BACKGROUND: Although rapid progression (RP) of coronary artery disease (CAD) has been shown to be a powerful predictor of cardiovascular events, predictors of RP are not fully understood in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: We prospectively investigated the clinical impact of glycemic variability (GV), as determined on continuous glucose monitoring system (CGMS), on RP of non-culprit lesions in 88 patients with ACS. RP was defined as ≥10% diameter reduction in a pre-existing stenosis ≥50%; ≥30% diameter reduction in a stenosis <50%; development of a new stenosis ≥30% in a previously normal segment; or progression of any stenosis to total occlusion. Patients were classified into 2 groups according to the presence (progressor, n=20) or absence (non-progressor, n=68) of RP. All patients were equipped with a CGMS during the stable phase, and mean amplitude of glycemic excursion (MAGE) was calculated as a marker of GV. Mean MAGE was significantly higher in progressors than in non-progressors (55±19 mg/dl vs. 37±18 mg/dl, P<0.01). On multiple logistic regression analysis, MAGE was an independent predictor of RP (odds ratio, 1.06 per 1 mg/dl; P<0.01). CONCLUSIONS: MAGE early after the onset of ACS is a predictor of RP of non-culprit lesions.
BACKGROUND: Although rapid progression (RP) of coronary artery disease (CAD) has been shown to be a powerful predictor of cardiovascular events, predictors of RP are not fully understood in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: We prospectively investigated the clinical impact of glycemic variability (GV), as determined on continuous glucose monitoring system (CGMS), on RP of non-culprit lesions in 88 patients with ACS. RP was defined as ≥10% diameter reduction in a pre-existing stenosis ≥50%; ≥30% diameter reduction in a stenosis <50%; development of a new stenosis ≥30% in a previously normal segment; or progression of any stenosis to total occlusion. Patients were classified into 2 groups according to the presence (progressor, n=20) or absence (non-progressor, n=68) of RP. All patients were equipped with a CGMS during the stable phase, and mean amplitude of glycemic excursion (MAGE) was calculated as a marker of GV. Mean MAGE was significantly higher in progressors than in non-progressors (55±19 mg/dl vs. 37±18 mg/dl, P<0.01). On multiple logistic regression analysis, MAGE was an independent predictor of RP (odds ratio, 1.06 per 1 mg/dl; P<0.01). CONCLUSIONS: MAGE early after the onset of ACS is a predictor of RP of non-culprit lesions.