title: Eutrophic remodeling of small arteries in type 1 diabetes mellitus is enabled by metabolic control: a 10-year follow-up study.
abstract: Type 2 diabetes mellitus profoundly changes small artery remodeling in response to hypertension. Abnormal increases of both wall thickness and lumen diameter are associated with an increased mortality. Changes to small artery structure in response to blood pressure (BP) in patients with type 1 diabetes mellitus have never been examined. In 1997, 17 patients with type 1 diabetes mellitus and 9 control subjects underwent in vitro assessment of gluteal-fat small arteries using pressure myography. Patients with BP <140/90 mm Hg (systolic BP: 119+/-3 mm Hg; n=12) had normal-resistance artery structure. However, patients with BP >140/90 mm Hg (systolic BP: 152+/-5 mm Hg; n=5) demonstrated vascular hypertrophic remodeling with a significant increase in the medial cross-sectional area and wall thickness. In 2008, 8 of the original 17 diabetic patients returned for a repeat assessment. All 8 of the patients had significantly improved cholesterol (2008: 154+/-9 mg/dL versus 1997: 191+/-9 mg/dL; P=0.01) and low-density lipoprotein cholesterol (2008: 79+/-8 mg/dL versus 1997: 122+/-9 mg/dL; P=0.003) but higher BPs (systolic BP: 2008: 136+/-3 mm Hg versus 1997: 119+/-6 mm Hg; P=0.03). Glycemia was improved (2008: 7.9+/-0.3% versus 1997: 8.9+/-0.6%; P=0.17), but not significantly so. In the small arteries studied, there were significant increases in medial wall thickness and wall:lumen ratio, but cross-sectional area was unchanged, indicating eutrophic remodeling. Collectively, these findings suggest that, with poor metabolic control, small arteries from patients with type 1 diabetes mellitus show hypertrophic growth in response to elevated BP, similar to that seen in type 2 diabetes mellitus. However, metabolic improvements enable eutrophic remodeling to occur in response to an increase in BP. This has only been observed previously in patients without diabetes mellitus.
authors.affiliation: Department of Medicine, Manchester University, United Kingdom.
authors.forename: Adam S
authors.initials: AS
authors.lastname: Greenstein
authors.forename: Anna
authors.initials: A
authors.lastname: Price
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Sonoyama
authors.forename: Angela
authors.initials: A
authors.lastname: Paisley
authors.forename: Kaivan
authors.initials: K
authors.lastname: Khavandi
authors.forename: Sarah
authors.initials: S
authors.lastname: Withers
authors.forename: Linda
authors.initials: L
authors.lastname: Shaw
authors.forename: Oscar
authors.initials: O
authors.lastname: Paniagua
authors.forename: Rayaz A
authors.initials: RA
authors.lastname: Malik
authors.forename: Anthony M
authors.initials: AM
authors.lastname: Heagerty
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D004576:Electromyography; D004727:Endothelium / Q000503:physiopathology; D005500:Follow-Up Studies; D006801:Humans; D008875:Middle Aged; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D002784:Cholesterol