栓子源不明的栓塞性卒中的二级预防

栓子源不明的栓塞性卒中(embolic stroke of undetermined source, ESUS)的常用二级预防方案为抗血小板治疗。然而,ESUS的栓塞来源具有极大的异质性,抗栓治疗的效果不尽相同。文章阐述了ESUS的病因及二级预防研究进展,以期为临床诊疗提供参考。     

心房心肌病和栓塞性卒中的研究进展

心房颤动(简称房颤)是最常见的可持续性心律失常。近年来, 随着心房心肌病概念的提出, 房颤以外的卒中风险因素得到广泛关注, 房颤可能不是卒中的根本原因, 而是心房病变的外在表现。该文从心房心肌病的概念、与房颤的关系、与栓塞性卒中的关系以及这类患者的卒中预防等方面进行介绍。     

瓣膜性房颤血栓栓塞事件的危险因素和CHA2DS2-VASc评分对其血栓栓塞事件的预测价值

目的 分析瓣膜性房颤患者血栓栓塞危险因素和CHA2DS2-VASc评分对其血栓栓塞事件预测价值。 方法 纳入2016年9月至2019年9月就诊于本院的瓣膜性房颤患者137例,按是否发生血栓栓塞事件分为栓塞组（n=50)与非栓塞组（n=87),在单因素分析基础上,进行多因素logistic回归分析判定血栓栓塞危险因素,并进行Cochran-Armitage趋势检验判断CHA2DS2-VASc评分与血栓栓塞是否存在线性趋势,制作ROC曲线,判定曲线下面积和截断点,并计算评价指标。 结果 研究组年龄≥75岁占比、女性患者占比、高血压、糖尿病、心衰患病率与对照组差异均无统计学意义,而两组间血管疾病患病率及CHA2DS2-VASc评分差异均有统计学意义（P<0.01）。多因素回归分析显示,血管疾病（OR: 7.463,95%CI 1.575-35.714,P<0.05）是卒中/TIA/血栓栓塞发生的独立危险因素;在控制其他变量后,CHA2DS2-VASc评分与卒中/TIA/血栓栓塞事件显著相关（OR: 2.688,95%CI: 1.776-4.065,P<0.01）及对栓塞事件预测的ROC曲线下面积为0.869（95%CI: 0.809-0.928,P<0.01）。Cochran-Armitage趋势检验显示CHA2DS2-VASc评分与卒中/TIA/血栓栓塞间存在线性趋势,卒中/TIA/血栓栓塞发生率随着CHA2DS2-VASc评分升高而升高（P<0.01）。 结论 血管疾病是瓣膜性房颤血栓栓塞事件发生的独立危险因素;CHA2DS2-VASc评分与此类患者血栓栓塞事件发生显著相关且对其预测价值较好。     

肥厚型心肌病合并心房颤动患者血栓栓塞的预测与防治

心房颤动（房颤）是肥厚型心肌病（HCM）患者最常合并的一种心律失常,合并房颤的HCM患者发生血栓栓塞的风险较高,而血栓栓塞也是导致此类患者死亡的主要原因。目前尚缺乏关于HCM合并房颤患者血栓栓塞风险的有效的预测模型或评分系统。在血栓栓塞防治方面,抗凝药物治疗是目前认为唯一的可有效降低HCM合并房颤患者血栓栓塞风险的方法...     

左心耳结构与心房颤动卒中的关系

心房颤动患者发生卒中的血栓来源,一是左心耳,二是动脉性疾病,如主动脉弓、颈动脉或颅内动脉疾病等。而大部分心房颤动卒中均与左房血栓有关,90%的非瓣膜性心房颤动颅内血栓来源于左心耳。目前,左心耳封堵术是预防左心耳血栓形成及脱落栓塞的重要治疗手段,因此认识左心耳结构及功能、左心耳与心房颤动卒中的关系、左心耳封堵术的有效性及安全性至关重要。本文将对左心耳相关问题进行阐述。     

