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Lipoprotein(a) is associated with necrotic core progression of non-culprit coronary lesions in statin-treated patients with angina pectoris

Tsuyoshi Nozue1*, Shingo Yamamoto2, Shinichi Tohyama3, Kazuki Fukui4, Shigeo Umezawa5, Yuko Onishi5, Tomoyuki Kunishima6, Akira Sato7, Toshihiro Nozato8, Shogo Miyake9, Youichi Takeyama10, Yoshihiro Morino11, Takao Yamauchi12, Toshiya Muramatsu13, Kiyoshi Hibi14, Mitsuyasu Terashima15 and Ichiro Michishita1

Author Affiliations

1 Division of Cardiology, Department of Internal Medicine, Yokohama Sakae Kyosai Hospital, 132 Katsura-cho, Sakae-ku, Yokohama 247-8581, Japan

2 Department of Cardiology, Tsurumi Nishiguchi Hospital, Yokohama, Japan

3 Department of Cardiology, Yokohama Seamen’s Insurance Hospital, Yokohama, Japan

4 Department of Cardiology, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan

5 Department of Cardiology, Hiratsuka Kyosai Hospital, Hiratsuka, Japan

6 Fourth Department of Internal Medicine, Mizonokuchi Hospital, Teikyo University School of Medicine, Kawasaki, Japan

7 Cardiovascular Center, Yokosuka Kyosai Hospital, Yokosuka, Japan

8 Department of Cardiology, National Hospital Organization, Disaster Medical Center, Tokyo, Japan

9 Department of Cardiology, Ebina General Hospital, Ebina, Japan

10 Division of Cardiology, Showa University Fujigaoka Rehabilitation Hospital, Yokohama, Japan

11 Department of Cardiology, Tokai University School of Medicine, Isehara, Japan

12 Department of Cardiology, Tokyo Women’s Medical University, Tokyo, Japan

13 Department of Cardiology, Saiseikai Yokohama City Eastern Hospital, Yokohama, Japan

14 Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan

15 Cardiovascular Imaging Center, Toyohashi, Japan

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Lipids in Health and Disease 2014, 13:59  doi:10.1186/1476-511X-13-59

Published: 1 April 2014



Statin therapy results in regression and stabilization of coronary artery plaques, and reduces the incidence of coronary artery disease. However, statin therapy does not effectively halt the accumulation of necrotic core in all patients. The purpose of the present study was to identify the predictors associated with necrotic core progression during statin therapy.


Coronary atherosclerosis in non-culprit lesions was evaluated using virtual histology intravascular ultrasound at baseline and 8 months after statin therapy. One hundred nineteen patients were divided into 2 groups based on necrotic core progression or regression during an 8-month follow-up period.


Patients with necrotic core progression had higher serum lipoprotein(a) [Lp(a)] levels than patients with regression at baseline (16 mg/dL vs. 12 mg/dL, p = 0.02) and at the 8-month follow-up (17 mg/dL vs. 10 mg/dL, p = 0.006). Patients with necrotic core progression had a higher fibro-fatty plaque volume (1.28 mm3/mm vs. 0.73 mm3/mm, p = 0.002), and less necrotic core (0.56 mm3/mm vs. 1.04 mm3/mm, p < 0.0001) and dense calcium (0.35 mm3/mm vs. 0.56 mm3/mm, p = 0.006) plaque volumes at baseline than patients with regression. Multivariate logistic regression analysis showed that Lp(a) was a significant independent predictor associated with necrotic core progression during statin therapy (odds ratio [OR]: 3.514; 95% confidence interval [CI]: 1.338-9.228; p = 0.01).


Serum Lp(a) is independently associated with necrotic core progression in statin-treated patients with angina pectoris.

Lipoprotein (a); Necrotic core; Statin; Virtual histology intravascular ultrasound