title: Compensatory remodeling of coronary microvasculature maintains shear stress in porcine left-ventricular hypertrophy.
abstract: BACKGROUND
  Hypertension-induced left-ventricular hypertrophy (LVH) is generally accompanied with coronary neovascularization. The extent of vascular growth or rarefaction depends on many factors (e.g. age, duration of hypertension, degree of hypertrophy). Here, we hypothesize that there is a compensatory vascular growth that maintains uniform wall shear stress (WSS) in perfusion arterioles (diameters of 8-60 μm) in LVH of young porcine.
  
  
  METHODS
  To test this hypothesis, we investigated LVH in young porcine after 5 weeks of supravalvular aortic stenosis (3 months of age). The morphometry (diameters, lengths, number and connectivity of vessels) of the entire left circumflex (LCx) arterial tree was determined and a hemodynamic network analysis was used to calculate the distribution of pressure, flow and WSS throughout the tree in the control and LVH groups.
  
  
  RESULTS
  It was found that the number of vessels and the weight of left ventricle (LV) in hypertrophy increased 1.5 and 1.2 times, respectively, and the length of the LCx main trunk increased by 3 cm (36% increase), as compared with those in control group. There were similar myocardial blood flows of 0.87 ± 0.24 and 0.94 ± 0.38 ml/min per g in control and LVH hearts, respectively. The compensatory remodeling in early LVH restores WSS in the smaller perfusion arterioles, but not in the larger epicardial branches.
  
  
  CONCLUSIONS
  The present findings quantify the structural and functional remodeling in the entire LCx arterial tree in response to LVH, which reflect heterogeneity in vascular morphometry and hemodynamics from small to large vessels. These conclusions enhance our understanding of compensatory vascular remodeling in LVH of pediatric heart.
authors.affiliation: Department of Biomedical Engineering, Surgery and Cellular and Integrative Physiology, IUPUI, Indianapolis, Indianapolis, Indiana 46202, USA.
authors.forename: Yunlong
authors.initials: Y
authors.lastname: Huo
authors.forename: Ghassan S
authors.initials: GS
authors.lastname: Kassab
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D021921:Aortic Stenosis, Supravalvular / Q000150:complications; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D055806:Microvessels / Q000473:pathology* / Q000503:physiopathology; D013552:Swine