Rates and determinants of coronary and abdominal aortic artery calcium progression in the Veterans Affairs Diabetes Trial (VADT).
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.
Saremi
Aramesh
A
Phoenix VA Health Care System, Phoenix, Arizona, USA.
Moritz
Thomas E
TE
Anderson
Robert J
RJ
Abraira
Carlos
C
Duckworth
William C
WC
Reaven
Peter D
PD
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
D007004:Hypoglycemic Agents; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase
Radiology. 1998 Sep;208(3):807-14
9722864
Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):216-21
15499045
Circulation. 2007 May 29;115(21):2722-30
17502571
Arterioscler Thromb Vasc Biol. 2001 Dec;21(12):2051-8
11742884
Atherosclerosis. 2008 Nov;201(1):1-7
18561934
J Am Coll Cardiol. 2007 Dec 4;50(23):2218-25
18061069
AJR Am J Roentgenol. 2004 May;182(5):1327-32
15100140
Diabetes Care. 2009 Jan;32(1):141-6
18852333
Arterioscler Thromb Vasc Biol. 2004 Feb;24(2):331-6
14656730
Nephrol Dial Transplant. 2005 Nov;20(11):2472-8
16077143
Hypertension. 2005 Jul;46(1):238-43
15851627
Am J Cardiol. 2007 Nov 15;100(10):1543-7
17996516
Am Heart J. 2005 Apr;149(4):695-700
15990755
MMW Fortschr Med. 2007 Jun 28;149(27-28 Suppl):75-84
17619604
Biochem J. 1999 Mar 1;338 ( Pt 2):479-87
10024526
Arch Intern Med. 2009 Jul 27;169(14):1307-16
19636033
Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1272-7
15059806
Diabetologia. 2005 Feb;48(2):379-85
15688207
Diabetes Care. 2004 May;27(5):1115-20
15111530
Am J Cardiol. 2007 Jun 15;99(12):1714-7
17560880
Atherosclerosis. 2008 Apr;197(2):777-83
17920067
J Am Coll Cardiol. 2007 May 8;49(18):1860-70
17481445
N Engl J Med. 2009 Jan 8;360(2):129-39
19092145
Diabetes. 2009 Nov;58(11):2642-8
19651816
J Diabetes Complications. 2003 Nov-Dec;17(6):314-22
14583175