扩张型心肌病合并左心室血栓的研究进展

<正>左心室血栓形成是扩张型心肌病的严重并发症之一，栓子脱落可引发卒中或体循环栓塞而产生不良后果。左心室血栓的诊断、危险因素识别、预防和治疗在临床诊疗中尤为重要。本文对扩张型心肌病合并左心室血栓形成的研究现状和最新进展做一综述。扩张型心肌病是一类表现为心腔扩大、心脏收缩力下降、心力衰竭、心律失常和血栓栓塞的异质性心肌病。左心室血栓形成是扩张型心肌病的常见严重并发症，血栓脱落可导致脑、肾和肢体动脉栓塞，增加致残和死亡风险。现对扩张型心肌病合并左心室血栓形成的发生机制、危险因素、预防和治疗进展做一综述。     

栓子源不明的栓塞性卒中的病因学

隐源性卒中是指虽经全面筛查仍未明确病因的缺血性卒中.研究显示,大部分隐源性卒中为栓塞性.近年来,有学者提出将栓子源不明的栓塞性卒中作为一种新的卒中亚型,并将其定义为除外颅内外血管狭窄和主要心源性栓子来源的非腔隙性缺血性卒中,有望为隐源性卒中的诊治提供新的思路.文章就其可能的潜在病因,例如低危心源性栓塞、反常性栓塞、非狭窄性易损斑块等进行了综述.     

新型口服抗凝药物在老年非瓣膜性心房颤动患者抗凝治疗中的作用

心房颤动（房颤）是临床上常见的快速性心律失常,是卒中和栓塞的独立危险因素。大多数非瓣膜性房颤患者超过65岁,对老年房颤患者行抗凝治疗可有效预防血栓栓塞事件,降低患者的致残率和致死率。目前指南推荐老年房颤患者使用新型口服抗凝药,该文介绍老年房颤患者抗凝治疗选择。     

心房心肌病与心房颤动：病与症的纠葛

近年来心房心肌病的概念引起重视, 以心房电重构、解剖重构、功能障碍、心房纤维化、血液高凝状态为主要特点, 常与心房颤动(房颤)同时存在, 明显增加血栓栓塞风险。房颤与心房心肌病具有共同的危险因素和病理生理过程, 相互促进、互为病症, 是"一枚硬币的两面"。心房心肌病可能是房颤患者血栓形成的主要原因。心房纤维化作为心房心肌病的主要表现之一, 可通过延迟增强核磁显像技术评价, 并对评估房颤血栓风险及射频消融手术成功率具有重要价值。针对房颤、心房心肌病的上游治疗及危险因素控制有望改善患者的预后。     

心房高频事件研究进展

心房高频事件（atrial high-rate episodes,AHRE）是指通过心脏植入式电子装置（cardiac implantable electronic device,CIED）检测到的无症状的快速房性心律失常,在无心房颤动诊断的老年患者中检测到AHRE的比例为10%～30%。AHRE与卒中、血栓栓塞等严重并发症的风险增加有关。目前对于AHRE的临床意义及是否需长期抗凝等问题尚未完全明确。本文综述了AHRE的流行病学特征、危险因素和预测因子,并介绍了AHRE的处理方法。     

Atrial fibrillation: A progressive atrial myopathy or a distinct disease?

Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance. However, the exact pathophysiological mechanisms of atrial fibrillation are not completely understood and whether atrial fibrillation is an unclassified cardiomyopathy or a distinct disease still remains to be answered. This review highlights proarrhythmic and pathophysiological mechanisms of atrial fibrillation and approaches the molecular basis underlying atrial fibrillation susceptibility.     

