Background: Cardiac remodeling underpinning progressive hypertensive heart disease alters the three-dimensional structure of the extracellular matrix, as well as the laminar organization of myocardial sheetlets. The effect of pharmacological intervention on microstructural remodeling is not known. Objective: To examine the changes in myocardial microstructure that occur as a result of hypertensive heart disease, and the effect of pharmacological treatment. Methods: The spontaneously hypertensive rat (SHR) model of hypertensive heart disease was studied, and compared with the normotensive Wistar Kyoto (WKY) rat, and SHRs treated with angiotensin converting enzyme inhibitors (TSHR). Cardiac magnetic resonance was used to assess cardiac function and ventricular geometry. Excised myocardium was stained (picrosirius red) for collagen and extended volume confocal microscopy used to produce high-resolution image stacks. Results: At 24 months, TSHRs had significantly greater ejection fraction (P < 0.05), and performed significantly less stroke work than the untreated diseased SHRs (P < 0.01). TSHR hearts displayed no increased collagen deposition between sheetlets at 14 months, unlike SHR hearts at the same age, which showed thick collagen and scarring. Laminar organization was retained in aged TSHR hearts, while it was progressively lost in aged SHR hearts. Conclusions: In aged SHRs, angiotensin converting enzyme inhibition attenuates remodeling of myocardial extracellular matrix, preserves the laminar organization of myocardial sheetlets, and helps to maintain normal cardiac function.
We have developed techniques to automatically generate personalised biomechanical models of patients' hearts based on 3D cardiac images. We demonstrate this approach using multi-slice computed tomography images. Unsupervised segmentation was performed using non-rigid image registration with a segmented image. A finite element model was automatically fitted to the segmented data of the left ventricle. Passive and contractile myocardial mechanical properties were tuned to match the segmented surface geometries at end-diastole and end-systole, respectively. Global and regional indices of myocardial mechanics, including cardiac wall and myofibre strain distributions, were then quantified. This automated biomechanical modelling approach to cardiac image analysis provided noninvasive methods to characterise heart function, and may provide new quantitative diagnostic markers for heart failure.
International audiencen this study, we propose a methodology to estimate 3D+time maps of left ventricular fibre strain from human structural and dynamic MRI data. A finite element model integrates fibre principal direction throughout the left ventricle from an ex vivo human diffusion tensor MRI acquisition and motion from tagged MRI. This combination enables the estimation of fibre strain and its variation throughout the cardiac cycle. The long-term goal of this study is to apply this technique to an atlas of human fibre orientations and to investigate the importance of having subject-specific fibre orientation for fibre strain analysis
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