Fat infiltration in the infarcted heart as a paradigm for ventricular arrhythmias.
Fat infiltration in the infarcted heart as a paradigm for ventricular arrhythmias.
复制标题
DOI：
10.1038/s44161-022-00133-6
复制
发表时间：
2022-10
期刊：
影响因子：
--
通讯作者：
Trayanova, Natalia A
中科院分区：
文献类型：
--
作者：
Sung, Eric;Prakosa, Adityo;Zhou, Shijie;Berger, Ronald D;Chrispin, Jonathan;Nazarian, Saman;Trayanova, Natalia A
最近发现浸润性脂肪组织（inFAT）与梗死心脏中的瘢痕共定位，并可能导致室性心律失常（VA），一种危及生命的心律失常。然而，inFAT对VA的贡献尚未得到充分证实。我们通过一项前瞻性临床和机械计算研究，研究了inFAT与瘢痕在VA中的作用。使用个性化的计算心脏模型，并比较VA动力学模拟结果与临床手术过程中测得的电生理异常，我们证明了inFAT，而不是疤痕，是致瘤倾向的主要驱动因素，并经常出现在VA电路的关键区域。我们确定，在VA回路中，与瘢痕相反，inFAT主要负责关键部位的传导减慢，机械地促进VA。我们的研究结果暗示inFAT是梗死相关VA的主要参与者，挑战了现有的范式，并为未探索的抗心律失常策略打开了大门。
Infiltrating adipose tissue (inFAT) has been recently found to co-localize with scar in infarcted hearts and may contribute to ventricular arrhythmias (VAs), a life-threatening heart rhythm disorder. However, the contribution of inFAT to VA has not been well-established. We investigated the role of inFAT versus scar in VA through a combined prospective clinical and mechanistic computational study. Using personalized computational heart models and comparing the results from simulations of VA dynamics with measured electrophysiological abnormalities during the clinical procedure, we demonstrate that inFAT, rather than scar, is a primary driver of arrhythmogenic propensity and is frequently present in critical regions of the VA circuit. We determined that, within the VA circuitry, inFAT, as opposed to scar, is primarily responsible for conduction slowing in critical sites, mechanistically promoting VA. Our findings implicate inFAT as a dominant player in infarct-related VA, challenging existing paradigms and opening the door for unexplored anti-arrhythmic strategies.