Atrial fibrillation: the mother rotor and its rebellious offspring take turns sustaining the family.
Atrial fibrillation: the mother rotor and its rebellious offspring take turns sustaining the family.
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心房颤动：母亲转子及其叛逆的后代轮流维持家庭。
DOI：
10.1016/j.hrthm.2009.04.019
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发表时间：
2009
期刊：
影响因子：
5.5
通讯作者：
Valderrábano,Miguel
中科院分区：
文献类型：
--
作者：
Valderrábano,Miguel
我们对心房颤动(房颤)的机制缺乏了解是令人羞愧的。尽管经过几十年的积极研究已经获得了有价值的见解，但它是由重返大气层还是焦点活动引起的这个简单的问题仍然没有得到回答，即使我们试图仅仅从相对的角度来这样做。一个多世纪前，温特伯格提出房颤是多个异位病灶的结果。1十年后，单个快速放电部位可导致房颤的想法被Scherf2和普林兹金属3证实，他们指出，局部注射乌头碱(一种钠通道开放剂)可在注射部位产生快速、规则的焦点激活，但全球心房颤动激活模式。然而，当Moe和Abildskov4，5提出多子波假说时，人们接受了房颤是由传播在异质心房组织上的自持激活子波引起的。事实上，标测研究能够证明这样的多个子波，6并且人们接受了至少需要4-6个子波才能维持房颤。然而，Allessie等人之前也证明了在没有解剖底物的情况下，心房有功能折返，8这支持了折返--根据定义，一个自我维持的过程--可能是房颤永久存在的机制的想法。像再入这样的周期性现象怎么可能是像房颤这样的混沌和非周期性现象的基础呢？快速激活转子可能会导致全球纤颤激活模式，如果漂移，9或如果来自转子的激活不能1：1传导到邻近组织。这种所谓的纤颤传导已被证明是由解剖学上确定的位置，如梳状肌的波破裂引起的。10支持相对稳定的转子，因为房颤的引擎来自Jalife实验室的一系列工作，显示出快速的局部周期性11和左心房的折返12，导致在持续房颤期间从左到右的稳定频率梯度13。左房折返发生在肺静脉附近的倾向也很明显：Arora等人14显示了这种局部折返的详细光学标测，Chen的研究小组强调了该区域复杂的潜在组织学模式(包括马歇尔韧带)，这可能导致折返，15这是SPACH几十年前预测的一个概念16，似乎也与室颤有关。17在临床领域，局灶性放电作为房颤的原因得到了巨大的支持，Haissaguerre等人的开创性发现是来自肺静脉的异位搏动引发了房颤。在机制上，在钙超载的情况下，触发房颤的焦点搏动是由电生性钠/钙交换引起的。19、20
Our poor understanding of the mechanisms of atrial fibrillation (AF) is humbling. Although valuable insights have been gained after decades of active research, the simple question of whether it is caused by reentry or focal activity remains unanswered, even if we tried to do so just in relative terms. More than a century ago, Winterberg suggested that AF was the consequence of multiple ectopic foci. 1 Decades later, the idea that a single rapid-firing site could lead to AF was proven by Scherf2 and Prinzmetal, 3 who showed that focal injection of aconitine (a sodium channel opener) produced rapid regular focal activations at the injection site, but global atrial fibrillatory activation patterns. However, when Moe and Abildskov4, 5 proposed the multiple wavelet hypothesis, it became accepted that AF was caused by selfperpetuating activation wavelets that propagated on heterogeneous atrial tissue. Indeed, mapping studies were able to demonstrate such multiple wavelets, 6 and it became accepted that a minimum of 4–6 wavelets were required to sustain AF. 7However, Allessie et al had also previously demonstrated functional reentry in the atrium in the absence of an anatomical substrate, 8 which supported the idea that reentry–by definition a self-sustainable process-could underlie the mechanisms of perpetuation of AF. How could a periodic phenomenon such as reentry underlie a chaotic and aperiodic one such as AF? Rapidly activating rotors may lead to global fibrillatory activation patterns if drifting, 9 or if activations stemming from the rotor fail to conduct 1: 1 to neighboring tissues. This so-called fibrillatory conduction has been shown to be caused by wavebreak in anatomically-determined locations, such as pectinate muscles. 10 Support for relatively stable rotors as the engine of AF came from a series of works from Jalife’s laboratory, showing fast, local periodicity11 and reentry in the left atrium12 that led to stable left-to-right frequency gradients13 during sustained AF. A predilection for left atrial reentry to occur in the neighborhood of the pulmonary veins was also evident: Arora et al14 showed detailed optical mapping of such local reentry, and Chen’s group emphasized the complex underlying histological patterns in this region (including the ligament of Marshall), that could lead to reentry, 15 a concept that had been predicted by Spach decades earlier16 and that seems to be relevant in ventricular fibrillation as well. 17 In the clinical realm, the concept of focal discharges as a cause of AF got enormous support with Haissaguerre et al’s seminal finding that ectopic beats from the pulmonary veins initiated AF. 18 Mechanistically, focal beats triggering AF were shown to arise from electrogenic sodium/calcium exchange in situations of calcium overload. 19, 20