Boriani Giuseppe, Gerra Luigi, Mantovani Marta, Tartaglia Enrico, Mei Davide A, Imberti Jacopo F, Vitolo Marco, Bonini Niccolò
Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy.
Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy.
Eur J Intern Med. 2023 Oct 26. doi: 10.1016/j.ejim.2023.10.023.
Since 1995, the concept of atrial cardiomyopathy (ACM) has been associated with myocardial fibrosis. Despite a consensus document in 2016, ACM's definition primarily relies on histopathological findings. The focus on diagnostic criteria for ACM is driven by the potential link to thromboembolic events even independently on atrial fibrillation (AF). The complexity of the mutual relationships between ACM and AF makes difficult any assessment of the thromboembolic risk associated to ACM per se. ACM's thrombogenicity is a multifaceted clinical phenomenon involving electrical, functional, and structural modifications. Factors such as cardiovascular risk factors (e.g., hypertension), common cardiac comorbidities (e.g., heart failure), and extracardiac conditions (e.g., neuromuscular disorders) can promote atrial derangement, triggering atrial fibrillation (AF) and increasing the risk of thromboembolic events. Several diagnostic methods are available to detect the key features of ACM, including electrical changes assessed by surface and intracavitary ECG, and structural and functional alterations evaluated through echocardiography and cardiac magnetic resonance (CMR). These methods can be complemented by electro-anatomical mapping (EAM) to enhance the accuracy of myocardial tissue characterization and assessment of atrial fibrosis. Although certain clinical conditions (e.g., atrial high-rate episodes, AHREs; embolic stroke of undetermined source, ESUS) often exhibit atrial alterations in their thromboembolic presentations, recent randomized trials have failed to demonstrate the benefits of oral anticoagulation in patients with ACM without AF. However, ACM constitutes the substrate for the development of AF, as proposed in the AF European guidelines under the 4S-AF scheme. This review emphasizes the lack of a diagnostic gold standard and the need for clinical criteria for ACM, aiming to better understand the potential therapeutic implications of atrial structural and functional derangements, even in the absence of clinical evidence of AF.
自1995年以来，心房心肌病（ACM）的概念一直与心肌纤维化相关。尽管在2016年有一份共识文件，但ACM的定义主要依赖于组织病理学发现。对ACM诊断标准的关注是由其与血栓栓塞事件的潜在联系驱动的，即使独立于心房颤动（AF）也是如此。ACM和AF之间相互关系的复杂性使得难以评估与ACM本身相关的血栓栓塞风险。ACM的血栓形成性是一种多方面的临床现象，涉及电、功能和结构改变。心血管危险因素（如高血压）、常见心脏合并症（如心力衰竭）和心外疾病（如神经肌肉疾病）等因素可促进心房紊乱，引发心房颤动（AF）并增加血栓栓塞事件的风险。有几种诊断方法可用于检测ACM的关键特征，包括通过体表和心腔内心电图评估的电变化，以及通过超声心动图和心脏磁共振（CMR）评估的结构和功能改变。这些方法可以通过电解剖标测（EAM）来补充，以提高心肌组织特征描述和心房纤维化评估的准确性。尽管某些临床情况（如心房高频率发作，AHREs；不明来源的栓塞性卒中，ESUS）在其血栓栓塞表现中常出现心房改变，但最近的随机试验未能证明在没有AF的ACM患者中口服抗凝治疗的益处。然而，正如欧洲AF指南在4S-AF方案中所提出的，ACM构成了AF发生发展的基础。本综述强调了缺乏诊断金标准以及对ACM临床标准的需求，旨在更好地理解心房结构和功能紊乱的潜在治疗意义，即使在没有AF临床证据的情况下也是如此。
