Diggelmann Flavia, Bengs Susan, Haider Achi, Epprecht Gioia, Beeler Anna Luisa, Etter Dominik, Wijnen Winandus J, Portmann Angela, Warnock Geoffrey I, Treyer Valerie, Grämer Muriel, Todorov Atanas, Mikail Nidaa, Rossi Alexia, Fuchs Tobias A, Pazhenkottil Aju P, Buechel Ronny R, Tanner Felix C, Kaufmann Philipp A, Gebhard Catherine, Fiechter Michael
Department of Nuclear Medicine, University Hospital Zurich, 8091 Zurich, Switzerland.
Center for Molecular Cardiology, University of Zurich, 8952 Schlieren, Switzerland.
J Pers Med. 2021 Apr 1;11(4):261. doi: 10.3390/jpm11040261.
Recent studies indicate that enhanced neuronal stress responses are associated with adverse cardiovascular outcomes. A chronic inflammatory state seems to mediate this detrimental neuro-cardiac communication. Statins are among the most widely prescribed medications in primary and secondary cardiovascular disease (CVD) prevention and not only lower lipid levels but also exhibit strong anti-inflammatory and neuroprotective effects. We therefore sought to investigate the influence of statins on neuronal stress responses in a patient cohort at risk for CVD.
563 patients (61.5 ± 14.0 years) who underwent echocardiography and F-fluorodeoxyglucose (F-FDG) positron emission tomography (PET) were retrospectively identified. Metabolic activity of the amygdala, a part of the brain's salience network, was quantified by F-FDG uptake, while normal cardiac morphology and function were assured by echocardiography. Vertebral bone marrow metabolism, a marker of inflammatory activity, was measured by F-FDG PET.
Increased neuronal stress responses were associated with an increased inflammatory activity in the bone marrow (r = 0.152, = 0.015) as well as with a subclinical reduction in left ventricular ejection fraction (LVEF, r = -0.138, = 0.025). In a fully-adjusted linear regression model, statin treatment was identified as an independent, negative predictor of amygdalar metabolic activity (B-coefficient -0.171, = 0.043).
Our hypothesis-generating investigation suggests a potential link between the anti-inflammatory actions of statins and reduced neuronal stress responses which could lead to improved cardiovascular outcomes. The latter warrants further studies in a larger and prospective population.
近期研究表明，增强的神经元应激反应与不良心血管结局相关。慢性炎症状态似乎介导了这种有害的神经-心脏通讯。他汀类药物是初级和二级心血管疾病（CVD）预防中最常用的药物之一，不仅能降低血脂水平，还具有强大的抗炎和神经保护作用。因此，我们试图研究他汀类药物对有CVD风险的患者队列中神经元应激反应的影响。
回顾性确定了563例接受超声心动图和F-氟脱氧葡萄糖（F-FDG）正电子发射断层扫描（PET）的患者（61.5±14.0岁）。通过F-FDG摄取对杏仁核（大脑显著性网络的一部分）的代谢活性进行量化，同时通过超声心动图确保心脏形态和功能正常。通过F-FDG PET测量椎体骨髓代谢，这是炎症活动的一个标志物。
神经元应激反应增强与骨髓炎症活动增加相关（r = 0.152，P = 0.015），也与左心室射血分数（LVEF）的亚临床降低相关（r = -0.138，P = 0.025）。在一个完全调整的线性回归模型中，他汀类药物治疗被确定为杏仁核代谢活性的独立负预测因子（B系数 -0.171，P = 0.043）。
我们的探索性研究表明，他汀类药物的抗炎作用与降低的神经元应激反应之间可能存在联系，这可能导致心血管结局改善。后者值得在更大规模的前瞻性人群中进一步研究。
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