Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, Dana 3, PO Box 208017, New Haven, CT, 06520-8017, USA.
Nuclear Cardiology Laboratory, Yale-New Haven Hospital, New Haven, CT, USA.
J Nucl Cardiol. 2022 Apr;29(2):798-809. doi: 10.1007/s12350-020-02372-1. Epub 2020 Oct 8.
Acute psychological stressors such as anger can precipitate ventricular arrhythmias, but the mechanism is incompletely understood. Quantification of regional myocardial sympathetic activity with I-metaiodobenzylguanidine (I-mIBG) SPECT imaging in conjunction with perfusion imaging during mental stress may identify a mismatch between perfusion and sympathetic activity that may exacerbate a mismatch between perfusion and sympathetic activity that could create a milieu of increased vulnerability to ventricular arrhythmia.
Five men with ischemic cardiomyopathy (ICM), and five age-matched healthy male controls underwent serial I-mIBG and Tc-Tetrofosmin SPECT/CT imaging during an anger recall mental stress task and dual isotope imaging was repeated approximately 1 week later during rest. Images were reconstructed using an iterative reconstruction algorithm with CT-based attenuation correction. The mismatch of left ventricular myocardial I-mIBG and Tc-Tetrofosmin was assessed along with radiotracer heterogeneity and the I-mIBG heart-to-mediastinal ratios (HMR) were calculated using custom software developed at Yale.
The hemodynamic response to mental stress was similar in both groups. The resting-HMR was greater in healthy control subjects (3.67 ± 0.95) than those with ICM (3.18 ± 0.68, P = .04). Anger recall significantly decreased the HMR in ICM patients (2.62 ± 0.3, P = .04), but not in normal subjects. The heterogeneity of I-mIBG uptake in the myocardium was significantly increased in ICM patients during mental stress (26% ± 8.23% vs. rest: 19.62% ± 9.56%; P = .01), whereas the Tc-Tetrofosmin uptake pattern was unchanged.
Mental stress decreased the I-mIBG HMR, increased mismatch between sympathetic activity and myocardial perfusion, and increased the heterogeneity of I-mIBG uptake in ICM patients, while there was no significant change in myocardial defect size or the heterogeneity of Tc-Tetrofosmin perfusion. The changes observed in this proof-of-concept study may provide valuable information about the trigger-substrate interaction and the potential vulnerability for ventricular arrhythmias.
急性心理应激源，如愤怒，可引发室性心律失常，但发病机制尚不完全清楚。在心理应激时，使用碘-间位胍（I-mIBG）SPECT 成像结合灌注成像来量化局部心肌交感神经活性，可能会发现灌注和交感神经活性之间不匹配的情况，这可能会加剧灌注和交感神经活性之间的不匹配，从而导致室性心律失常易感性增加的环境。
5 名缺血性心肌病（ICM）男性患者和 5 名年龄匹配的健康男性对照者在愤怒回忆心理应激任务期间接受了连续的 I-mIBG 和 Tc-四氮茂 SPECT/CT 成像，大约 1 周后在休息时重复进行双同位素成像。使用基于 CT 的衰减校正的迭代重建算法重建图像。使用耶鲁大学开发的定制软件评估左心室心肌 I-mIBG 和 Tc-Tetrofosmin 的不匹配情况，以及放射性示踪剂异质性，并计算 I-mIBG 心脏与纵隔比值（HMR）。
两组的心理应激血流动力学反应相似。健康对照组的静息-HMR 较大（3.67±0.95），而 ICM 患者的静息-HMR 较小（3.18±0.68，P=0.04）。愤怒回忆明显降低了 ICM 患者的 HMR（2.62±0.3，P=0.04），但对正常受试者没有影响。在心理应激时，ICM 患者心肌 I-mIBG 摄取的异质性显著增加（26%±8.23%比休息时：19.62%±9.56%；P=0.01），而 Tc-Tetrofosmin 摄取模式保持不变。
心理应激降低了 I-mIBG HMR，增加了交感神经活性与心肌灌注之间的不匹配，增加了 ICM 患者 I-mIBG 摄取的异质性，而心肌缺损大小或 Tc-Tetrofosmin 灌注的异质性没有显著变化。这项概念验证研究中观察到的变化可能提供有关触发-底物相互作用和室性心律失常潜在易感性的有价值信息。
