BACKGROUND: Previous studies demonstrated the inverse association of adiponectin with coronary artery disease (CAD) especially in men with acute coronary syndrome, however their association with in vivo plaque vulnerability in stable CAD, which may be reflected by the thin-cap fibroatheroma (TCFA) prevalence, remains unknown. METHODS: In 50 men with stable CAD, we identified TCFA with multi-vessel examination of combined use of virtual histology intravascular ultrasound (VH-IVUS) and optical coherence tomography (OCT). The definition of TCFA was described as follows; necrotic-core rich lesion (% necrotic-core >10%) without evidence of an overlying fibrous component and % plaque-volume >40% in at least 3 consecutive frames by VH-IVUS, and the thinnest fibrous-cap thickness <65 microm by OCT. The patients were divided into two groups, patients with TCFA and without TCFA, and plasma adiponectin level was compared between the groups. RESULTS: Among 50 patients, we could observe 116 vessels (2.32+/-0.47 vessel/patient). At least one TCFA was identified in 20 patients. Patients with TCFA had significantly lower plasma adiponectin levels than patients without TCFA (P<0.0001). Furthermore, the plasma adiponectin levels in patients with multi-vessel TCFA were significantly lower than those in patients with single-vessel TCFA (P=0.049). Multivariate logistic regression analysis revealed that plasma adiponectin was the strongest predictive factor of the presence of TCFA (P=0.0007). CONCLUSIONS: Low plasma adiponectin was associated with the presence of TCFA in men with stable CAD. This finding suggests that, in these subjects, it may be a biomarker that can be used to stratify "vulnerable patients" into risk categories. Copyright (c) 2009. Published by Elsevier Ireland Ltd.
BACKGROUND: Previous studies demonstrated the inverse association of adiponectin with coronary artery disease (CAD) especially in men with acute coronary syndrome, however their association with in vivo plaque vulnerability in stable CAD, which may be reflected by the thin-cap fibroatheroma (TCFA) prevalence, remains unknown. METHODS: In 50 men with stable CAD, we identified TCFA with multi-vessel examination of combined use of virtual histology intravascular ultrasound (VH-IVUS) and optical coherence tomography (OCT). The definition of TCFA was described as follows; necrotic-core rich lesion (% necrotic-core >10%) without evidence of an overlying fibrous component and % plaque-volume >40% in at least 3 consecutive frames by VH-IVUS, and the thinnest fibrous-cap thickness <65 microm by OCT. The patients were divided into two groups, patients with TCFA and without TCFA, and plasma adiponectin level was compared between the groups. RESULTS: Among 50 patients, we could observe 116 vessels (2.32+/-0.47 vessel/patient). At least one TCFA was identified in 20 patients. Patients with TCFA had significantly lower plasma adiponectin levels than patients without TCFA (P<0.0001). Furthermore, the plasma adiponectin levels in patients with multi-vessel TCFA were significantly lower than those in patients with single-vessel TCFA (P=0.049). Multivariate logistic regression analysis revealed that plasma adiponectin was the strongest predictive factor of the presence of TCFA (P=0.0007). CONCLUSIONS: Low plasma adiponectin was associated with the presence of TCFA in men with stable CAD. This finding suggests that, in these subjects, it may be a biomarker that can be used to stratify "vulnerable patients" into risk categories. Copyright (c) 2009. Published by Elsevier Ireland Ltd.
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