Article
The heart-brain axis in the setting of subarachnoid hemorrhage
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Authors
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Ran Xu
- Charité – Universitätsmedizin Berlin , Neurochirurgische Klinik, Berlin, Deutschland
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Christian Oeing
- Charité Universitätsmedizin Berlin, Department of Cardiology, Berlin, Deutschland
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Jane Vorbäumen
- Charité – Universitätsmedizin Berlin , Neurochirurgische Klinik, Berlin, Deutschland
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Ulf C. Schneider
- Neurochirurgische Klinik, Campus Virchow Klinikum, Charité - Universitätsmedizin Berlin, Berlin, Deutschland
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Peter Vajkoczy
- Charité - Universitätsmedizin Berlin, Campus Mitte, Neurochirurgische Klinik, Berlin, Deutschland
| Published: | June 9, 2017 |
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Outline
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Objective: Cardiac dysfunction occurs in up to 20% after subarachnoid hemorrhage (SAH), which has been previously described as neurogenic stunned myocardium. Current paradigm suggests that the interplay between cardiac dysfunction and cerebral perfusion may be triggered via hypercatecholaminergic events, which in turn may lead to secondary brain injury; however, this effect is poorly understood. Thus, the aim of the study was to investigate cardiac function after experimental SAH.
Methods: Using male C57Bl/6 mice, experimental SAH was induced via a filament perforation model (n=18), while Sham operation was conducted for the corresponding control group (n=9). The presence of SAH was verified with Magnetic Resonance Imaging (MRI) in all operated animals. Transthoracic cardiac echocardiography was then performed on all mice to elicit diastolic and systolic function on day 1, day 7, and day 14. Diastolic function was assessed by determining mitral inflow patterns (E/E’ ratio) and mitral annulus velocities (E/A ratio), while left ventricular ejection fraction (LVED) was measured for systolic function. Furthermore, the heart weight on each time point was determined following scarification.
Results: In SAH mice, impaired diastolic function was observed as demonstrated by reduced E/A ratio (Sham vs. SAH: 2,3 vs. 1,5; p=0,04). This effect was most prominently seen after 1 week, but a trend was already apparent after 1 day. Left ventricular ejection fraction was not affected in the setting of SAH (Sham vs. SAH: 68% vs. 64%). To elicit whether diastolic dysfunction may stem from cardiac hypertrophy, heart weight was measured after mice sacrification. Indeed, the heart weight increased in SAH mice by 11,7% (Sham vs. SAH: 136 mg vs. 152 mg; p<0,05).
Conclusion: The above-mentioned model can be utilized to examine the brain-heart axis in the setting of SAH. In experimental SAH mice, a significant impact on diastolic dysfunction is observed after inducing SAH injury, paralleled by an increase in heart weight. Further studies are needed to investigate the pathophysiological patterns that underlie this axis in neurogenic stunned myocardium.
