著者
Junya Ako Kiyoshi Hibi Kenichi Tsujita Takafumi Hiro Yoshihiro Morino Ken Kozuma Toshiro Shinke Hiromasa Otake Kiyoko Uno Michael J Louie Yoshiharu Takagi Katsumi Miyauchi
出版者
The Japanese Circulation Society
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
pp.CJ-19-0412, (Released:2019-08-20)
参考文献数
20
被引用文献数
34

Background:In patients with acute coronary syndrome (ACS), alirocumab reduced the risk of recurring ischemic events. ODYSSEY J-IVUS assessed the effect of alirocumab on coronary atheroma volume in Japanese patients recently hospitalized with ACS and hypercholesterolemia, using intravascular ultrasound imaging analysis.Methods and Results:Patients (n=206) who at index ACS diagnosis either had low-density lipoprotein cholesterol (LDL-C) ≥2.59 mmol/L (≥100 mg/dL) despite stable statin therapy, or were not on statins with LDL-C levels above target after statin initiation, were randomized (1:1) to alirocumab (75 mg every 2 weeks [Q2 W]/up to 150 mg Q2 W), or standard of care (SoC; atorvastatin ≥10 mg/day or rosuvastatin ≥5 mg/day) for 36 weeks. The primary efficacy endpoint (week [W] 36 mean [standard error] percent change in normalized total atheroma volume [TAV] from baseline) was −3.1 (1.0)% with SoC vs. −4.8 (1.0)% with alirocumab (between-group difference: −1.6 [1.4]; P=0.23). W36 absolute change from baseline in percent atheroma volume was −1.3 (0.4)% (SoC) and −1.4 (0.4)% (alirocumab; nominal P=0.79). At W36, LDL-C was reduced from baseline by 13.4% (SoC) vs. 63.9% (alirocumab; nominal P<0.0001). In total, 61.8% (SoC) and 75.7% (alirocumab) of patients reported treatment-emergency adverse events.Conclusions:In Japanese patients with ACS and hypercholesterolemia inadequately controlled despite statin therapy, from baseline to W36, a numerically greater percent reduction in normalized TAV was observed with alirocumab vs. SoC, which did not reach statistical significance.
著者
Takafumi Hiro
出版者
日本循環器学会
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
pp.CJ-17-0416, (Released:2017-04-27)
参考文献数
12
被引用文献数
2

The 66thAnnual Scientific Sessions and Expo of the American College of Cardiology (ACC) were held at the Walter E. Washington Convention Center, Washington DC, from March 17thto 19th, 2017. This meeting offered 23 Late-Breaking Clinical Trial (LBCT) presentations, 17 Featured Clinical Research presentations with and without LBCT, and 2,572 abstracts presented in oral and poster sessions by over 2,000 experts. This report presents the highlights of this meeting, including the opening showcase, several important LBCTs and some international joint symposiums.
著者
Junnichi Ishii Kosuke Kashiwabara Yukio Ozaki Hiroshi Takahashi Fumihiko Kitagawa Hideto Nishimura Hideki Ishii Satoshi Iimuro Hideki Kawai Takashi Muramatsu Hiroyuki Naruse Hiroshi Iwata Sadako Tanizawa-Motoyama Hiroyasu Ito Eiichi Watanabe Yutaka Matsuyama Yoshihiro Fukumoto Ichiro Sakuma Yoshihisa Nakagawa Kiyoshi Hibi Takafumi Hiro Seiji Hokimoto Katsumi Miyauchi Hiroshi Ohtsu Hideo Izawa Hisao Ogawa Hiroyuki Daida Hiroaki Shimokawa Yasushi Saito Takeshi Kimura Masunori Matsuzaki Ryozo Nagai
出版者
Japan Atherosclerosis Society
雑誌
Journal of Atherosclerosis and Thrombosis (ISSN:13403478)
巻号頁・発行日
vol.29, no.10, pp.1458-1474, 2022-10-01 (Released:2022-10-01)
参考文献数
33
被引用文献数
1 9

