Abstract
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.
Highlights
Cerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (SAH)
To the best of our knowledge, this is the first study to analyze the relationship between cardiac function and cerebral perfusion in a murine model of SAH
The most important findings of our study are: (i) Overall, SAH enhances left ventricular (LV) contractility in the early period after SAH but with marked inter-individual variability, (ii) only a specific subset of animals developed echocardiographic and ECG signs of neurogenic stress cardiomyopathy (NSC), a pattern similar to SAH patients[6,7,34,35], and (iii) left ventricular end-diastolic volume (LVEDV) correlated significantly with cerebral perfusion at defined time points post-SAH, and there was a non-significant trend for correlation of cardiac output and stroke volume with cerebral perfusion
Summary
Cerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (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. Several studies have shown that decreased cardiac output (CO) can induce both acute[9,10] and chronic cerebral hypoperfusion[11,12], and that impaired left ventricular (LV) function is associated with cognitive decline[13,14]. Impaired LV function leads to cerebral hypoperfusion after SAH This assumption is supported by a clinical study that found an association between cardiac dysfunction and cerebral hypoperfusion during the first 24 h after hospital admission in patients with S AH15. Function appears essential for mitigating cerebral hypoperfusion and optimal neurological outcome after SAH. The link between post-stroke cardiac dysfunction and cerebral hypoperfusion has not been established in experimental studies
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