gms | German Medical Science

70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12.05. - 15.05.2019, Würzburg

Interrogating the heart-brain interaction after subarachnoid haemorrhage in the experimental and clinical setting

Untersuchungen von Herz-Hirn Interaktionen im Rahmen der Subarachnoidalblutung im experimentellen und klinischen Modell

Meeting Abstract

  • presenting/speaker Ran Xu - Charité – Universitätsmedizin Berlin, Klinik für Neurochirurgie, Berlin, Deutschland
  • Christian Oeing - Johns Hopkins University, Dept. of Cardiology, Baltimore, United States
  • Jane Vormbäumen - Charité – Universitätsmedizin Berlin, Klinik für Neurochirurgie, Berlin, Deutschland
  • Ulf Schneider - Charité – Universitätsmedizin Berlin, Klinik für Neurochirurgie, Berlin, Deutschland
  • Peter Vajkoczy - Charité – Universitätsmedizin Berlin, Klinik für Neurochirurgie, Berlin, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie. Würzburg, 12.-15.05.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocV009

doi: 10.3205/19dgnc009, urn:nbn:de:0183-19dgnc0096

Veröffentlicht: 8. Mai 2019

© 2019 Xu et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objective: Cardiac pathologies occur in up to 30% after subarachnoid hemorrhage (SAH), ultimately contributing to systemic complications. The underlying pathology of the interplay between cardiac dysfunction and cerebral perfusion is poorly understood. We sought to describe an in-vivo mouse model to investigate cardiac function after experimental SAH, and based on these findings, to establish an algorithm in the clinical setting to dissect pathophysiological mechanisms of heart-brain axis.

Methods: Experimental SAH was induced in male C57Bl/6 mice via a filament perforation model and confirmed via MRI, while Sham operation was conducted for the control group. Transthoracic echocardiography (TTE) was performed to elicit diastolic and systolic function on three timepoints (d1, d7, d14; ntotal=72). 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. Cardiomyocyte size was quantified using Hematoxylin/Eosin stainings, as well as Masson Trichrome to quantify fibrotic tissue. For the human study protocol (EA2/124/18), an algorithm was established to evaluate cardiac function via consecutive TTE (day 1, 4, 7, and 14 post SAH) and to investigate potential underlying pathways in SAH patients utilizing CSF and blood samples.

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), while left ventricular ejection fraction was not affected in the setting of SAH (Sham vs. SAH: 68% vs. 64%). This was paralleled by a significant increase in cardiomyocyte size in SAH mice (Sham vs. SAH: 114 mm2 vs. 141 mm2; p<0,01), as well as a significant increase in interstitial fibrosis. This data was then synthesized to establish a clinical pipeline to investigate heart-brain interactions in SAH patients in vivo and ex vivo. Preliminary data show a decrease in diastolic function comparing the acute phase to the subacute period after SAH (day 1 vs. day 14: E/E’=5,3 vs. 7,8).

Conclusion: In our mouse model, a significant impact on diastolic dysfunction is observed after inducing SAH injury, paralleled by an increase in cardiomyocyte size and interstitial fibrosis. The above-mentioned model can be not only utilized to examine the brain-heart axis in the setting experimental SAH, but also further used to establish a clinical algorithm to recapitulate these effects in SAH patients.

Figure 1 [Fig. 1]