Abstract
The long-standing high blood pressure (also known as hypertension) overworks the heart. Microstructural remodeling is a key factor of hypertensive heart disease progression. Diffusion tensor magnetic resonance imaging (DT-MRI) is a powerful tool for the rapid noninvasive nondestructive delineation of the cardiomyocyte organization. The spontaneously hypertensive rat (SHR) is a well-established model of genetic hypertension. The goal of this study was to employ high-resolution DT-MRI and the SHR animal model to assess the transmural layer-specific remodeling of myocardial microstructure associated with hypertension. Ex vivo experiments were performed on excised formalin-fixed hearts of aged SHRs (n = 4) and age-matched controls (n = 4). The DT-MRI-derived fractional anisotropy (FA), longitudinal diffusivity (λL), transversal diffusivity (λT), and mean diffusivity (MD) served as the readout parameters investigated at three transmural zones (i.e., endocardium, mesocardium, and epicardium). The helix angles (HAs) of the aggregated cardiomyocytes and the orientation of laminar sheetlets were also studied. Compared with controls, the SHRs exhibited decreased epicardial FA, while FA changes in the other two transmural regions were insignificant. No substantial differences were observed in the diffusivity parameters and the transmural course of HAs between the two groups. A consistent distribution pattern of laminar sheetlet orientation was not identified for either group. Our findings are in line with the known cellular microstructure from early painstaking histological studies. Biophysical explanations of the study outcomes are provided. In conclusion, our experimental findings indicate that the epicardial microstructure is more vulnerable to high blood pressure leading to more pronounced changes in this region during remodeling. DT-MRI is well-suited for elucidating these alterations. The revealed transmural nonuniformity of myocardial reorganization may shed light on the mechanisms of the microstructure-function relationship in hypertension progression. Our results provide insights into the management of patients with systemic arterial hypertension, thus prevent the progression toward heart failure. The findings of this study should be acknowledged by electromechanical models of the heart that simulate the specific cardiac pathology.
Highlights
Elevated blood pressure in the arteries is a serious condition that can lead to heart failure, stroke, kidney failure, and blindness among others1
From a clinical perspective, depicting the remodeling of cardiomyocyte arrangement in hypertension is of vital significance, as this would provide us with a novel insight on the structure-function relationship allowing us to better interpret and model the cardiac behavior in this pathology
The average ejection fraction (EF) was 69% for the Wistar Kyoto rats (WKYs) and 50% for the spontaneously hypertensive rat (SHR), confirming that the SHRs were in borderline heart failure stage
Summary
Elevated blood pressure in the arteries ( known as hypertension) is a serious condition that can lead to heart failure, stroke, kidney failure, and blindness among others. More than 1 in 5 adults live with hypertension all around the globe, and complications from persistent high blood pressure account for 12.8% of the total of all deaths worldwide every year. The chronic elevated arterial pressure adversely affects the cardiac function by compromising the organ’s ability to work as a pump which escalates into heart failure. From a clinical perspective, depicting the remodeling of cardiomyocyte arrangement in hypertension is of vital significance, as this would provide us with a novel insight on the structure-function relationship allowing us to better interpret and model the cardiac behavior in this pathology
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