Right ventricle hypertrophy in a porcine model restored capillary perfusion and wall shear stress to nearly homeostatic levels throughout most of the vasculature after 5 weeks.
Compensatory vascular remodeling in right ventricular hypertrophy functionally restores perfusion at the arteriolar and capillary level and normalizes wall shear stress.
It has been shown that right ventricle (RV) hypertrophy involves significant compensatory vascular growth and remodeling. The objective of the present study was to determine the functional implications of the vascular growth and remodeling through a full flow analysis of arterial tree down to first capillary segments. A computer reconstruction of RV branches including the proximal right coronary artery to the posterior descending artery was established based on measured morphometric data in arrested, vasodilated porcine heart. The flows were computed throughout the reconstructed trees based on conservation of mass and momentum and appropriate pressure boundary conditions. It was found that the flow rate was significantly increased in large epicardial coronary arteries in hypertrophic as compared with control hearts but normalized in the intramyocardial coronary arteries and smaller vessels in RV hypertrophy primarily because of the significant increase in number of arterioles. Furthermore, the wall shear stress was restored to nearly homeostatic levels throughout most of the vasculature after 5 weeks of RV hypertrophy. The compensatory remodeling in RV hypertrophy functionally restores the perfusion at the arteriolar and capillary level and wall shear stress in most of larger vessels. This is the first full analysis of coronary arterial tree, with millions of vessels, in cardiac hypertrophy that reveals the compensatory adaptation of structure to function.
Huo et al. (2007) studied Right ventricle hypertrophy. Right ventricle hypertrophy vs. Control hearts was evaluated on Flow rate and wall shear stress. Right ventricle hypertrophy in a porcine model restored capillary perfusion and wall shear stress to nearly homeostatic levels throughout most of the vasculature after 5 weeks.