Dr Wilson completed a Bachelor of Science in Biomedical Science (University of Auckland, New Zealand, 2007), and a Postgraduate Diploma in Medical Sciences (UoA, 2008).
He then changed his focus to engineering and applied mathematics, and completed a Masters of Operations Research (UoA, Faculty of Engineering, 2011). In his Master's thesis, he developed a mixed-integer linear formulation for determining optimal electricity distribution tariffs under a range of power generation conditions.
Dr Wilson then switched back his focused to the Medical Sciences and completed a PhD in Bioengineering with a joint appointment in the Department of Physiology and the Auckland Bioengineering Institute. His Doctoral thesis (2018) focused on the physiology and biomechanics of cardiac remodeling underpinning heart failure.
During his first Postdoctoral position (University of South Florida Heart Institute, 2018-2019), Dr Wilson developed nanoparticle therapies for myocardial ischemia-reperfusion injury, as well as anti-thrombin nanoparticles to reduce thrombus formation while limiting bleeding risk.
Dr Wilson is currently a member of the Cardiac MRI Research Group at Stanford University (PI: Professor Daniel Ennis), and works on a range of projects including (i) using tissue clearing techniques to understand the fundamental branching structure of the myocardium (ii) developing new diffusion tensor MRI reconstruction techniques for extracting cardiac microstructure and pathology (iii) using MRI and histology to understand the myocardial structural and functional improvements brought about by ACE inhibitor treatment.
● Wilson et al "Myocardial Mesostructure and Mesofunction" [2022 AJP-H&C]
● Wilson et al "Restored Torsion and Longitudinal Strain in ACE Inhibitor Treated Hypertension" [2022 ISMRM]
● Wilson et al "Assessment of Microstructural Remodeling in Myocardial InfarctionUsing Advanced Diffusion Metrics" [2022 SCMR]
● Wilson et al "Graph-based Analysis Of Cardiomyocyte Network Connectivity" [2021 AHA:SS]
● Wilson et al "Collagen Remodeling Of Spontaneously Hypertensive Rats Undergoing Quinapril Treatment Measured By Three Dimensional Shape Analysis" [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
Myocardial Mesostructure and Mesofunction.
American journal of physiology. Heart and circulatory physiology
The complex and highly organized structural arrangement of some five billion cardiomyocytes directs the coordinated electrical activity and mechanical contraction of the human heart. The characteristic transmural change in cardiomyocyte orientation underlies base-to-apex shortening, circumferential shortening, and left ventricular torsion during contraction. Individual cardiomyocytes shorten approximately 15% and increase in diameter approximately 8%. Remarkably, however, the left ventricular wall thickens by up to 30-40%. To accommodate this, the myocardium must undergo significant structural rearrangement during contraction. At the mesoscale, collections of cardiomyocytes are organized into sheetlets, and sheetlet shear is the fundamental mechanism of rearrangement that produces wall thickening. Herein we review the histological and physiological studies of myocardial mesostructure that have established the sheetlet shear model of wall thickening. Recent developments in tissue clearing techniques allow for imaging of whole hearts at the cellular scale, while magnetic resonance imaging (MRI) and computed tomography (CT) can image the myocardium at the mesoscale (tens to hundreds of microns) to resolve cardiomyocyte orientation and organization. Through histology, cardiac diffusion tensor imaging (cDTI) and other modalities, mesostructural sheetlets have been confirmed in both animal and human hearts. Recent in vivo cDTI methods have measured reorientation of sheetlets during the cardiac cycle. We also examine the role of pathological cardiac remodeling on sheetlet organization and reorientation, and the impact this has on ventricular function and dysfunction. We also review the unresolved mesostructural questions and challenges that may direct future work in the field.
View details for DOI 10.1152/ajpheart.00059.2022
View details for PubMedID 35657613
Formulation and Characterization of Antithrombin Perfluorocarbon Nanoparticles.
Methods in molecular biology (Clifton, N.J.)
2020; 2118: 111-120
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