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1 Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA
2 Department of Internal Medicine, Division of Nephrology & Hypertension, Mayo Clinic College of Medicine, Rochester, MN, USA
3 Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Physiology & Biomedical Enginnering, Mayo Clinic College of Medicine, Rochester, MN, USA
4 Department of Internal Medicine, Division of Nephrology & Hypertension, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: lerman.lilach{at}mayo.edu.
Advanced hypertension (HT), associated with left ventricular hypertrophy (LVH), impairs myocardial microvascular function and structure and leads to increased myocardial hypoxia and growth factor activation. However, the effect of HT on microvascular architecture and its relation to microvascular function, prior to the development of LVH (early HT), remain unclear. Methods: Pigs were studied after 12 weeks of renovascular HT (n=7) or control (n=7). Myocardial microvascular function (blood volume and blood flow at baseline and in response to adenosine) was assessed using electron beam computed-tomography (CT). Microvascular architecture was subsequently studied ex-vivo using micro-CT, and microvessels (diameter<500µm) counted in-situ in 3-D images (40µm on-a-side cubic voxels). Myocardial expression of vascular endothelial growth factor, basic fibroblast growth factor, and hypoxia inducible factor-1
were also measured. Results: Left ventricular muscle mass was similar between the groups. The blood volume response to intravenous adenosine was attenuated in HT compared to normal animals (+7.4±17.0 vs. +46.2±12.3 % compared to baseline, p=0.48 and p=0.01, respectively). Microvascular spatial density in HT was significantly elevated compared to normal (246±26 vs. 125±20 vessels/cm2, p<0.05) and correlated inversely with the blood volume response to adenosine. Growth factors expression was increased in HT compared to control. Conclusion: Early HT elicits changes in myocardial microvascular architecture, which are associated with microvascular dysfunction and precede changes in muscle mass. These observations underscore the direct and early effects of HT on the myocardial vasculature.
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