Establishing the link between a specific pathology and atrial fibrillation.
Establishing the link between a specific pathology and atrial fibrillation.
复制标题
建立特定病理学与心房颤动之间的联系。
DOI：
10.1016/s0008-6363(01)00455-2
复制
发表时间：
2001
影响因子：
10.8
通讯作者：
Schuessler,RB
中科院分区：
文献类型：
--
作者：
Schuessler,RB
参见Shi et al的文章。[5]（第217-225页）在这个问题上，Shi等人研究了心力衰竭如何引起问题。快速心室起搏，影响房颤的脆弱性[5]。同样重要的是，他们将房颤（AF）发生的变化与心力衰竭重塑中发生的变化以及正常衰老过程进行了比较。最快速的心房起搏。本文扩展了Stanley Nattel博士实验室的一项关于瓣膜和缺血性心脏病的早期研究，该研究涉及疾病、甲状腺功能亢进症、高血压和心脏病，使用快速心室起搏产生心力衰竭心肌病。不太常见的病因，但仍然很清楚[6]。他们在该研究中表明，与AF相关的AF易感性包括心脏肿瘤、心室起搏引起的各种增加而不改变炎症性疾病、异常自主神经张力和亚量级或分散的不应性。然而，这是一种滥用[1]。在过去的100年中，由于多年的房颤研究，已经清楚的是传播速度的异质性增加，这是在电生理学上增加的间质纤维化。在本研究中，他们认为有四种相互作用的基质有助于检查左心房和右心房舒张期AF的时间过程。这些基质包括：（1）过早冲动形成;（2）收缩面积以及收缩面积分数缩短复极的幅度和分布，以及快速心房起搏和起搏引起的心力衰竭。不应期;（3）心房的大小、分布和不均匀性与传播速度的不应期熵沿着相关，（4）心房的微观结构和诱发房颤的持续时间相关。在心力衰竭模型中，这些AF持续时间的相互作用取决于决定是否启动AF的因素和心房大小，而不是不应期。在快速心房维持。然而，尽管我们了解潜在的起搏动物，但它们显示出完全相反的效果，AF的病理学和机制，药理学持续时间对心房大小的依赖性很小，但AF治疗的成功率有限。部分与不应期相关。这项研究表明，这种失败是由于缺乏理解为什么它是重要的，以了解如何特定的病理学的各种病理学与电生理学的相互作用影响的基础基板AF。1995年，两项重要的治疗研究已经很清楚了。例如，如果Wijffels等人和Morillo等人的治疗策略改变了我们预防或逆转房颤重塑的设计方式[2，3]。他们证明了孤立性房颤患者的不应期，底物是动态的，特别是他们表明，你可以预期一个积极的结果。然而，如果快速心房率改变了不应性和心房大小。将其应用于心力衰竭患者，这些变化增加了心房对纤维的脆弱性-方法可能成功有限。缺乏的是什么，并导致Wijffels等人提出，“心房动物模型，为不同的临床病理。只有心房颤动才会引起心房颤动。随后，在这些模型中，我们可以跟踪研究的进展，现在已经阐明了每种底物发生的细胞离子通道变化，并测试了负责重塑电选择的治疗变化。应该谨慎使用...
See article by Shi et al.[5](pages 217–225) in this In this issue, Shi et al. examine how heart failure, caused issue. by rapid ventricular pacing, affects the vulnerability to AF [5]. Just as important, they compare the changes that occur Atrial fibrillation (AF) is associated with numerous inaheartfailuremodelwiththosethatoccurinamodelof pathologies, as well as the normal aging process. The most rapid atrial pacing. This paper extends an earlier excellent common pathologies are valvular and ischemic heart study out of the laboratory of Dr. Stanley Nattel by Li et disease, hyperthyroidism, hypertension, and car- al. using rapid ventricular pacing to produce heart failure diomyopathies. Less common etiologies, but still clearly[6]. They showed in that study that vulnerability to AF associated with AF, include cardiac tumors, various in- increased with ventricular pacing without changing the flammatory diseases, abnormal autonomic tone, and sub- magnitude or dispersion of refractoriness. However, there stance abuse [1]. What has become clear over the last 100 was an increased heterogeneity of propagation velocity due years of AF research is that at the electrophysiological to increased interstitial fibrosis. In the present study, they level there are four interacting substrates that contribute to examine the time course of left and right atrial diastolic AF. These include:(1) premature impulse formation;(2) and systolic areas as well as the fractional area shortening the magnitude and distribution of repolarization and re- during rapid atrial pacing and pacing induced heart failure. fractory period;(3) the magnitude, distribution, and aniso- They correlated these data along with the refractory period tropy of propagation velocity; and (4) the microscopic and with the duration of induced AF. They showed that the macroscopic anatomy of the atria. The interaction of these duration of AF in the heart failure model was dependent on factors determines whether or not AF will be initiated and the atrial size and not refractory period. In the rapid atrial maintained. Yet despite our knowledge of the underlying pacing animals, they showed exactly the opposite effect, pathologies and the mechanisms of AF, pharmacological with little dependence of duration on atrial size, but with a treatments for AF have met with limited success. In part, correlation with refractory period. This study demonstrates this failure is due to a lack of understanding of how why it is important to understand how specific pathologies various pathologies interact with the electrophysiological affect the underlying substrates for AF. Implications for substrates. In 1995, two important studies appeared by therapy are clear. As an example, if a treatment strategy Wijffels et al. and Morillo et al. that changed how we were designed for preventing or reversing the remodeling thought about AF [2, 3]. They demonstrated that these of refractory period in a patient with lone atrial fibrillation, substrates were dynamic, and in particular they showed then you could anticipate a positive outcome. However, if that rapid atrial rate altered refractoriness and atrial size. it were applied to a patient with heart failure, the same These changes increased the atrial vulnerability to fibrilla- approach may have limited success. What is lacking are tion and lead Wijffels et al. to propose that ‘atrial animal models for different clinical pathologies. It is only fibrillation begets atrial fibrillation’. Subsequently, numer- in these models that we can follow the evolution of the ous studies have now elucidated the cellular ion channel changes that occur with each substrate and test therapeutic changes that are responsible for remodeling the electro- options. Caution should be used …