著者

Hideki Nakamura Yosuke Nagasawa Hitomi Kobayashi Masako Tsukamoto Tadateru Takayama Noboru Kitamura

出版者

The Japanese Society of Internal Medicine

雑誌

Internal Medicine (ISSN:09182918)

巻号頁・発行日

pp.9433-22, (Released:2022-04-23)

参考文献数

24

被引用文献数

1

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We herein report a 60-year-old woman who experienced severe flare of rheumatoid arthritis (RA) and Epstein-Barr virus (EBV) positivity following administration of the mRNA-type SARS-CoV-2 vaccine. Since 40 years old, she had been in long-term remission of anti-citrullinated protein antibody-positive RA. Ten days after SARS-CoV-2 vaccination, she presented with a high fever and polyarthritis, active synovitis on joint ultrasound, a clinical disease activity index of 35, and positivity for anti-EA DR IgG and EBV deoxyribonucleic acid (EBV-DNA). Tocilizumab was introduced to treat RA. The RA disease activity disappeared, and anti-EA DR IgG and EBV-DNA became negative.

著者

Makoto Watanabe Kazutaka Aonuma Toyoaki Murohara Yasuo Okumura Takeshi Morimoto Sadanori Okada Sunao Nakamura Shiro Uemura Koichiro Kuwahara Tadateru Takayama Naofumi Doi Tamio Nakajima Manabu Horii Kenichi Ishigami Kazumiki Nomoto Daisuke Abe Koji Oiwa Kentaro Tanaka Terumasa Koyama Akira Sato Tomoya Ueda Tsunenari Soeda Yoshihiko Saito PREVENT CINC-J Investigators

出版者

The Japanese Circulation Society

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

pp.CJ-21-0869, (Released:2022-04-22)

参考文献数

37

被引用文献数

2

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Background: Previous studies have reported that high-dose strong statin therapy reduces the incidence of contrast-induced nephropathy (CIN) in statin naïve patients; however, the efficacy of high-dose strong statins for preventing CIN in real-world clinical practice remains unclear. The aim of this study was to evaluate the efficacy of strong statin therapy in addition to fluid hydration for preventing CIN after cardiovascular catheterization.Methods and Results: This prospective, multicenter, randomized controlled trial included 420 patients with chronic kidney disease who underwent cardiovascular catheterization. They were assigned to receive high-dose pitavastatin (4 mg/day × 4 days) on the day before and of the procedure and 2 days after the procedure (Statin group, n=213) or no pitavastatin (Control group, n=207). Isotonic saline hydration combined with a single bolus of sodium bicarbonate (20 mEq) was scheduled for administration to all patients. In the control group, statin therapy was continued at the same dose as that before randomization. CIN was defined as a ≥0.5 mg/dL increase in serum creatinine or ≥25% above baseline at 48 h after contrast exposure. Before randomization, 83% of study participants were receiving statin treatment. The statin group had a higher incidence of CIN than the control group (3.0% vs. 0%, P=0.01). The 12-month rate of major adverse cardiovascular events was similar between the 2 groups.Conclusions: High-dose pitavastatin increases the incidence of CIN in this study population.

著者

Kazuhisa Kodama Sei Komatsu Yasunori Ueda Tadateru Takayama Jyunji Yajima Shinsuke Nanto Hiroshi Matsuoka Satoshi Saito Atsushi Hirayama

出版者

日本循環器学会

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

vol.74, no.9, pp.1922-1928, 2010 (Released:2010-08-25)

参考文献数

31

被引用文献数

29 51

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Background: Few studies have serially monitored the change of coronary plaque after statin therapy using multiple plaque imaging modalities. Methods and Results: A prospective open-label trial was performed to assess coronary plaque regression and stabilization following 52 weeks of pitavastatin treatment (2 mg/day). Coronary segments that included the most diseased plaque of 90 patients determined on angioscopy were analyzed using intravascular ultrasound (IVUS). The yellow grade of each plaque of 46 patients who had matched angioscopy and IVUS data was evaluated on angioscopy. Low-density lipoprotein-cholesterol (LDL-C) was reduced 34.5% (145.0±24.0 mg/dl to 93.6±22.6 mg/dl, P<0.001), and high-density lipoprotein cholesterol increased 17.8% (44.9±11.1 mg/dl to 51.9±11.7 mg/dl, P<0.001). Yellow grade decreased (2.9±0.8 to 2.6±0.7, P=0.040) during 52 weeks. The reduction of yellow grade was not correlated with the LDL-C level at 52 weeks or its change. The change of yellow grade was inversely correlated with maximum yellow grade at baseline. Percent atheroma volume on IVUS did not change during 52 weeks, but its change for 52 weeks was significantly correlated with LDL-C level at 52 weeks (Spearman's rank correlation coefficient 0.312, P=0.035). Conclusions: Fixed dose pitavastatin stabilized vulnerable coronary plaques by the reduction of yellow grade without significant reduction of plaque volume. The stabilization and regression of atherosclerotic plaques by statin may differ, but both nonetheless contribute to the reduction of cardiovascular events (UMIN Clinical Trials Registry UMIN000001107).  (Circ J 2010; 74: 1922 - 1928)

著者

Atsushi Hirayama Satoshi Saito Yasunori Ueda Tadateru Takayama Junko Honye Sei Komatsu Osamu Yamaguchi Yuxin Li Junji Yajima Shinsuke Nanto Kenji Takazawa Kazuhisa Kodama

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.4, pp.718-725, 2009 (Released:2009-03-25)

参考文献数

27

被引用文献数

32 83

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Background: The aim of this study was to elucidate the time course of atorvastatin-induced changes in vulnerable plaque using angioscopy and intravascular ultrasound (IVUS). Methods and Results: Fifty-seven hypercholesterolemic patients with coronary artery disease (CAD) were treated with atorvastatin (10-20 mg/day) for 80 weeks and then coronary plaques were evaluated with angioscopy and IVUS. Angioscopic images were classified into 6 grades (0-5) based on yellow color intensity. A 20-mm segment containing angioscopically-identified yellow plaque was also examined by IVUS to measure atheroma volume. The mean angioscopic grade of 58 yellow plaques significantly decreased from 1.5 (95% confidence interval [CI] 1.2 to 1.8) to 1.1 (95%CI 0.9 to 1.3, P=0.012) at week 28 and 1.2 (95%CI 0.9 to 1.4, P=0.024) at week 80. Mean volume of 30 lesions, including the 58 yellow plaques, significantly reduced -8.3% (95%CI -11.5 to -5.2) at week 28 (P<0.001 for baseline vs week 28) and -17.8% (95%CI -23.9 to -11.8) at week 80 (P<0.001 for baseline vs week 80). Conclusions: In patients with CAD treated with atorvastatin, serial analysis with angioscopy demonstrated early loss of yellow color in plaques, and IVUS volumetric analysis showed subsequent plaque regression. Both changes possibly indicate reduction of plaque vulnerability in an additive manner. (Circ J 2009; 73: 718 - 725)

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

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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)