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
N1 - Funding Information:
The Japan Heart Foundation funded this study with an unrestricted grant from Kowa Pharmaceutical. Kowa pharmaceutical participated to prepare the study design. However, investigators or independent Clinical Research Coordinator conducted final decision of the study design, database maintenance, made manuscript, and decided to submit the article, independent statistician analysed the data.
Funding Information:
Dr. Ohashi, Shibata, Kanashiro, Ishii and Ichimiya have no conflict of interest. Dr. Hiro has received honoraria for the lectures from Kowa pharmaceutical, Pfizer and Astellas Pharma. Dr. Miyauchi has received honoraria for the lectures from Kowa pharmaceutical, Pfizer and Astellas Pharma. Dr. Nakagawa has received honoraria for the lectures from Kowa pharmaceutica, Pfizer and Astellas Pharma. Dr. Yamagishi has received honoraria for the lectures from Kowa pharmaceutical, Pfizer and Astellas Pharma. Dr. Ozaki is an advisory member of Kowa pharmaceutical and has received honoraria for the lectures from Pfizer and Kowa pharmaceutical. Dr. T Kimura is an advisory member of Kowa pharmaceutical, Pfizer and has received honoraria for the lectures from Kowa pharmaceutical, Pfizer and Astellas Pharma. Dr. Morimoto has received honoraria for the lectures from Kowa pharmaceutical and Pfizer. Dr. Daida is an advisory member of Kowa pharmaceutical, and has received honoraria for the lectures and research grants from Kowa pharmaceutical, Pfizer and Astellas Pharma. Dr. Murohara has no conflict of interest. Dr. Matsuzaki is an advisory member of Kowa pharmaceutical and Pfizer, has received honoraria for the lectures and research grants from Kowa pharmaceutical, Pfizer and Astellas Pharma.
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
SN - 0021-9150
VL - 212
SP - 237
EP - 242
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -