Clustering of metabolic syndrome components attenuates coronary plaque regression during intensive statin therapy in patients with acute coronary syndrome: the JAPAN-ACS subanalysis study
Hiroaki Takashima, Yukio Ozaki, Takeshi Morimoto, Takeshi Kimura, Takafumi Hiro, Katsumi Miyauchi, Yoshihisa Nakagawa, Masakazu Yamagishi, Hiroyuki Daida, Tomofumi Mizuno, Kenji Asai, Yasuo Kuroda, Takashi Kosaka, Yasushi Kuhara, Akiyoshi Kurita, Kazuyuki Maeda, Tetsuya Amano, Masunori Matsuzaki, JAPAN-ACS Investigators, Hiroaki Takashima, Yukio Ozaki, Takeshi Morimoto, Takeshi Kimura, Takafumi Hiro, Katsumi Miyauchi, Yoshihisa Nakagawa, Masakazu Yamagishi, Hiroyuki Daida, Tomofumi Mizuno, Kenji Asai, Yasuo Kuroda, Takashi Kosaka, Yasushi Kuhara, Akiyoshi Kurita, Kazuyuki Maeda, Tetsuya Amano, Masunori Matsuzaki, JAPAN-ACS Investigators
Abstract
Background: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) trial showed that intensive statin therapy could induce significant coronary plaque regression in acute coronary syndrome (ACS). We evaluated the impact of metabolic syndrome (MetS) and its components on coronary plaque regression in the JAPAN-ACS patients.
Methods and results: Serial intravascular ultrasound measurements over 8-12 months were performed in 242 ACS patients receiving pitavastatin or atorvastatin. Patients were divided into groups according to the presence of MetS or the number of MetS components. Although the percent change in plaque volume (%PV) was not significantly different between the MetS (n=119) and non-MetS (n=123) groups (P=0.50), it was significantly associated with an increasing number of MetS components (component 0: -24.0%, n=7; components 1: -20.8%, n=31; components 2: -16.1%, n=69; components 3: -18.7%, n=83; components 4: -13.5%, n=52; P=0.037 for trend). The percent change in body mass index (%BMI) significantly correlated with %PV (r=0.15, P=0.021), especially in the MetS components 4 group (r=0.35, P=0.017). In addition, %BMI was an independent predictor of plaque regression after adjustment for the changes of low- and high-density lipoprotein cholesterol, triglycerides and HbA(1c).
Conclusions: The clustering of MetS components, but not the presence of MetS itself, could attenuate coronary plaque regression during intensive statin therapy in ACS patients. Therefore, to achieve a greater degree of plaque regression, it is necessary to treat to each MetS component and use lifestyle modification.
Trial registration: ClinicalTrials.gov NCT00242944.
Source: PubMed