Embolic Stroke of Undetermined Source: Current Perspectives on Diagnosis,Investigations, and Management

In 2014, Hart et al. introduced the concept of “embolic stroke of undetermined source” (ESUS) to the clinical-research stroke community. The hypothesis underlying the development of the ESUS construct was that this potentially heterogenous group of stroke mechanisms were largely thromboembolic, and would thus benefit from anticoagulation over antiplatelet for secondary prevention. Since then, 2 large clinical trials have shown that, to date, there is not a clear uniform antithrombotic strategy for secondary prevention after ESUS as it was originally broadly defined. However, this work has yielded valuable information about the patient phenotypes that experience ESUS strokes, as well as hypothesis-generating substudies that have given rise to the next generation of secondary prevention trials aimed at more personalized approaches for different suspected mechanisms of embolic stroke. In parallel with the evolution of ESUS, several studies aimed at screening for atrial fibrillation in the secondary stroke prevention population have generated additional questions about the mechanistic relevance of atrial fibrillation detected after stroke, and how this should inform poststroke workup, and secondary prevention strategies. Herein, we provide a synthesis of the current understanding surrounding the patient phenotypes that experience ESUS strokes, and previous, ongoing, and anticipated clinical trials that will guide earlier and later secondary prevention strategies and poststroke cardiac investigations.     

Long-Term Cardiac Monitoring After Embolic Stroke of Undetermined Source: Search Longer,Look Harder

Embolic stroke of undetermined source (ESUS) represents a heterogeneous subgroup of patients with cryptogenic stroke, in which despite an extensive diagnostic workup the cause of stroke remains uncertain. Identifying covert atrial fibrillation among patients with ESUS remains challenging. The increasing use of cardiac implanted electronic devices (CIED), such as pacemakers, implantable defibrillators, and implantable loop recorders (ILR), has provided important information on the burden of subclinical atrial fibrillation. Accumulating evidence indicate that long-term continuous monitoring, especially in selected patients with ESUS, significantly increases the possibility of atrial fibrillation detection, suggesting it may be a cost-effective tool in secondary stroke prevention. This review summarizes available evidence related to the use of long-term cardiac monitoring and the use of implantable cardiac monitoring devices in patients with ESUS.     

Structural remodelling during chronic atrial fibrillation: act of programmed cell survival

Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes and chromatin redistribution. The absence of clear signs of degeneration in these models points towards cardiomyocyte adaptation or a mechanism of programmed cell survival. In patients with atrial fibrillation cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.     

脂联素在心房颤动中的保护作用及其研究进展

心房颤动是临床实践中最常见的心律失常。目前确切机制仍不清楚,病理生理机制复杂,且诸多可能的机制相互关联。近年来发现脂联素与心房颤动的发生及维持密切相关。由于脂联素具有减轻体重、逆转心肌重构、增强胰岛素敏感性、抗炎、抗动脉粥样硬化、抗高血压、保护血管内皮功能等作用。因此对心房颤动的保护作用具有巨大的潜力。     

Atrial remodeling in atrial fibrillation and some related microRNAs

Atrial fibrillation is the most common sustained arrhythmia associated with substantial cardiovascular morbidity and mortality, with stroke being the most critical complication. The role of atrial remodeling has emerged as the new pathophysiological mechanism of atrial fibrillation. Electrical remodeling and structural remodeling will increase the probability of generating multiple atrial wavelets by enabling rapid atrial activation and dispersion of refractoriness. MicroRNAs (miRNAs) are small non-coding RNAs of 20-25 nucleotides in length that regulate expression of target genes through sequence-specific hybridization to the 3' untranslated region of messenger RNAs and either block translation or direct degradation of their target messenger RNA. They have also been implicated in a variety of pathological conditions, such as arrhythmogenesis and atrial fibrillation. Target genes of miRNAs have the potential to affect atrial fibrillation vulnerability.     

