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Post‐challenge glucose predicts coronary atherosclerotic progression in non‐diabetic, post‐menopausal women 1
Author(s) -
Mellen P. B.,
Bittner V.,
Herrington D. M.
Publication year - 2007
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2007.02222.x
Subject(s) - medicine , diabetes mellitus , body mass index , quartile , post hoc analysis , cardiology , endocrinology , coronary atherosclerosis , cholesterol , pathogenesis , coronary artery disease , confidence interval
Aims We sought to determine whether fasting or post‐challenge glucose were associated with progression of coronary atherosclerosis in non‐diabetic women. Methods We performed a post‐hoc analysis of 132 non‐diabetic women who underwent 75‐g oral glucose tolerance testing. The primary outcome of interest was progression of atherosclerosis determined by baseline and follow‐up coronary angiography, a mean of 3.1 ± 0.9 years apart. We analysed the association of change in minimal vessel diameter (ΔMD) by quartile of fasting and post‐challenge glucose using mixed models that included adjustment for age, systolic blood pressure, total : high‐density lipoprotein cholesterol ratio, current smoking, lipid‐lowering and anti‐hypertensive medication use and other covariates. Results At baseline, participants had a mean age of 65.7 ± 6.7 years and a mean body mass index of 27.9 ± 8.5 kg/m 2 . Although there were no significant differences in atherosclerotic progression by fasting glucose category ( P for trend across quartiles = 0.99), there was a significant inverse association between post‐challenge glucose and ΔMD (in mm) (Q1 : 0.01 ± 0.03; Q2 : 0.08 ± 0.03; Q3 : 0.13 ± 0.03; Q4 : 0.11 ± 0.03; P for trend = 0.02). Conclusions In post‐menopausal women without diabetes, post‐challenge glucose predicts angiographic disease progression. These findings suggest that even modest post‐challenge hyperglycaemia influences the pathogenesis of atherosclerotic progression.