Department of Neurosurgery, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Center for Cardiology-Cardiology I, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Sci Rep. 2021 Feb 8;11(1):3317. doi: 10.1038/s41598-021-82583-9.
Cerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (SAH). A subset of SAH patients develop neurogenic stress cardiomyopathy (NSC), but it is unclear to what extent cerebral hypoperfusion is influenced by cardiac dysfunction after SAH. The aims of this study were to examine the association between cardiac function and cerebral perfusion in a murine model of SAH and to identify electrocardiographic and echocardiographic signs indicative of NSC. We quantified cortical perfusion by laser SPECKLE contrast imaging, and myocardial function by serial high-frequency ultrasound imaging, for up to 7 days after experimental SAH induction in mice by endovascular filament perforation. Cortical perfusion decreased significantly whereas cardiac output and left ventricular ejection fraction increased significantly shortly post-SAH. Transient pathological ECG and echocardiographic abnormalities, indicating NSC (right bundle branch block, reduced left ventricular contractility), were observed up to 3 h post-SAH in a subset of model animals. Cerebral perfusion improved over time after SAH and correlated significantly with left ventricular end-diastolic volume at 3, 24, and 72 h. The murine SAH model is appropriate to experimentally investigate NSC. We conclude that in addition to cerebrovascular dysfunction, cardiac dysfunction may significantly influence cerebral perfusion, with LVEDV presenting a potential parameter for risk stratification.
脑灌注不足是决定蛛网膜下腔出血（SAH）后结局的关键因素。一小部分 SAH 患者会发生神经源性应激性心肌病（NSC），但尚不清楚 SAH 后心脏功能障碍对脑灌注的影响程度。本研究旨在探讨 SAH 小鼠模型中心脏功能与脑灌注之间的关系，并确定心电图和超声心动图提示 NSC 的指标。通过血管内纤维蛋白丝穿孔诱导实验性 SAH 后，我们使用激光 speckle 对比成像技术来量化皮质灌注，使用高频超声成像技术连续测量心功能，最长可达 7 天。SAH 后皮质灌注明显下降，而心输出量和左心室射血分数明显升高。在一部分模型动物中，SAH 后 3 小时内可观察到短暂的病理性心电图和超声心动图异常，提示 NSC（右束支传导阻滞，左心室收缩功能降低）。SAH 后，脑灌注随时间逐渐改善，与 3、24 和 72 小时时的左心室舒张末期容积显著相关。SAH 小鼠模型适合用于实验性研究 NSC。我们得出结论，除了脑血管功能障碍外，心脏功能障碍可能会显著影响脑灌注，LVEDV 可能是一种用于风险分层的潜在参数。
