Risk Stratification and Sudden Cardiac Death: Is It Time to Include Autonomic Variables?
Risk Stratification and Sudden Cardiac Death: Is It Time to Include Autonomic Variables?
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风险分层和心源性猝死：是时候纳入自主变量了吗？
DOI：
10.1161/circimaging.117.006819
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Vaseghi,Marmar
中科院分区：
文献类型：
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作者：
Khakpour,Houman;Vaseghi,Marmar
2 Khakpour和Vaseghi交感神经去神经和心源性猝死（去神经、左心室舒张末期容积指数和未使用血管紧张素转换酶抑制剂; BNP升高替代肌酐升高）。因此，交感神经和心肌重塑的组合似乎优先增加这些患者的心肌梗死性死亡的风险。正电子发射断层扫描11 C-间羟麻黄碱评估的失神经支配心肌的程度，最有可能是异质性交感神经支配的标志物，导致心室复极离散度增加。一些影响回顾性研究的局限性同样适用于当前的研究。研究人群较少，主要为男性（90%）。考虑到人群规模和事件数量，先前与死亡率相关的某些变量（包括房颤和慢性阻塞性肺疾病）未被收集或未纳入模型。有限的患者数量也可能解释了为什么左心室射血分数和纽约心脏协会分级等变量与心脏死亡率没有达到统计学显著性，因为它们与其他研究中的死亡率相关。15，16此外，对死因特异性死亡率和心脏骤停的回顾性判定可能存在偏倚。缺损大小的量化也有局限性，这是基于使用75%的左心室最大活动阈值，这是一个有点随意的阈值，如果存在更全面的神经支配减少，可能会导致不准确，这已经在心肌梗死动物模型和缺血性心肌病患者中显示。10，11，17区域保留指数计算或更标准化的患者量化将是有价值的。尽管存在这些局限性，但Fallavollita等人的贡献值得称赞，他们指出，越来越多的证据支持在评估SCD风险时纳入心脏自主神经变量。本研究与之前的研究沿着强调了将自主神经指数纳入危险分层算法的必要性，以提高医生预测病因特异性死亡率的预后能力，并更好地分配昂贵的资源和治疗，如ICD。对病理性心脏交感神经和副交感神经支配模式背后的机制的进一步理解也代表了神经调节疗法未来发展的重要方法，其中一些已经显示出在治疗室性心律失常中的益处。18在这方面，未来的步骤应包括前瞻性验证这些自主变量，包括交感神经去神经，并实施旨在调节心脏自主神经系统以预防SCD的随机前瞻性研究。
2 Khakpour and Vaseghi Sympathetic Denervation and Sudden Cardiac Death (denervation, left ventricular end-diastolic volume index, and lack of angiotensin-converting enzyme inhibitor use; elevated BNP replaced elevated creatinine). Hence, a combination of sympathetic and myocardial remodeling seem to preferentially increase the risk of arrhythmic deaths in these patients. The extent of denervated myocardium, as assessed by positron emission tomography 11C-meta-hydroxyephedrine, is most likely a marker for heterogeneous sympathetic innervation, leading to increased dispersion of ventricular repolarization. Some of the same limitations that afflict retrospective studies apply to the current study. The studied population is small and predominantly men (90%). Certain variables, previously associated with mortality, including atrial fibrillation and chronic obstructive pulmonary disease, either were not collected or not included in the model given the population size and number of events. The limited number of patients also may potentially explain why variables such as left ventricular ejection fraction and New York Heart Association Class did not reach statistical significance for cardiac mortality, given their association with mortality in other studies. 15, 16 Furthermore, retrospective adjudication of cause-specific mortality and sudden cardiac arrest may be biased. There are also limitations with the quantification of defect size, which was based on using a 75% threshold for left ventricular maximum activity, a somewhat arbitrary threshold that can lead to inaccuracies if there exists a more global reduction in innervation, which has been shown in animal models of myocardial infarction and in patients with ischemic cardiomyopathy. 10, 11, 17 A regional retention index calculation or more standardized quantification across patients would have been valuable. Despite these limitations, Fallavollita et al are to be commended for their contribution, which points to the growing body of evidence supporting the inclusion of cardiac autonomic variables in assessing risk of SCD. This study, along with its predecessors, emphasize the need for incorporation of autonomic indices into risk stratification algorithms, in order to improve the prognostic ability of physicians to predict cause-specific mortality and to better allocate expensive resources and therapies, such as ICDs. Improved understanding of the mechanisms behind pathological cardiac sympathetic and parasympathetic innervation patterns also represent an important approach for future development of neuromodulatory therapies, some of which have already shown benefit in treatment of ventricular arrhythmias. 18 In this regard, future steps should include prospective validation of these autonomic variables, including sympathetic denervation, and implementation of randomized prospective studies aimed at modulating the cardiac autonomic nervous system for prevention of SCD.