Improvement in coronary endothelial function is independently associated with a slowed progression of coronary artery calcification in type 2 diabetes mellitus.
OBJECTIVE
To examine a relationship between alterations of structure and function of the arterial wall in response to glucose-lowering therapy in type 2 diabetes mellitus (DM) after a 1-year follow-up (FU).


RESULTS
In DM (n = 22) and in healthy controls (n = 17), coronary artery calcification (CAC) was assessed with electron beam tomography and carotid intima-media thickness (IMT) with ultrasound, whereas coronary function was determined with positron emission tomography-measured myocardial blood flow (MBF) at rest, during cold pressor testing (CPT), and during adenosine stimulation at baseline and after FU. The decrease in plasma glucose in DM after a mean FU of 14 +/- 1.9 months correlated with a lower progression of CAC and carotid IMT (r = 0.48, P < or = 0.036 and r = 0.46, P < or = 0.055) and with an improvement in endothelium-related DeltaMBF to CPT and to adenosine (r = 0.46, P < or = 0.038 and r = 0.36, P < or = 0.056). After adjusting for metabolic parameters by multivariate analysis, the increases in DeltaMBF to CPT after glucose-lowering treatment remained a statistically significant independent predictor of the progression of CAC (P < or = 0.001 by one-way analysis of variance).


CONCLUSIONS
In DM, glucose-lowering treatment may beneficially affect structure and function of the vascular wall, whereas the observed improvement in endothelium-related coronary artery function may also mediate direct preventive effects on the progression of CAC.
Schindler
Thomas H
TH
Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, University of California at Los Angeles, 650 Charles E. Young Drive South, B2-085J CHS, Box 95648, Los Angeles, CA 90095-6948, USA.
Cadenas
Jerson
J
Facta
Alvaro D
AD
Li
Yanjie
Y
Olschewski
Manfred
M
Sayre
James
J
Goldin
Jonathan
J
Schelbert
Heinrich R
HR
D000328:Adult; D002114:Calcinosis / Q000188:drug therapy* / Q000503:physiopathology; D002340:Carotid Artery Diseases / Q000473:pathology; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology
D007004:Hypoglycemic Agents