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Comparative Study
. 2017 Feb 1;24(2):123-132.
doi: 10.5551/jat.32615. Epub 2016 Aug 4.

Enhanced Impact of Cholesterol Absorption Marker on New Atherosclerotic Lesion Progression After Coronary Intervention During Statin Therapy

Kenta Mori  1 , Tatsuro Ishida, Shigeyasu Tsuda, Toshihiko Oshita, Masakazu Shinohara, Tetsuya Hara, Yasuhiro Irino, Ryuji Toh, Ken-Ichi Hirata
Affiliations
Comparative Study

Enhanced Impact of Cholesterol Absorption Marker on New Atherosclerotic Lesion Progression After Coronary Intervention During Statin Therapy

Kenta Mori et al. J Atheroscler Thromb. .

Abstract

Aim: Clinical trials suggest that residual risks remain for coronary artery disease (CAD) during low-density lipoprotein cholesterol (LDL-C) lowering therapy. We aimed to investigate the role of exogenous lipids in the prognosis of CAD after percutaneous coronary intervention (PCI).

Methods: A total of 145 patients with CAD, who underwent elective PCI, and 82 non-CAD (control) patients were enrolled in this study. CAD patients underwent follow-up coronary angiography 6-9 months after PCI, and were classified into three groups: 1) patients who showed in-stent restenosis (ISR) in the original stented segment, 2) patients with other non-target coronary atherosclerotic lesions (de novo), and 3) patients with neither ISR nor a de novo lesion. Biochemical analyses were performed on fasting serum samples at the time of follow-up coronary angiography.

Results: Despite the controlled serum LDL-C levels, CAD patients with statin showed elevated cholesterol absorption marker campesterol/total cholesterol (TC), synthesis marker lathosterol/TC, campesterol/lathosterol ratio, and apolipoprotein B48 (apoB48) concentration compared with non-CAD patients. The high campesterol/TC, campesterol/lathosterol ratio, and apoB48 concentration were associated with de novo lesion progression after PCI. In stepwise multivariate logistic regression analysis, campesterol/TC and apoB48 concentrations were independent risk factors for de novo lesion progression in statin-treated CAD patients after PCI.

Conclusion: The increase of cholesterol absorption marker and apoB48 concentration may lead to the progression of de novo lesions, and these markers may represent a residual risk during statin treatment after PCI.

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Conflict of interest statement

COI Tatsuro Ishida has received lecture honoraria from MSD, and Mochida Pharmaceutical. Ken-ichi Hirata has received resarch funds from Acterion Pharmaceuticals Japan, Sysmex, GlaxoSmithKline, Dai-ichi Sankyo, Japan Medtronics, St. Jude Medical Japan, Sumitomo Dainippon Pharma, Takeda Pharmaceutical, Nippon Boehringer Ingelheim, Boston Scientific Japan, Bristol-Myers Squibb, Mochida Pharmaceutical, FUJI-FILM RI Pharma, Nihon Medi-Physics, Bayer Yakuhin, Astellas Pharma, Eizai, MSD, Kaneka Medix, Novartis Pharma, and Otsuka Pharmaceutical, and lecture honoraria from MSD, AstraZeneca, Takeda Pharmaceutical, Pfizer, Dai-ichi Sankyo, Mochida Pharmaceutical, Kowa Pharmaceutical, and Japanese Society of Internal Medicine. The other authors report no conflicts of interest.

Figures

Fig. 1.
Fig. 1.
Cholesterol absorption and synthesis markers in CAD patients with or without statin During statin therapy, compared with the non-CAD patients, cholesterol absorption marker (campesterol/TC, a) was significantly increased in CAD patients. Cholesterol synthesis marker (lathosterol/TC, b) was decreased in the patients with statin therapy compared with the patients without statin, whereas in he statin (+) group, it was still higher in patients with CAD than in those without CAD. The campesterol/lathosterol ratio (c) was higher in patients with CAD than in corresponding patients without CAD, with and without statin therapy. CAD, coronary artery disease and TC, total cholesterol. p values were calculated using t-test unpaired.
Fig. 2.
Fig. 2.
Impact of cholesterol absorption and synthesis markers on CAD prognosis Cholesterol absorption marker (campesterol/TC, a) and campesterol/lathosterol ratio (c) was higher in CAD patients with de novo lesion progression after coronary intervention than in patients with in-stent restenosis (ISR) or no lesion. Cholesterol synthesis marker (lathosterol/TC, b) was similar in the three groups. Abbreviations similar to those in Fig. 1. p values were calculated using one-way ANOVA in the three groups. We adjusted significance levels by Bonferroni correction in multiple comparison tests.
See this image and copyright information in PMC

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