, whereas renal dysfunction reflects systemic microvascular, neurohormonal, and inflammatory alterations. Although these processes may coexist, current evidence supports correlation rather than directional causality. The study would benefit from integration of imaging-based fibrosis quantification or biomarkers of extracellular matrix turnover to substantiate mechanistic claims (Pegoraro et al. <span>2025</span>). As it stands, the prognostic","PeriodicalId":8074,"journal":{"name":"Annals of Noninvasive Electrocardiology","volume":"31 1","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12719601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}