
Karoline Marie Bornemann
Postdoctoral Scholar, Cardiology
Bio
Karoline-Marie Bornemann, PhD, is a biomedical engineer interested in cardiovascular flows, specifically the computational modeling of heart valves using fluid-structure interaction simulations. Her current postdoctoral research in the Marsden lab at Stanford University focuses on the simulation of congenital valve pathologies and valve repair in pediatrics working with Alexander D. Kaiser, Alison Marsden and Michael Ma. She obtained her PhD in Biomedical Engineering from the University of Bern where she investigated instability mechanisms leading to laminar-turbulent transition past bioprosthetic aortic valves with Dominik Obrist and Peter Schmid. During her PhD, she performed a secondment at KTH Royal Institute of Technology collaborating with Ardeshir Hanifi and Dan Henningson assessing the stability of flow fields past valve prostheses. Visualizations of her PhD research were showcased in a winning entry of the Gallery of Fluid Motion 2024 and her PhD thesis won the GCB Best PhD Thesis 2024 Award.
Honors & Awards
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GCB Best PhD Thesis 2024, GCB, University of Bern (06/2025)
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Winner of the Gallery of Fluid Motion, American Physical Society (APS), Division of Fluid Mechanics (11/2024)
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UniBE Short Travel Grant for (Post)Docs, University of Bern (04/2024)
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Best poster award in the category 'Pathology, Mechanisms and Outcomes', Heart Valve Society (HVS) (02/2024)
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PROMOS International Scholarship, German Academic Exchange Service (DAAD) (04/2019)
Professional Education
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Doctor of Philosophy, University of Bern (Bern, Switzerland), Biomedical Engineering (2024)
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Diplom (Master of Science), Technische Universität Dresden (Dresden, Germany), Aerospace Engineering (2020)
Stanford Advisors
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Alison Marsden, Postdoctoral Faculty Sponsor
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Alexander Kaiser, Postdoctoral Research Mentor
All Publications
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Leaflet fluttering changes laminar-turbulent transition mechanisms past bioprosthetic aortic valves
PHYSICS OF FLUIDS
2025; 37 (5)
View details for DOI 10.1063/5.0270405
View details for Web of Science ID 001493187300033
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The relation between aortic morphology and transcatheter aortic heart valve thrombosis: Particle tracing and platelet activation in larger aortic roots with and without neo-sinus.
Computers in biology and medicine
2024; 179: 108828
Abstract
Transcatheter aortic heart valve thrombosis (THVT) affects long-term valve durability, transvalvular pressure gradient and leaflet mobility. In this study, we conduct high-fidelity fluid-structure interaction simulations to perform Lagrangian particle tracing in a generic model with larger aortic diameters (THVT model) with and without neo-sinus which is compared to a model of unaffected TAVI patients (control model). Platelet activation indices are computed for each particle to assess the risk of thrombus formation induced by high shear stresses followed by flow stagnation. Particle tracing indicates that fewer particles contribute to sinus washout of the THVT model with and without neo-sinus compared to the control model (-34.9%/-34.1%). Stagnating particles in the native sinus of the THVT model show higher platelet activation indices than for the control model (+39.6% without neo-sinus, +45.3% with neo-sinus). Highest activation indices are present for particles stagnating in the neo-sinus of the larger aorta representing THVT patients (+80.2% compared to control). This fluid-structure interaction (FSI) study suggests that larger aortas lead to less efficient sinus washout in combination with higher risk of platelet activation among stagnating particles, especially within the neo-sinus. This could explain (a) a higher occurrence of thrombus formation in transcatheter valves compared to surgical valves without neo-sinus and (b) the neo-sinus as the prevalent region for thrombi in TAV. Pre-procedural identification of larger aortic roots could contribute to better risk assessment of patients and improved selection of a patient-specific anti-coagulation therapy.
View details for DOI 10.1016/j.compbiomed.2024.108828
View details for PubMedID 38996554
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Instability mechanisms initiating laminar-turbulent transition past bioprosthetic aortic valves
JOURNAL OF FLUID MECHANICS
2024; 985
View details for DOI 10.1017/jfm.2024.309
View details for Web of Science ID 001209376100001
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Altered blood flow due to larger aortic diameters in patients with transcatheter heart valve thrombosis.
APL bioengineering
2023; 7 (4): 046120
Abstract
The etiology of transcatheter heart valve thrombosis (THVT) and the relevance of the aortic root geometry on the occurrence of THVT are largely unknown. The first aim of this pilot study is to identify differences in aortic root geometry between THVT patients and patients without THVT after transcatheter aortic valve implantation (TAVI). Second, we aim to investigate how the observed difference in aortic diameters affects the aortic flow using idealized computational geometric models. Aortic dimension was assessed using pre-TAVI multi-detector computed tomography scans of eight patients with clinical apparent THVT and 16 unaffected patients (two for each THVT patient with same valve type and size) from the Bern-TAVI registry. Among patients with THVT the right coronary artery height was lower (-40%), and sinotubular junction (STJ) and ascending aorta (AAo) diameters tended to be larger (9% and 14%, respectively) compared to the unaffected patients. Fluid-structure interaction (FSI) in two idealized aortic models with the observed differences in STJ and AAo diameter showed higher backflow rate at the STJ (+16%), lower velocity magnitudes in the sinus (-5%), and higher systolic turbulent dissipation rate in the AAo (+8%) in the model with larger STJ and AAo diameters. This pilot study suggests a direct effect of the aortic dimensions on clinically apparent THVT. The FSI study indicates that larger STJ and AAo diameters potentially favor thrombus formation by increased backflow rate and reduced wash-out efficiency of the sinus. The reported observations require clinical validation but could potentially help identifying patients at risk for THVT.
View details for DOI 10.1063/5.0170583
View details for PubMedID 38125699
View details for PubMedCentralID PMC10732696