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GW24-e1865 Association between cholesterol synthesis/absorption markers and effects of cholesterol lowering by atorvastatin among patients with high risk of coronary heart disease
  1. Yue Qi1,
  2. Jing Liu1,
  3. Changsheng Ma2,
  4. Wei Wang1,
  5. Xiaohui Liu2,
  6. Miao Wang1,
  7. Qiang Lv2,
  8. Jiayi Sun1,
  9. Jun Liu1,
  10. Yan Li1,
  11. Dong Zhao1
  1. 1Department of Epidemiology, Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases
  2. 2Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University

Abstract

Objectives No indices are available to facilitate clinicians to identify patients who need either statin monotherapy or statin-ezetimibe combined treatment. We aimed to test whether cholesterol synthesis and absorption markers can predict the cholesterol-lowering response to statin.

Methods A total of 306 statin naïve patients with high risk of coronary heart disease (CHD) were treated with atorvastatin 20 mg/day for 1 month. Cholesterol synthesis markers (desmosterol and lathosterol), absorption markers (campesterol and sitosterol) and low-density lipoprotein cholesterol (LDL-C) levels were measured before and after treatment. The association of these markers with baseline LDL-C levels and its changes were analysed.

Results Atorvastatin decreased LDL-C by 36.8% (range: decrease of 74.5% to increase of 31.9%). Baseline lathosterol and campesterol levels co-determined baseline LDL-C levels and the effect of atorvastatin treatment. The inhibiting effects of atorvastatin on cholesterol synthesis and related LDL-C lowering were significantly associated with baseline lathosterol levels. However, the effect of atorvastatin treatment on LDL-C was modified bi-directionally by baseline campesterol levels. In patients with the highest baseline campesterol levels, atorvastatin treatment decreased cholesterol absorption by 46.1%, which enhanced the effect of LDL-C lowering. Atorvastatin treatment increased cholesterol absorption by 52.3% in those with the lowest baseline campesterol levels, which attenuated the effect of LDL-C reduction. Those with the highest lathosterol but the lowest campesterol levels at baseline had significantly less LDL-C reduction than those with the same baseline lathosterol levels but the highest campesterol levels (27.3% vs. 42.4%, P = 0.002).

Conclusions Our findings suggest that combined patterns of cholesterol synthesis/absorption markers rather than the single value of each marker are potential predictors of the LDL-C lowering effects of statins in high-risk CHD patients.

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