Relationship between Advanced Glycation End Products and Plaque Progression in Patients with Acute Coronary Syndrome: The JAPAN-ACS Sub-study

Intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment (either 4 mg/day of pitavastatin or 20 mg/day of atorvastatin), in patients with ACS. In the 208 JAPAN-ACS subjects, PV using IVUS in non-culprit segment > 5 mm proximal or distal to the culprit lesion and, serum levels of AGEs and soluble RAGE (sRAGE) were measured at baseline and 8–12 months after PCI.At baseline, no differences in the levels of either AGEs or sRAGE were found between patients with DM and those without DM. The levels of AGEs decreased significantly with statin therapy from 8.6 ± 2.2 to 8.0 ± 2.1 U/ml (p < 0.001), whereas the levels of sRAGE did not change. There were no significant correlations between changes in PV and the changes in levels of AGEs as well as sRAGE. However, high baseline AGEs levels were significantly associated with plaque progression (odds ratio, 1.21; 95% confidence interval, 1.01 - 1.48; p = 0.044) even after adjusting for DM in multivariate logistic regression models.High baseline AGEs levels were associated with plaque progression in the JAPAN-ACS trial. This relationship was independent of DM. These findings suggest AGEs may be related to long-term glucose control and other oxidative stresses in ACS.NCT00242944Recent advances in plaque imaging have enabled the quantitative measurement of plaque volume (PV) and their characteristics[1,2]. Several clinical trials have observed significant plaque regression after treatment with HMG CoA-reductase inhibitors (statins) using intravascular ultrasound (IVUS) [3-6].Using IVUS, the Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN–ACS) trial has demonstrated that early aggressive statin therapy (either pitavastatin or atorvastatin) in patients with acute coronary syndrome (ACS) significantly reduces PV of non-culprit coronary lesions during the first 8–12 months after ACS [7]. In this trial, the regression o