心脏磁共振成像(MRI)显示,未确定来源(ESUS)患者的栓塞性中风中的纤维化与心房颤动(AFib)中的水平相当。我们使用计算模型来了解ESUS中不存在心律失常,尽管存在推定的致心律失常纤维化。对45例ESUS和45例AFib患者重建了基于MRI的心房模型。计算评估每位患者的纤维化基质致心律失常能力。在24/45(53%)ESUS和22/45(49%)AFib模型中诱导了折返驱动。诱导模型比非诱导模型(11.07±3.61%;p<0.0001)有更多的纤维化(16.7±5.45%);然而,ESUS和AFib模型的可诱导亚群具有相似的纤维化水平(p=0.90),这意味着ESUS和AFib中纤维化的内在致心律失常底物特性是无法区分的。这表明一些ESUS患者具有潜在的临床前纤维化底物,这可能是心律失常的未来来源。因此,我们的工作提示了这样一个假设,即有纤维化心房的ESUS患者由于没有心律失常触发因素而免于AFib治疗.
心脏通常以规律的节奏跳动,将携带氧气和营养物质的血液泵送到不同的器官。有时候,可以发生称为心律失常的心律改变。心房颤动,也被称为AFib,是一种心律失常,心脏跳动迅速而不规则,导致异常血流,导致血凝块的形成。如果这些血凝块之一进入大脑,它可以阻塞血管,导致中风。然而,许多中风的发生没有任何AFib的证据。与AFib无关的卒中的一个子集是未确定来源的栓塞性卒中(ESUS)。占所有中风的25%。根据定义,ESUS和AFib不会一起发生,但两者都与疾病相关的重塑水平相似(即,纤维化)在心脏组织中,当心脏受伤时就会出现。纤维化损害心脏的正常电活动。Bifulco等人。我们希望确定AFib患者和发生ESUS事件的患者之间在纤维化方面是否存在一些根本差异。要做到这一点,他们使用一种计算方法对45例ESUS患者和45例AFib患者的心脏纤维化的几何形状和模式进行建模,本质上是每个病人心脏的虚拟版本。Bifulco等人。然后将虚拟起搏器(在超速模式下工作)应用于每个心脏模型,以确定可能导致AFib的电输入是否对ESUS和AFib患者有不同的影响.结果表明,电输入在所有心脏模型中都具有相似的效果。这导致了Bifulco等人。得出结论,ESUS和AFib患者有难以区分的纤维化模式。关键的区别在于ESUS患者缺少启动纤颤过程的触发因素-如果心房纤维化是前庭的火药盒,这些触发器是点火所需的火花。进一步研究,包括Bifulco等人的确认。在活的病人身上的发现,将需要确认以下假设:ESUS患者缺乏AFib主要是由于缺乏触发因素。如果真是这样,这些发现可能更容易识别AFib或进一步卒中风险较高的ESUS患者.此外,更好地理解纤维化作为卒中和AFib之间的联系将有助于临床医生提供更好的,更多个性化治疗,例如指导患者是否应该服用血液稀释剂或接受更严格的心脏监测。
Cardiac magnetic resonance imaging (MRI) has revealed fibrosis in embolic stroke of undetermined source (ESUS) patients comparable to levels seen in atrial fibrillation (AFib). We used computational modeling to understand the absence of arrhythmia in ESUS despite the presence of putatively pro-arrhythmic fibrosis. MRI-based atrial models were reconstructed for 45 ESUS and 45 AFib patients. The fibrotic substrate\'s arrhythmogenic capacity in each patient was assessed computationally. Reentrant drivers were induced in 24/45 (53%) ESUS and 22/45 (49%) AFib models. Inducible models had more fibrosis (16.7 ± 5.45%) than non-inducible models (11.07 ± 3.61%; p<0.0001); however, inducible subsets of ESUS and AFib models had similar fibrosis levels (p=0.90), meaning that the intrinsic pro-arrhythmic substrate properties of fibrosis in ESUS and AFib are indistinguishable. This suggests that some ESUS patients have latent pre-clinical fibrotic substrate that could be a future source of arrhythmogenicity. Thus, our work prompts the hypothesis that ESUS patients with fibrotic atria are spared from AFib due to an absence of arrhythmia triggers.
The heart usually beats with a regular rhythm to pump the blood that carries oxygen and nutrients to different organs. Sometimes, alterations in the heart’s rhythm known as arrhythmias can occur. Atrial fibrillation, also called AFib, is a type of arrhythmia in which the heart beats rapidly and irregularly, causing abnormal blood-flow that can lead to the formation of blood clots. If one of these blood clots travels to the brain, it can block a blood vessel, causing a stroke. However, many strokes occur without any evidence of AFib. One subset of strokes that are not associated with AFib are embolic strokes of undetermined source (ESUS), which account for 25% of all strokes. By definition ESUS and AFib do not occur together, but both are associated with similar elevated levels of disease-related remodeling (i.e., fibrosis) in the heart tissue, which appears when the heart is injured. Fibrosis impairs the heart’s normal electrical activity. Bifulco et al. wanted to determine whether there is some fundamental difference in fibrosis between people with AFib and those who have had an ESUS event. To do this, they used a computational approach to model the geometries and patterns of fibrosis of the hearts of 45 ESUS patients and 45 patients with AFib, essentially producing a virtual version of each patient’s heart. Bifulco et al. then applied a virtual pace-maker (working in overdrive mode) to each heart model to determine whether electrical inputs that can lead to AFib had different effects on ESUS and AFib patients. The results showed that the electrical inputs had similar effects in all of the heart models. This led Bifulco et al. to conclude that ESUS and AFib patients have indistinguishable patterns of fibrosis. The key difference is that ESUS patients are missing the trigger to initiate the fibrillation process – if atrial fibrosis is the proverbial tinderbox, these triggers are the spark needed to ignite a fire. Further research, including confirmation of Bifulco et al.’s findings in live patients, will be needed to confirm the hypothesis that ESUS patients lack AFib primarily due to an absence of triggers. If this is indeed the case, these findings may make it easier to identify ESUS patients at higher risk for AFib or further strokes. Additionally, a better understanding of fibrosis as a link between stroke and AFib will help clinicians provide better, more personalized treatments, for example guiding whether a patient should take blood thinners or undergo more rigorous cardiac monitoring.