● Cardiac anatomy and microstructure using histology and diffusion tensor MRI, and the structural underpinning of cardiac function.
● Ex vivo cardiac MRI, confocal microscopy, image analysis, preclinical models of cardiovascular disease, cardiac Langendorff preparations.
● Assessment of diastolic function and myocardial stiffness
● Animal handling and surgery
● Cardiac MRI scanning
● Preclinical echocardiography
● Image processing
● Langendorff heart preparations
● Computational mechanics
● Programming (Matlab, Python, R, ImageJ)
● Wilson et al "Graph-based Analysis Of Cardiomyocyte Network Connectivity" (Accepted) [2021 AHA:SS]
● Wilson et al "Collagen Remodeling Of Spontaneously Hypertensive Rats Undergoing Quinapril Treatment Measured By Three Dimensional Shape Analysis" (Accepted) [2021 BCVS]
● Wilson et al "Analysis of Location-Dependent Cardiomyocyte Branching" [2021 FIMH]
● Wilson et al "Microstructure-Based Simulation of Myocardial Diffusion Using Extended Volume Confocal Microscopy" [2021 ISMRM]
● Wilson et al "ACE Inhibitor Treatment Normalizes Apparent Diffusion Coefficient in Spontaneously Hypertensive Rats" [2021 SCMR]
● Wilson et al "Relationship Between Myocyte Branching and Location Within Myocardial Sheetlet" [2020 AHA:SS]
● Wilson et al "Comparison of MRI-Derived Left Ventricular End-Diastolic Pressure-Volume Relationship with Ex Vivo Measurements" [2020 VPH]
● Wilson et al "Myocardial Laminar Organization Is Retained in Angiotensin-Converting Enzyme Inhibitor Treated SHRs" [2020 Exp Mech]
● Wilson et al "Formulation and Characterization of Antithrombin Perfluorocarbon Nanoparticles" [2020 Methods]
Honors & Awards
First Prize, AIMI-HIAE COVID-19 Researchathon, Stanford University (2020)
Finalist, John Hubbard Memorial Prize in recognition of excellence in studies towards a PhD, New Zealand Medical Sciences Congress (2017)
Travel Fellowship, World Congress of Biomechanics (2014)
First Class Honors, Master of Operations Research, University of Auckland (2012)
First Prize, John Carman Prize for best oral presentation by a graduate student, New Zealand Medical Sciences Congress (2012)
Distinction in Theoretical Statistics, University of Auckland (2009)
Merit, Postgraduate Diploma in Science (Medical Sciences), University of Auckland (2009)
Boards, Advisory Committees, Professional Organizations
Member, Society for Cardiovascular Magnetic Resonance (2020 - Present)
Member, International Society for Magnetic Resonance in Medicine (2020 - Present)
Trainee Committee Member, Functional Imaging and Modeling of the Heart (2020 - 2021)
Organization Committee Member, 2020 Radiological Sciences Laboratory Retreat, Stanford University (2020 - 2020)
Member, American Heart Association (2019 - Present)
Daniel Ennis, Postdoctoral Faculty Sponsor
Formulation and Characterization of Antithrombin Perfluorocarbon Nanoparticles.
Methods in molecular biology (Clifton, N.J.)
2020; 2118: 111–20
Thrombin, a major protein involved in the clotting cascade by the conversion of inactive fibrinogen to fibrin, plays a crucial role in the development of thrombosis. Antithrombin nanoparticles enable site-specific anticoagulation without increasing bleeding risk. Here we outline the process of making and the characterization of bivalirudin and D-phenylalanyl-L-prolyl-L-arginyl-chloromethyl ketone (PPACK) nanoparticles. Additionally, the characterization of these nanoparticles, including particle size, zeta potential, and quantification of PPACK/bivalirudin loading, is also described.
View details for DOI 10.1007/978-1-0716-0319-2_8
View details for PubMedID 32152974
Myocardial Laminar Organization Is Retained in Angiotensin-Converting Enzyme Inhibitor Treated SHRs
View details for DOI 10.1007/s11340-020-00622-4
Microstructurally Motivated Constitutive Modeling of Heart Failure Mechanics.