Dementia and Atrial Fibrillation: Pathophysiological Mechanisms and Therapeutic Implications

Atrial fibrillation increases the risk of stroke by a factor of four- to fivefold, and dementia is a common consequence of stroke. However, atrial fibrillation has been associated with cognitive impairment and dementia, even in patients without prior overt stroke. Nonischemic mechanisms include cerebral hypoperfusion, vascular inflammation, brain atrophy, genetic factors, and shared risk factors such as age or hypertension. Critical appraisal of studies evaluating the association between atrial fibrillation and dementia in stroke-free patients reveals that several suffer from methodological issues, such as not including silent stroke or anticoagulation therapy in multivariate analyses. Some studies show a close relationship between atrial fibrillation and dementia due to silent stroke, in the absence of overt stroke. Evidence is accumulating that anticoagulation may be effective to decrease the risk of dementia in atrial fibrillation patients. Overall, the pathogenesis linking atrial fibrillation to dementia is likely multifactorial. Cerebral infarctions, including silent stroke, play a central role. These findings underscore the importance of stroke prevention measures in atrial fibrillation patients.     

Anti-thrombotic strategies for patients with atrial fibrillation and heart failure

Atrial fibrillation occurs commonly in the setting of congestive heart failure and, in fact can cause left ventricular dysfunction due to a rapid ventricular response over time, termed tachycardia-mediated cardiomyopathy. The combination of atrial fibrillation and congestive heart failure leads to a high risk of stroke for the patient and appropriate antithrombotic therapy can minimize this incidence of stroke. Stroke risk can be markedly reduced by treatment with warfarin and complications of anticoagulation minimized by close attention to maintaining the INR between 2.0 and 3.0.     

Lessons from the Stroke Prevention in Atrial Fibrillation trials

Atrial fibrillation predisposes to left atrial thrombus formation and carries a sixfold increased risk for stroke. Antithrombotic therapies are the mainstay for stroke prevention. The National Institute of Neurological Disorders and Stroke-sponsored Stroke Prevention in Atrial Fibrillation (SPAF) studies assessed the value of warfarin, aspirin, and their combination for preventing stroke in six multicenter trials involving 3950 participants. This review presents the major results and implications, which offer unique perspectives on antithrombotic therapies for stroke prevention in atrial fibrillation. Warfarin and aspirin reduce stroke. Anticoagulation substantially benefits high-risk patients with atrial fibrillation, while many younger patients with atrial fibrillation have a low stroke rate when given aspirin. Pathogenetic and transesophageal echocardiographic correlations shed light on mechanisms by which antithrombotic agents prevent stroke. Warfarin inhibits formation of atrial appendage thrombi and markedly reduces cardioembolic strokes, while aspirin primarily prevents smaller, noncardioembolic strokes. The SPAF III stroke risk stratification scheme has been validated for identifying patients with high versus moderate versus low risk for stroke. Women with atrial fibrillation benefit from anticoagulation significantly more than men do. Many elderly patients with recurrent paroxysmal atrial fibrillation have high rates of stroke. Antithrombotic prophylaxis should be individualized on the basis of the estimated risk for stroke during aspirin therapy and the risk for bleeding during anticoagulation. Overall, nearly one third of patients with atrial fibrillation are low risk and should be treated with aspirin, and about one third are high risk and should receive warfarin if it can be given safely. For patients at moderate risk for stroke, patient preferences and access to reliable anticoagulation monitoring are particularly relevant.     

Postprandial hyperglycemia is a possible contributor to paroxysmal atrial fibrillation: a case report

Atrial fibrillation, a major risk factor for stroke, is believed to occur first as paroxysmal episodes, gradually becoming more persistent, and finally progressing to chronic atrial fibrillation. Treatment of paroxysmal atrial fibrillation is an important target to prevent chronic atrial fibrillation. We describe a very unique case with postprandial hyperglycemia and obesity associated with drug-refractory paroxysmal atrial fibrillation. A 73-year-old Japanese woman with postprandial hyperglycemia suffered from drug-refractory paroxysmal atrial fibrillation. A 1600 kcal/day diet and walking three times/day for more than 30 min eliminated paroxysmal atrial fibrillation after 6 months. Diet and exercise should be considered as the initial therapy in patients with paroxysmal atrial fibrillation who also have postprandial hyperglycemia. This case suggests that postprandial hyperglycemia and insulin resistance might be one of the possible underlying mechanisms of paroxysmal atrial fibrillation.