title: Rates and determinants of coronary and abdominal aortic artery calcium progression in the Veterans Affairs Diabetes Trial (VADT).
abstract: OBJECTIVE
  To determine the predictors of progression of calcified atherosclerosis and the effect of intensive glycemic control on this process in patients with type 2 diabetes.
  
  
  METHODS
  As part of the Risk Factors, Atherosclerosis, and Clinical Events in Diabetes (RACED) substudy of the Veterans Affairs Diabetes Trial (VADT), 197 and 189 individuals with type 2 diabetes received baseline and follow-up computed tomographic scans for measurement of coronary and abdominal artery calcium, respectively. Standard and novel risk factors were assessed at baseline, and progression of calcified atherosclerosis was determined by several methods. Progression was defined both as a categorical (square root increase of volumetric scores ≥ 2.5 mm(3)) and continuous variable. In addition, annualized percent change of volume scores was determined.
  
  
  RESULTS
  After an average follow-up of 4.6 years, >75% of individuals demonstrated coronary (CAC) and abdominal artery calcification (AAC) progression. Progression increased with higher baseline calcium categories but was not influenced by standard risk factors. However, the albumin-to-creatinine ratio (ACR) (P = 0.02) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) (P = 0.01) predicted progression of CAC, and these results were not altered by adjustment for age and other traditional risk factors. Treatment assignment (intensive versus standard) within the VADT did not influence CAC or AAC progression, irrespective of baseline calcium category.
  
  
  CONCLUSIONS
  In patients with long-standing type 2 diabetes, baseline CAC, Lp-PLA(2), and ACR predicted progression of CAC. Intensive glycemic control during the VADT did not reduce progression of calcified atherosclerosis.
authors.affiliation: Phoenix VA Health Care System, Phoenix, Arizona, USA.
authors.forename: Aramesh
authors.initials: A
authors.lastname: Saremi
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Moritz
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Anderson
authors.forename: Carlos
authors.initials: C
authors.lastname: Abraira
authors.forename: William C
authors.initials: WC
authors.lastname: Duckworth
authors.forename: Peter D
authors.initials: PD
authors.lastname: Reaven
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism; D000368:Aged; D002114:Calcinosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D002986:Clinical Trials as Topic; D003324:Coronary Artery Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D006349:Heart Valve Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D007004:Hypoglycemic Agents; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase
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