Heart failure (HF) is one of the leading causes of death worldwide. HF is associated with substantial microstructural remodeling, which is linked to changes in left ventricular geometry and impaired cardiac function. The role of myocardial remodeling in altering the mechanics of failing hearts remains unclear. Structurally based constitutive modeling provides an approach to improve understanding of the relationship between biomechanical function and tissue organization in cardiac muscle during HF. In this study, we used cardiac magnetic resonance imaging and extended-volume confocal microscopy to quantify the remodeling of left ventricular geometry and myocardial microstructure of healthy and spontaneously hypertensive rat hearts at the ages of 12 and 24months. Passive cardiac mechanical function was characterized using left ventricular pressure-volume compliance measurements. We have developed a, to our knowledge, new structurally based biomechanical constitutive equation built on parameters quantified directly from collagen distributions observed in confocal images of the myocardium. Three-dimensional left ventricular finite element models were constructed from subject-specific invivo magnetic resonance imaging data. The structurally based constitutive equation was integrated into geometrically subject-specific finite element models of the hearts and used to investigate the underlying mechanisms of ventricular dysfunction during HF. Using a single pair of material parameters for all hearts, we were able to produce compliance curves that reproduced all of the experimental compliance measurements. The value of this study is not limited to reproducing the mechanical behavior of healthy and diseased hearts, but it also provides important insights into the structure-function relationship of diseased myocardium that will help pave the way toward more effective treatments for HF.
View details for DOI 10.1016/j.bpj.2019.09.038
View details for PubMedID 31653449
Increased cardiac work provides a link between systemic hypertension and heart failure
2017; 5 (1)
The spontaneously hypertensive rat (SHR) is an established model of human hypertensive heart disease transitioning into heart failure. The study of the progression to heart failure in these animals has been limited by the lack of longitudinal data. We used MRI to quantify left ventricular mass, volume, and cardiac work in SHRs at age 3 to 21 month and compared these indices to data from Wistar-Kyoto (WKY) controls. SHR had lower ejection fraction compared with WKY at all ages, but there was no difference in cardiac output at any age. At 21 month the SHR had significantly elevated stroke work (51 ± 3 mL.mmHg SHR vs. 24 ± 2 mL.mmHg WKY; n = 8, 4; P < 0.001) and cardiac minute work (14.2 ± 1.2 L.mmHg/min SHR vs. 6.2 ± 0.8 L.mmHg/min WKY; n = 8, 4; P < 0.001) compared to control, in addition to significantly larger left ventricular mass to body mass ratio (3.61 ± 0.15 mg/g SHR vs. 2.11 ± 0.008 mg/g WKY; n = 8, 6; P < 0.001). SHRs showed impaired systolic function, but developed hypertrophy to compensate and successfully maintained cardiac output. However, this was associated with an increase in cardiac work at age 21 month, which has previously demonstrated fibrosis and cell death. The interplay between these factors may be the mechanism for progression to failure in this animal model.
View details for DOI 10.14814/phy2.13104
View details for Web of Science ID 000392243200001
View details for PubMedID 28082430
View details for PubMedCentralID PMC5256162
- Three-Dimensional Quantification of Myocardial Collagen Morphology from Confocal Images SPRINGER INTERNATIONAL PUBLISHING AG. 2017: 3–12
- Image-driven constitutive modeling of myocardial fibrosis INTERNATIONAL JOURNAL FOR COMPUTATIONAL METHODS IN ENGINEERING SCIENCE & MECHANICS 2016; 17 (3): 211–21
- Microstructural Remodelling and Mechanics of Hypertensive Heart Disease SPRINGER-VERLAG BERLIN. 2015: 382–89
- Field-Based Parameterisation of Cardiac Muscle Structure from Diffusion Tensors SPRINGER-VERLAG BERLIN. 2015: 146–54