TY - JOUR
T1 - Correlation between circulating adiponectin levels and coronary plaque regression during aggressive lipid-lowering therapy in patients with acute coronary syndrome
T2 - Subgroup analysis of JAPAN-ACS study
AU - Ohashi, Taiki
AU - Shibata, Rei
AU - Morimoto, Takeshi
AU - Kanashiro, Masaaki
AU - Ishii, Hideki
AU - Ichimiya, Satoshi
AU - Hiro, Takafumi
AU - Miyauchi, Katsumi
AU - Nakagawa, Yoshihisa
AU - Yamagishi, Masakazu
AU - Ozaki, Yukio
AU - Kimura, Takeshi
AU - Daida, Hiroyuki
AU - Murohara, Toyoaki
AU - Matsuzaki, Masunori
PY - 2010/9
Y1 - 2010/9
N2 - Objective: The Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome (JAPAN-ACS) study demonstrated that aggressive lipid-lowering therapy with a statin resulted in a significant regression of coronary atherosclerotic plaques in patients with ACS. Adiponectin is an adipocyte-derived protein with anti-atherogenic properties. Here, we investigated the association between adiponectin levels and the change in the plaque volume in ACS patients. Methods: Intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment, in 238 patients with ACS. Follow-up IVUS was performed between 8 and 12 months after the PCI. The percent change in the plaque volume (%PV) in a non-culprit coronary artery segment was evaluated. The serum adiponectin and lipid parameters were measured both at baseline and at the follow-up. Results: At baseline, adiponectin was correlated positively with HDL-cholesterol and negatively correlated with triglyceride, but no correlation was observed with the PV. Adiponectin levels increased significantly from 7.8 ± 4.6 μg/mL at baseline to 10.3 ± 6.9 μg/mL at the 8-12 months follow-up. The increase in adiponectin was also associated with an increase of HDL-cholesterol and decrease of triglyceride, however, no significant correlation was observed with the %PV. A significantly higher incidence of major adverse cardiac events (MACE) was observed in patients with hypo-adiponectinemia at baseline. A multiple logistic regression analysis identified adiponectin as a significant independent predictor of MACE. Conclusion: Adiponectin levels measured after PCI could serve as a marker of MACE in patients with ACS.
AB - Objective: The Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome (JAPAN-ACS) study demonstrated that aggressive lipid-lowering therapy with a statin resulted in a significant regression of coronary atherosclerotic plaques in patients with ACS. Adiponectin is an adipocyte-derived protein with anti-atherogenic properties. Here, we investigated the association between adiponectin levels and the change in the plaque volume in ACS patients. Methods: Intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment, in 238 patients with ACS. Follow-up IVUS was performed between 8 and 12 months after the PCI. The percent change in the plaque volume (%PV) in a non-culprit coronary artery segment was evaluated. The serum adiponectin and lipid parameters were measured both at baseline and at the follow-up. Results: At baseline, adiponectin was correlated positively with HDL-cholesterol and negatively correlated with triglyceride, but no correlation was observed with the PV. Adiponectin levels increased significantly from 7.8 ± 4.6 μg/mL at baseline to 10.3 ± 6.9 μg/mL at the 8-12 months follow-up. The increase in adiponectin was also associated with an increase of HDL-cholesterol and decrease of triglyceride, however, no significant correlation was observed with the %PV. A significantly higher incidence of major adverse cardiac events (MACE) was observed in patients with hypo-adiponectinemia at baseline. A multiple logistic regression analysis identified adiponectin as a significant independent predictor of MACE. Conclusion: Adiponectin levels measured after PCI could serve as a marker of MACE in patients with ACS.
UR - http://www.scopus.com/inward/record.url?scp=77956228825&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77956228825&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2010.05.005
DO - 10.1016/j.atherosclerosis.2010.05.005
M3 - Article
C2 - 20684825
AN - SCOPUS:77956228825
VL - 212
SP - 237
EP - 242
JO - Atherosclerosis
JF - Atherosclerosis
SN - 0021-9150
IS - 1
ER -