Abstract
BackgroundPressure overload left ventricular (LV) hypertrophy is characterized by increased cardiomyocyte width and ventricle wall thickness, however the regional variation of this remodeling is unclear. Cardiovascular magnetic resonance (CMR) diffusion tensor imaging (DTI) may provide a non-invasive, comprehensive, and geometrically accurate method to detect regional differences in structural remodeling in hypertrophy. We hypothesized that DTI parameters, such as fractional and planar anisotropy, would reflect myocyte remodeling due to pressure overload in a regionally-dependent manner.MethodsWe investigated the regional distributions of myocyte remodeling in rats with or without transverse aortic constriction (TAC) via direct measurement of myocyte dimensions with confocal imaging of thick tissue sections, and correlated myocyte cross-sectional area and other geometric features with parameters of diffusivity from ex-vivo DTI in the same regions of the same hearts.ResultsWe observed regional differences in several parameters from DTI between TAC hearts and SHAM controls. Consistent with previous studies, helix angles from DTI correlated strongly with those measured directly from histological sections (p < 0.001, R2 = 0.71). There was a transmural gradient in myocyte cross-sectional area in SHAM hearts that was diminished in the TAC group. We also found several regions of significantly altered DTI parameters in TAC LV compared to SHAM, especially in myocyte sheet angle dispersion and planar anisotropy. Among others, these parameters correlated significantly with directly measured myocyte aspect ratios.ConclusionsThese results show that structural remodeling in pressure overload LV hypertrophy is regionally heterogeneous, especially transmurally, with a greater degree of remodeling in the sub-endocardium compared to the sub-epicardium. Additionally, several parameters derived from DTI correlated significantly with measurements of myocyte geometry from direct measurement in histological sections. We suggest that DTI may provide a non-invasive, comprehensive method to detect regional structural myocyte LV remodeling during disease.
Highlights
Pressure overload left ventricular (LV) hypertrophy is characterized by increased cardiomyocyte width and ventricle wall thickness, the regional variation of this remodeling is unclear
In transverse aortic constriction (TAC) animals, a hemo-clip was inserted between the brachiocephalic and left carotid arteries, constricted to a fixed width of 0.5 mm, which constricts the aortic lumen to approximately 50–60% of its original cross-sectional area
The helix angles in this region were consistently slightly higher in TAC animals compared to SHAM controls by approximately 7–8 degrees at all points across the wall, whereas in the anterior region of the equator and base, the opposite was true
Summary
Pressure overload left ventricular (LV) hypertrophy is characterized by increased cardiomyocyte width and ventricle wall thickness, the regional variation of this remodeling is unclear. The well-known response of the left ventricle (LV) to such pressure overload is concentric hypertrophy, which is characterized by the addition of sarcomeres in parallel within cardiomyocytes, resulting in LV wall thickening without chamber dilation Such remodeling in pressure overload hypertrophy is considered a compensatory mechanism to maintain cardiac output despite increased downstream resistance to blood flow. This compensatory state, often leads to impaired diastolic filling, accompanied by wall thinning, chamber dilation, impaired systolic function, and eventual heart failure [2, 3]. These transmural gradients, together with other factors, are thought to contribute to normalizing the otherwise large gradients in stress and strain along the long-axis of the myocytes (sometimes referred to as “fiber” stress or strain) during both diastolic filling and systolic contraction [10,11,12,13,14,15]
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