Chronic total occlusion of infarct-related artery: A bystander or a risk factor of electrical storm?
Chronic total occlusion of infarct-related artery: A bystander or a risk factor of electrical storm?
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梗塞相关动脉慢性完全闭塞：旁观者还是雷暴的危险因素？
DOI：
10.1016/j.ijcard.2022.04.016
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发表时间：
2022
影响因子：
3.5
通讯作者：
Dobrev Dobromir
中科院分区：
文献类型：
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作者：
Tsuji Yukiomi;Dobrev Dobromir
电风暴（ES）通常定义为24 h内≥ 3次室性心动过速/心室颤动（VT/VF）事件，是植入式心律转复除颤器（ICD）治疗的主要并发症。这在各种结构性心脏病中发展，包括缺血性和非缺血性心肌病、心肌梗死（MI）和致血栓性右心室心肌病[1，2]。缺血性心肌病是诱发ES的最常见疾病，急性缺血事件是引发ES的众所周知的因素[1，2]。然而，冠状动脉血管造影检测到的异常与ES还没有得到很好的建立。在这个问题上，国际J Cardiol Faga et al. [3]在一项大规模多中心队列研究中证实，未进行血运重建的梗死相关动脉慢性完全闭塞（CTO）（IRA-CTO）独立预测ES的发生。作者还提出了一种新的ES风险预测模型，包括IRA-CTO、既往室性心律失常和左室射血分数<38% 3个类别。CTO在约20%的冠状动脉疾病患者中检出，可明确提供室性心律失常的易损基质。在ICD接受者中进行的几项用于心脏性猝死（SCD）一级和/或二级预防的临床研究报告称，CTO是适当ICD治疗发生的独立预测因素[4]，并对长期死亡率有不良影响[[5]，[6]，[7]]。此外，与CTO相比，IRA-CTO的致瘤性更高，CTO与其所在区域的既往梗死无关（非IRA-CTO）：IRA-CTO患者接受适当ICD治疗的比例高于非IRA-CTO患者[8]。Assaf等人的一篇综述文章评估了CTO和VA之间的相关性，沿着假定的潜在机制[9]。瘢痕相关性室性心动过速通常是由MI后发生的解剖学确定的大折返性回路引起的。小股存活心肌在瘢痕区域或瘢痕与正常心肌之间的边界区域中产生缓慢且各向异性的传导区域，这是瘢痕相关折返回路演变的关键部分。IRA-CTO区域的瘢痕边界区大于无CTO的梗死相关动脉，并且在CTO血运重建后立即减少[9]。瘢痕重塑，其特征在于瘢痕大小及其边缘区和核心区的组分以及边缘区通道数量的动态变化，边缘区通道被定义为连接到2个健康组织区域的瘢痕核心周围的边缘区的连续走廊，在MI发作后的前6个月内开始发展，并持续4年以上，复极异质性持续增加[10].此外，大多数CTO患者具有缺血性血流储备分数，即使是那些侧支血管发育良好的患者，也会导致慢性缺血诱导的心肌适应，称为冬眠[9]。这表现出异常和不均匀的电特性，并有助于形成折返基质，这可能导致更容易发生室性心律失常和SCD [9]。
Electrical storm (ES), generally defined as≥ 3 ventricular tachycardia/fibrillation (VT/VF) events within 24 h, is a major complication of implantable cardioverter-defibrillator (ICD) therapy. This develops in a variety of structural heart diseases including ischemic and non-ischemic cardiomyopathy, myocardial infarction (MI) and arrhythmogenic right ventricular cardiomyopathy [1, 2]. Ischemic cardiomyopathy is the most prevalent disorder predisposing to ES and acute ischemic events are a well-known factor to initiate ES [1, 2]. However, coronary arterial abnormalities detected by angiography relate to ES are not well-established. In this issue of Int J Cardiol Faga et al.[3] demonstrated in a large-scale multicenter cohort study that chronic total occlusion (CTO) of infarct-related artery (IRA-CTO) that was not revascularized independently predicted the occurrence of ES. The authors also showed a novel risk-prediction model of ES, which comprises of 3 categories including IRA-CTO, prior ventricular arrhythmias and left ventricular ejection fraction< 38%.A CTO, which is detected in approximately 20% of patients with coronary artery disease, can clearly provide a vulnerable substrate for ventricular arrhythmias. There are several clinical studies in ICD recipients for the primary and/or secondary prevention of sudden cardiac death (SCD) reporting that CTO is an independent predictor for the occurrence of appropriate ICD therapies [4] and has an adverse impact on long-term mortality [[5],[6],[7]]. Moreover, IRA-CTO is more arrhythmogenic compared to CTO which is not associated with a prior infarction in their territory (non-IRA-CTO): patients with IRA-CTO had a higher proportion of appropriate ICD therapies than those with non-IRA-CTO [8]. A review article by Assaf et al. has assessed the association between CTO and VAs, along with the putative underlying mechanism [9]. Scar-related VT usually is caused by anatomically determined macro-reentrant circuits that develop after MI. Small strands of surviving myocardium create zones of slow and anisotropic conduction in the scar area or in the border zone between scar and normal myocardium, which are critical parts for the evolution of the scar-related reentrant circuit. A territory of IRA-CTO has a larger scar border zone than that of infarct-related artery without CTO and it immediately decreases after CTO revascularization [9]. Scar remodeling, characterized by dynamic changes in the scar size and its components of border zone and core zone as well as number of border zone channels defined as continuous corridors of border zone surrounding by scar core that connect to 2 areas of healthy tissue, starts to develop within the first 6 months after the onset of MI and lasts over a 4-year period with a persistent increase in repolarization heterogeneity [10]. In addition, the majority of CTO patients have ischemic fraction flow reserve, even those with well-developed collateral vessels, that causes chronic ischemia-induced myocardial adaptation termed hibernation [9]. This exhibits abnormal and heterogeneous electrical properties and contributes to the formation of a substrate for reentry, which likely contributes to the higher vulnerability to ventricular arrhythmias and SCD [9].