Aim: We investigated the relationship between small dense low-density cholesterol (sdLDL-C) and risk of major adverse cardiovascular events (MACE) in patients treated with high- or low-dose statin therapy.Methods: This was a prospective case-cohort study within the Randomized Evaluation of Aggressive or Moderate Lipid-Lowering Therapy with Pitavastatin in Coronary Artery Disease (REAL-CAD) study, a randomized trial of high- or low-dose (4 or 1 mg/d pitavastatin, respectively) statin therapy, in patients with stable coronary artery disease (CAD). Serum sdLDL-C was determined using an automated homogenous assay at baseline (randomization after a rule-in period, >1 month with 1 mg/d pitavastatin) and 6 months after randomization, in 497 MACE cases, and 1543 participants randomly selected from the REAL-CAD study population.Results: High-dose pitavastatin reduced sdLDL-C by 20% than low-dose pitavastatin (p for interaction <0.001). Among patients receiving low-dose pitavastatin, baseline sdLDL-C demonstrated higher MACE risk independent of LDL-C (hazard ratio [95% confidence interval], 4th versus 1st quartile, 1.67 [1.04–2.68]; p for trend=0.034). High-dose (versus low-dose) pitavastatin reduced MACE risk by 46% in patients in the highest baseline sdLDL-C quartile (>34.3 mg/dL; 0.54 [0.36–0.81]; p=0.003), but increased relative risk by 40% in patients with 1st quartile (≤ 19.5 mg/dL; 1.40 [0.94–2.09]; p=0.099) and did not alter risk in those in 2nd and 3rd quartiles (p for interaction=0.002).Conclusions: These findings associate sdLDL-C and cardiovascular risk, independent of LDL-C, in statin-treated CAD patients. Notably, high-dose statin therapy reduces this risk in those with the highest baseline sdLDL-C.
著者
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 for the JAPAN-ACS Investigators
出版者
日本循環器学会
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
vol.76, no.12, pp.2840-2847, 2012 (Released:2012-11-22)
参考文献数
32
被引用文献数
4 6

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 HbA1c. 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.  (Circ J 2012; 76: 2840–2847)
著者
Tadateru Takayama Takafumi Hiro Masakazu Yamagishi Hiroyuki Daida Atsushi Hirayama Satoshi Saito Tetsu Yamaguchi Masunori Matsuzaki The COSMOS Investigators
出版者
日本循環器学会
雑誌
Circulation Journal (ISSN:13469843)
巻号頁・発行日
vol.73, no.11, pp.2110-2117, 2009 (Released:2009-10-23)
参考文献数
29
被引用文献数
109 153

Background: It has been suggested that intensive lipid-lowering therapy using statins significantly decreases atheromatous plaque volume. The effect of rosuvastatin on plaque volume in patients with stable coronary artery disease (CAD), including those receiving prior lipid-lowering therapy, was examined in the present study. Methods and Results: A 76-week open-label trial was performed at 37 centers in Japan. Eligible patients began treatment with rosuvastatin 2.5 mg/day, which could be increased at 4-week intervals to ≤20 mg/day. A total of 214 patients underwent intravascular ultrasound (IVUS) at baseline; 126 patients had analyzable IVUS images at the end of the study. The change in the serum low-density lipoprotein-cholesterol level from baseline to end of follow-up was -38.6 ±16.9%, whereas that of high-density lipoprotein-cholesterol was +19.8 ±22.9% (both P<0.0001). Percent change of plaque volume, the primary endpoint, was -5.1 ±14.1% (P<0.0001). Conclusions: Rosuvastatin exerted significant regression of coronary plaque volume in Japanese patients with stable CAD, including those who had previously used other lipid-lowering drugs. Rosuvastatin might be useful in the setting of secondary prevention in patients with stable CAD. (Circ J 2009; 73: 2110-2117)